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Hekmat, A.;  Saso, L.;  Lather, V.;  Pandita, D.;  Kostova, I.;  Saboury, A.A. Nanomaterials of Group XIV Elements in Breast Cancer. Encyclopedia. Available online: https://encyclopedia.pub/entry/38487 (accessed on 15 December 2025).
Hekmat A,  Saso L,  Lather V,  Pandita D,  Kostova I,  Saboury AA. Nanomaterials of Group XIV Elements in Breast Cancer. Encyclopedia. Available at: https://encyclopedia.pub/entry/38487. Accessed December 15, 2025.
Hekmat, Azadeh, Luciano Saso, Viney Lather, Deepti Pandita, Irena Kostova, Ali Akbar Saboury. "Nanomaterials of Group XIV Elements in Breast Cancer" Encyclopedia, https://encyclopedia.pub/entry/38487 (accessed December 15, 2025).
Hekmat, A.,  Saso, L.,  Lather, V.,  Pandita, D.,  Kostova, I., & Saboury, A.A. (2022, December 10). Nanomaterials of Group XIV Elements in Breast Cancer. In Encyclopedia. https://encyclopedia.pub/entry/38487
Hekmat, Azadeh, et al. "Nanomaterials of Group XIV Elements in Breast Cancer." Encyclopedia. Web. 10 December, 2022.
Nanomaterials of Group XIV Elements in Breast Cancer
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This entry is adapted from the peer-reviewed paper 10.3390/pharmaceutics14122640

Breast cancer is one of the most common malignancies and a leading cause of cancer-related mortality among women worldwide. The elements of group XIV in the periodic table exhibit a wide range of chemical manners. There have been remarkable developments in the field of nanobiomedical research, especially in the application of engineered nanomaterials in biomedical applications.

group XIV breast cancer nanopharmaceuticals graphene nanomaterials

1. Breast Cancer Subtypes

Breast cancer is a heterogeneous disease with various subtypes and diverse biological characteristics that lead to different responses to clinical treatments. More than 75% of breast cancers are positive for estrogen receptors (ER) and/or progesterone receptors (PR). The ER-positive tumors express genes that encode typical proteins of luminal epithelial cells; therefore, they are named the luminal group. According to the combined data set, two main luminal-like subclasses were identified: luminal A and luminal B [1]. The other subtypes of breast cancer are HER2-positive, claudin-low, and basal-like (triple-negative) subtypes.
Luminal A tumors are marked by a high level of ER (ER-positive) and/or PR (PR-positive), a low level of Ki67 (proliferating cell nuclear antigen) index, as well as negative human epidermal growth factor receptor-2 (HER2) expression. They are also characterized by the expression of luminal epithelial cytokeratins (CK) 18 and 8 and other luminal-associated markers. The luminal A subtype represents about 50–60% of all breast cancers and commonly has a low degree of nuclear pleomorphism, low mitotic activity, and low histological grade. Of the five major subtypes, luminal A tumors possess a good prognosis (chance of survival) and relatively low recurrence rates [1].
Luminal B tumors tend to be ER-positive; however, they can be HER2-negative or HER2-positive. Luminal B tumors are marked by a high level of growth receptor signaling genes. Compared to the luminal A subtype, this subtype has a higher histological grade, more aggressive phenotype, worse prognosis, higher level of proliferation-related gene expression, higher recurrence rate, and lower survival rates after relapse. The luminal B subtype represents about 15–20% of all breast cancers [1][2].
The HER2-enriched subtype is characterized by a high level of HER2 and other genes associated with the HER2 pathway and/or HER2 amplicon expression. HER2 is a one of a family of four membrane tyrosine kinases. The HER2 receptor (a proto-oncogene mapped in chromosome 17q21) is encoded by the HER2 gene. Approximately half of the HER2-enriched breast cancers are positive for ER, although they generally express a lower level of ER. HER2-enriched tumors represent about 15–20% of all breast cancers. This subtype has about 40% p53 mutations, high histological and nuclear grade, and a high degree of proliferative activity. In the absence of treatment, HER2-enriched tumors have a poor prognosis [1][2][3].
Basal-like subtype tumors express high levels of basal myoepithelial markers but do not express HER2, PR, and ER; consequently, they are referred to as triple-negative [4]. Basal-like tumors are marked by aggressive clinical behavior, a high rate of metastasis to the lung and brain, high proliferative indices and mitosis, the presence of central necrotic or fibrotic zones, and poor tubule formation. Tumors belonging to this subtype overexpress epidermal growth factor receptor (EGFR), alpha-beta crystallin, caveolins 1 and 2, fascin, and P-cadherin. Patients with basal-like tumors have poor clinical outcomes. It is crucial to explain that there is an 80% overlap between the intrinsic basal-like and triple-negative subtypes. The basal-like subtype is defined through gene expression microarray analysis; nevertheless, the term triple-negative belongs to the immunohistochemical classification of breast cancers lacking HER2, PR, and ER protein expression [1][2].
Claudin-low tumors are described by a low level of expression of genes involved in cell–cell adhesions and tight junctions (including E cadherin, occluding, and claudins 3, 4, and 7), a high level of epithelial to mesenchymal transition gene expression, and zero level of HER2, PR, and ER expression. it has been confirmed that patients with claudin-low tumors have poor clinical outcomes [1][2].
According to current studies, each subtype has a different treatment response. Since ER is a therapeutic target, the luminal A and luminal B subtypes can be treated with hormone therapy. The HER2-enriched tumors are potential candidates for trastuzumab therapy. However, basal-like tumors are not easy to treat and regularly have a poor prognosis [2].

2. Silisium (Silicon)-Based Nanomaterials

Silisium is well known as the earth crust’s second-most abundant element, behind oxygen, supplying low-cost and rich resource support for numerous silicon-based applications. By virtue of its outstanding mechanical and semiconductor properties, silisium materials dominate the electronics industry and act as the prominent semiconductor materials to date. [5]. To date, silicon materials of numerous nanostructures (nanodots, nanoparticles, nanorods, nanoribbons, and nanowires) have been manipulated. Silicon nanoparticles (SiNPs) and silicon nanowires (SiNWs) are identified as the most significant zero- and one-dimensional silicon nanostructures, respectively. Consistently, SiNPs are utilized in pharmaceutical technology. Conversely, SiNWs could serve as a platform for SERS studies [6]. In a recent study, the organotin(IV) complex and chlorambucil (two different cytotoxic agents) were loaded on fibrous silica NPs and then decorated with folic acid and Alexa Fluor 647. The study demonstrated enhanced cytotoxicity of two chemotherapeutic agents against MDA-MB-231 cells as well as a higher cell migration inhibition [7]. A successful encapsulation of breast cancer-specific gene 1-small interference RNA (BCSG1-siRNA) in chitosan-silicon dioxide NPs was reported by CUI et al. The authors observed the cytotoxic effect of chitosan-silicon dioxide/BCSG1-siRNA NPs on the growth of MCF-7 cells. They observed that the designed BCSG1-siRNA plasmid could selectivity and significantly downregulate BCSG1 gene expression. Thus, their nanomaterials demonstrated considerable antitumor influences in breast cancer cells [8].
Usually, three types of Si-based nanomaterials can be utilized in nanopharmaceutical research: mesoporous SiNPs (MSNs), periodic mesoporous SiNPs (PMONPs), and porous SiNPs (pSiNPs). Recently, MSNs were proposed as imaging or drug delivery agents [9]. MSNs have a well-defined internal mesoporous structure (2–10 nm diameter) and a large pore volume (0.6−1 cm3/g). The shape, surface, and pore sizes of MSNs can be custom designed, offering several unique possibilities for the loading of antitumor agents. Many studies examined the cytotoxicity of MSNs loaded with DOX; for instance, the anticancer effects of DOX-MSNs@hyaluronic acid-gelatin-PEG on MDA-MB-231 cells by upregulation of the MMP-2 mechanism [10], niclosamide-DOX-COOH-Chi-MSNs on MDA-MB-231, SK-BR-3, and MCF-7 cells by inhibition of Wnt/β-catenin signaling mechanism [11], and MSN-siRNA/Aptamer@DOX on MDA-MB-231 cells by downregulation of TIE2 (tyrosine kinase with immunoglobulin-like and EGF-like domains 1) mechanism [12] have been reported. In addition, the antiproliferative effects of MSNs loaded with other anticancer agents have been studied. Konoplyannikov et al. prepared MSNs loaded with salinomycin and showed that this nanomaterial has a major cytotoxic effect on MCF-7/MDR1 cells (breast cancer and multidrug-resistant cells). Thus, their work revealed that salinomycin-loaded MSNs could be utilized for moderate chemotherapy of both primary cancer tumors and metastasis [13]. In a more recent study, Mohan Viswanathan et al. observed that prepared gallium nitrate and curcumin complex loaded on MSNs (GaC-HMSNAP) could significantly reduce the growth of MCF-7 cells by increasing PARP (Poly (ADP-ribose) polymerase), GSK 3β(S9), cleaved caspase-6, caspase-9, and caspase-6 expression. Furthermore, GaC-HMSNAP reduced mitochondrial proteins; for example, SOD1 (superoxide dismutase 1), HSP60 (heat shock protein 60), and prohibitin1. Consequently, their results showed that GaC-HMNSAP could provoke cell death through the mitochondrial intrinsic cell death pathway [14].
pSiNPs could also offer a platform for the vectorization of anticancer agents, especially hydrophobic agents, into the pores. Landgraf et al. loaded camptothecin (a highly cytotoxic chemotherapeutic compound) into pSiNP (160 nm) that was conjugated with EGFR-targeting antibody cetuximab. The authors revealed that the CPT-pSiNP-anti-EGFR decreased the growth of MDA-MB-231BO cells, increased survival rate, reduced primary tumor growth, and decreased metastases in a mouse model [15].
Consequently, most of the reported cases revealed that silica-based nanomaterials could be utilized in breast cancer therapy and combination therapy. Thus, developing simpler methods to synthesize silica-based nanomaterials is a high priority, as is enhancing their cancer- targeting abilities. Furthermore, the existing research about silica-based nanomaterials’ combination therapies is immature. Surely, chemotherapy-based nanosystems applying silica-based nanomaterials have a brilliant adaptable future and excellent potential for clinical translation.

3. Germanium-Based Nanomaterials

Germanium (Ge) is a metalloid with a semiconductor feature and is nonessential for human health. Ge exists in plants, animals, and soil as a natural compound. Ge possesses a diversity of interesting properties, for instance, narrow bandgap, high charge carrier mobility, high refractive index, and high ion intercalation capacity. Organic Ge and its compounds have the potential to enter the human body through the respiratory tract, digestive tract, skin, blood circulation system, and other ways. In October 2003, the FDA rejected adding organic germanium to human supplements because it had caused nephrotoxicity (kidney damage) and death in humans, even when people were healthy. The American Cancer Society also determined that organic Ge and its compounds have the potential to interfere with drugs and consequently are harmful to humans. It further warned that the usage of organic Ge alone could have serious health consequences for conventional cancer care [16][17][18].
Studies into the use of Ge nanomaterials in biological applications have been neglected. Ma et al. showed that water-soluble GeNPs (less than 10 nm) have high toxicity to cells. These GeNPs initiated cell necrosis by elevating intracellular calcium concentration, which increases ROS levels [19]. Hence, the intrinsic poor biodegradation of most Ge nanomaterials may prevent their further in vivo applications and clinical translation in biomedicine. However, there have been few reports available on Ge nanomaterials’ application in biology. Amongst these studies, one includes the study of Bezuidenhout et al., who revealed that there are no adverse cytotoxic effects of self-seeded Ge nanowires on L929 (murine aneuploid fibrosarcoma) and MCF-7 cells [20]. In 2016, McVey et al. compared the synthetic protocols of Si and Ge nanocrystals (NCs). They found that Si and Ge NCs possess low toxicity, so they could be used in biomedical applications [21]. In 2021, Ge et al. also synthesized a novel type of 2-D germanene nanosheets (GeH NSs) with excellent oxidative biodegradability, which has excellent degradability and biocompatibility [22]. Accordingly, Ge-based nanostructures have received considerably less attention, probably owing to their complex chemistry and the lack of convenient/predictable methods for their preparation.

4. Tin-Based Nanomaterials

According to archaeological reports, people from ancient civilizations began utilizing bronze (an alloy that mostly contains tin and copper) for the design of durable and harder weapons and tools. Therefore, the earliest manipulation of tin (Sn) is during the bronze age. Today, tin is utilized for the manufacture of tin cans for the canning of processed food [23]. The oxide form of tin is the common form of tin. Sn(II)O (stannous oxide) and Sn(IV)O2 (stannic oxide) are the two primary oxides of tin. Tin oxide (SnO2) is a critical metal oxide semiconductor with a stable n-type wide bandgap (3.6 eV at 300 K). SnO2 belongs to the category of surface-sensitive materials, i.e., when molecules get adsorbed on the surface, charge transfer between the frontier orbitals of the adsorbates and the support surface may occur. Diverse morphologies of low-dimensional SnO2 nanostructure have been described as 0-D NPs, 1-D nanorods, nanobelts, nanowires, nanotubes, and 2-D nanosheets. Furthermore, recently, three-dimensional (3-D) hierarchical architecture has also been reported by a few researchers. Moreover, the doping of SnO2-based nanomaterials offers a convenient way to tailor their electrical, structural, and optical properties [24]. SnO2 has been employed extensively in various fields, including chemical sensors, environmental monitoring, solar cells, catalysis, and leakage detection [25]. However, despite their widespread use in many fields, in vitro molecular studies evaluating the safety/toxicity issues of SnO2 nanomaterials are limited. In 1929, the earliest experiments on the cytotoxicity of Sn compounds against mouse cancer were performed. Some 40 years later, various Sn(IV) compounds were surveyed for their in vivo antitumor activity against some cancer cells in mice. However, many of them were found to be inactive against other solid tumor cells [26]. Between 2016 and 2021, several articles were published on the effects of Sn NPs on breast cancer cells. For example, Guo et al. demonstrated that SnO2 NPs (30 nm) can prevent the proliferation of MCF-7 cells with mitigation of mitochondrial membrane potential, deactivation of catalase and superoxide dismutase activity, downregulation of p-PI3K/p-AKT/p-mTOR, and overexpression of the Bax/Bcl-2 signaling pathway [27]. Ahamed et al. observed the same results when they explored the effects of SnO2 NPs (21 nm) in MCF-7 cells. They reported that SnO2 NPs can induce toxicity in MCF-7 cells via oxidative stress [28]. The anticancer effects of SnO2 NPs (40 nm) extracted from Rheum emodi root on MDA-MB-231 cells were also examined and the potential cytotoxic effects of these NPs were proved [29]. In another study, undoped SnO2 and cobalt-doped NPs were biosynthesized and the significant in vitro anticancer and antioxidant effect of these NPs on MCF-7 cells was demonstrated [30]. Zhai et al. showed that the green synthesized SnNPs (18.13 nm) could induce cytotoxicity in MCF-10, MCF-7, and Hs 319.T (breast infiltrating ductal cell carcinoma) [31]. There is a great potential for Sn nanomaterials and future investigations about Sn on the nanoscale could provide some more encouraging results in drug delivery systems. It is anticipated that Sn NPs would give rise to the design of better antitumor agents with improved specificity.

5. Lead-Based Nanomaterials

Throughout cell evolution, about 24 (biogenic) metal species have been selected and assigned biological functions based on their intrinsic physicochemical properties and bioavailability. The most frequently found biogenic metal ions are Na+, K +, Mg 2+, Ca2+, Zn2+, Mn2+, Fe2+/3+, Co2+/3+, Ni 2+, and Cu+/2+, which play vital roles in a multitude of essential tasks such as protein structure stabilization, enzyme catalysis, blood coagulation, signal transduction, muscle contraction, hormone secretion, taste and pain sensation, respiration, and photosynthesis. Other abiogenic/xenobiotic metal species, e.g., Hg2+, Pb2+, Al3+, or Tl+/Tl3+, upon entering organisms lacking efficient defensive mechanisms against such intruders, can adversely impact the cellular processes by competing with the native cations in various proteins.
Lead (Pb2+), with an unknown biological function in higher organisms, is commonly found in soil and water at concentrations ∼1000-fold higher than its natural levels, a consequence of utilizing leaded fuel, lead-containing water pipes, and leaded paint. This metal has harmful impacts on human health, as manifested through severe neurological, cardiovascular, reproductive, renal, endocrine, hematological, and/or immune dysfunctions. This is mainly because lead is a potent neurotoxin that interferes with signaling cascades in the brain, causing cognitive and psychiatric disorders [32]. Due to its strong toxicity, several government agencies have set strict regulations on the maximum permitted Pb levels. For instance, the maximum Pb concentration in drinking water defined by the World Health Organization (WHO) is 0.01 mg L−1 (48 nM) [33][34][35]. Some reports have indicated that high levels of heavy metals (lead, selenium, mercury, and cadmium) can accumulate in cancerous breasts and their presence can be one of the causes of cancer initiation [36]. Pb can activate estrogen receptor α (ERα) to direct the estrogen target genes’ expression and breast cancer cell reproduction [36]. There is only limited information about lead oxide nanoparticles (PbONPs) regarding their toxicological impacts [37]. Thus, although experiments on the mechanism concerning pb-based nanomaterials in breast cancer are limited, it seems that pb nanomaterials can induce oxidative stress in cells [37]. Collectively, although a few articles showed the biocompatibility of their synthesized Pb NPs [38], there are no articles to date about the effects of nanolead on the growth of breast cancer cells.

6. Mechanisms of Cell Death

Before nanomaterials (herein the elements of G14 nanomaterials) reach the outer membranes of tumor cells, they should interact with the microenvironment around the tumor cells [39]. The microenvironment, such as extracellular matrix and fibrosis, can alter the properties of nanomaterials and modify their interactions with the cell membrane and their intracellular fate [39]. Furthermore, the zone of nanomaterial–cell interactions can be influenced by the interplay of several microenvironmental factors, including MMPs, prostaglandins, vascular endothelial growth factor (VEGF), and bradykinin [40]. The pH of the tumor microenvironment can also alter the nanomaterial–cell interactions and the entry of nanomaterials [41]. Once nanomaterials reach the exterior membrane of a tumor cell, they can interact with the extracellular matrix or components of the plasma membrane and enter the cell. It has been demonstrated that nanomaterials can enter the tumor cell mainly through endocytosis pathways [42]. The five main mechanisms of endocytosis by which nanomaterials can enter cells are phagocytosis, caveolin-mediated endocytosis, clathrin-mediated endocytosis, macropinocytosis, and clathrin/caveolae-independent endocytosis. Other entry mechanisms are direct microinjection, disruption of the cell membrane, hole formation, and passive diffusion [40][42]. It should be noted that the physicochemical properties of nanomaterials, such as shape, size, surface charge, hydrophobicity, and surface functionality, can affect their cellular uptake [40].
Intracellular trafficking of nanomaterials has a crucial role in the cellular fate of nanomaterials and their therapeutic efficacy. After the entry of nanomaterials into tumor cells via endocytic vesicles, generally, their fate is determined by the intracellular trafficking/sorting mechanisms, mostly mediated by a network of cellular endosomes in conjunction with the lysosomes, endoplasmic reticulum (ER), and Golgi apparatus [43]. Several hidden factors affect the cellular trafficking of nanomaterials, including protein corona and cell vision. The set of proteins that bind to the surface of the nanomaterial is referred to as the protein corona, i.e., what cells “see” is corona-coated nanomaterials rather than their pristine surfaces [43]. Cell vision indicates the behaviors/mechanisms that each cell can employ in response to nanomaterials [44]. These two issues can alter the intracellular trafficking of nanomaterials.

6.1. Most Common Mechanisms of Cell Death Induced by Nanomaterials

When nanomaterials enter tumor cells could interfere with cell components, for instance, mitochondria, and generate damage affecting their functions. In response to stress, mitochondria can produce ROS [45]. Thus, following exposure to nanomaterials, the intracellular generation of ROS can rapidly and sharply increase. ROS are chemically reactive particles that contain oxygen, including hydroxyl radicals (•OH), reactive superoxide anion radicals (O2−), and hydrogen peroxide (H2O2) [46]. The excess ROS induced by nanomaterials can affect the organelles and biomolecules (DNA/RNA, lipids, and protein) structures of tumor cells, which causes cell death [45][47][48]. Furthermore, overburdened ROS can initiate further irreversible cell damage such as the inactivation of cell receptors, the leakage of the organelles’ contents, cell cycle arrest, and the rupturing of the membranes of organelles [49][50]. It has been shown that during mitosis, nanomaterials could interact with chromosomes and cause breaks into chromosomes or disturb the process of mitosis, by chemical binding or mechanically. Nanomaterials could also bind or interact with DNA molecules during interphase and cause a variety of DNA strand breakages and DNA damage. They also can influence DNA replication and transcription of DNA into RNA [45].
Nanomaterials can also target signaling pathways and control cell capacities. All distinctive features of cancer cells are mediated through signaling pathways that have become deregulated. Currently, 12 signaling pathways that perform a vital function in cancer growth have been recognized, including RAS, cell cycle apoptosis, Notch, Hedgehog signaling (HH), transcriptional regulation, APC, signal transducers and activators of transcription (STAT), DNA damage control, transforming growth factor-beta (TGF-β), a mitogen-activated protein kinase (MAPK), phosphatidylinositol-3 kinase (PI3K), and chromatin modification [51][52]. Among these pathways, the relationship between kinase pathways and cancer has attracted the attention of several scientists. Thus, several nanomaterial-based inhibitors were designed for various families of kinases, for instance, the mTOR, receptor tyrosine kinases (RTKs), MAPK, and PI3K. The RTKs’ signaling cascades affect the motility of cells, mitogenesis, cell survival and differentiation, as well as gene expression [52][53]. One of the highly important RTK subfamilies in cancer is the ErbB or EGFR family. Three major intracellular signaling cascades stimulated by EGFR activation include the MAPK pathway, the PI3K pathway, and the antiapoptotic Akt/protein kinase B (PKB) pathway [52]. The activity of PI3K is crucial for cellular responses to malignant transformation and growth factors. The PI3K/mTOR network has detected actionable target proteins in breast cancers. mTOR refers to two protein complexes, mTORC1, and mTORC2, that have a fundamental role in integrating signals from nutrients and growth factors to monitor metabolism, cell cycle progression, and protein synthesis [54].

6.2. Mechanism of Cell Death Induced by Carbon-Based Nanomaterials

It has been reported that carbon-based nanomaterials can enter the cell, usually by adhesive interactions, and are found free in the cytoplasm; i.e., this group of nanomaterials has the potential to interact directly with the cytoskeleton to influence mechanotransduction. As a typical example, graphene-based nanomaterials have a great affinity with the cellular membrane [55]. It has been confirmed that the van der Waals interaction and hydrophobic interaction are the main driving force in GO–membrane contact [56]. The extraction of phospholipids through this interaction could induce serious membrane damage and even cell death. It should be noted that any modification on the surface of graphene-family nanomaterials could change their cellular uptake; for example, positively charged graphene sheets could enter MCF7 cells by receptor-mediated endocytosis and phagocytosis [57]. When graphene-family nanomaterials pass through the cell membranes of breast cancer, cell death is initiated by various mechanisms. One of the toxicological processes proposed for numerous graphene-based nanomaterials is ROS generation [58][59]. Graphene-based nanomaterials can also enter the nucleus and directly interact with DNA, mainly through π–π stacking and hydrogen bonding, causing DNA distortion and even DNA cleavage [60]. The large GQDs have a tendency to stick to the ends of the DNA molecule, causing the DNA to unfold; however, the small GQDs easily enter the DNA molecule, leading to DNA base mismatch [61]. Based on recent research, rGO could induce apoptosis in breast cancer cells by mitochondrial membrane potential reduction, deregulation of mitochondrial proteins, activation of caspase-9 and caspase-3, cell cycle arrest, and deregulated P21 expression. rGO also caused autophagy in breast cancer cells [62]. Graphene-based nanomaterials could also affect the cell signaling pathways. GQDs could downregulate the expressions of P-glycoprotein, multidrug resistance protein 1 (MRP1) [63]. It has been reported that the synthesized nanocomposite consisting of rGO incorporated with Cu (rGO-Cu) could downregulate MMP-9, cathepsin D, and Bcl-2 gene expression and upregulate P53 gene expression [64]. In breast cancer, MMP9 and cathepsin D are involved in cell invasion and metastasis through the hydrolysis of fibronectin, proteoglycans, and collagens by their lysosomal aspartic protease activity [65]. The Bcl-2 protein family can regulate the permeability of the mitochondrial inner membrane and also can mitigate the induction of apoptosis, whereas Bax causes permeability of the outside mitochondrial membrane, which releases soluble proteins into the cytosol, where they stimulate the activation of caspase [66].
The literature review showed that few surveys had been conducted to assess the mechanisms of cell death induced by CNTs in breast cancer. Recent studies revealed CNTs utilize either an endocytic pathway or passive diffusion to penetrate through cellular membranes [67]. Endocytosis is also the proposed mechanism for translocating CQDs and NDs into breast cancer cells. Nevertheless, some research demonstrated this process can be carried out through non-endocytic pathways; thus, the internalization mechanism theory for these nanomaterials still needs more investigation [68]. Based on recent studies NDs (0-D) and CNTs (1-D) show higher uptake rates than sheet-like GO (2-D). Thus, there is a positive relationship between shape, size, and surface modifications of carbon-based nanomaterials and cellular uptake. Prior studies have illustrated that when CNTs pass through cells, they can initiate cell death by downregulation of Bcl-2 and upregulation of Bax [69], mitochondria damage (induced by SWCNTs), and membrane integrity (induced by MWCNTs) [70]. It has been demonstrated that the mechanism of CNTs in cells could be related to the purity, size, fabrication route, length, structure, surface chemistry, and concentration of CNTs. Based on recent research, CQDs could induce apoptosis in breast cancer cells by cell cycle arrest in the G0/G1 phase, DNA damage [71], ROS generation, LDH release [72], and activation of caspase-3 [72][73]. Collectively, the mechanism of cell death induced by carbon-based nanomaterials in cancerous cells is different. As an example, compared with GO and NDs, CNTs induce a dramatic release of LDH owing to their needle-like structure, which could be more mobile and can more easily penetrate the cell membrane, causing greater cell membrane damage. Furthermore, CNTs and GO induce a high level of ROS. In contrast, NDs show the ability to scavenge ROS [74]. It should also be mentioned that carbon-based nanomaterials tend to interact with a variety of proteins in biological fluids, forming a protein corona on the surface of nanomaterials. Thus, the interaction of carbon-based nanomaterials with proteins can affect the cellular uptake and mechanism of cell death.

6.3. Mechanism of Cell Death Induced by Silisium-Based Nanomaterials

Recently, by utilizing the pharmacological inhibitors of major endocytic pathways, the uptake mechanisms of SiNPs in MCF-7 cells were demonstrated. The results proved that the uptake of SiNPs, especially amino-functionalized SiNPs, is strongly affected by actin depolymerization. Thus, F-actin plays a crucial role in the process of internalization of SiNPs. More importantly, positively charged SiNPs have higher cell uptake than negatively charged SiNPs, which is crucial in designing drug carriers that can cross the mucosal barriers and enable a noninvasive delivery of biological therapeutics [75]. It has also been shown that when nano-SiO2 passes through the cell membranes of breast cancer, it can downregulate EGFR, proto-oncogene c-Src, and signal transducer and activator of STAT3 phosphorylation. Furthermore, nano-SiO2 could reduce the expression of survivin, cyclins, fibronectin, and focal adhesion kinase (FAK). Thus, it could be proposed that nano-SiO2 could induce apoptosis in breast cancer cells by disruption of EGFR dimerization, modulation of downstream signaling cascades, and disruption of cellular adhesion, migration, and invasion [76]. Results of other investigations also indicate that mesoporous silica-based nanomaterials (<100 nm diameter) could not disorganize the actin filaments in the cytoskeleton; nevertheless, rod-shaped MSNs could disorganize and disrupt the actin filaments with poorly formed filament bundles in the area near the cell membrane and at the edges of lamellipodia and filopodia [77]. Such cytoskeleton destruction causes higher cellular penetration of rod-shaped MSNs, leading to more serious damage to the cytoskeleton. It should be noted that since MSNs demonstrate tunable pore size, porous interior, and large surface area, they could act as an excellent reservoir for various drug molecules and other pharmaceutical materials of interest. Various targeting moieties have been also utilized on the surface of MSNs, for example, targeting folate receptor, transferrin receptor, VEGF receptor, mannose receptor, HER2 receptor, and c-type lectin receptor [78]. However, in terms of the biological point of view, the clinical application of MSNs is limited, owing to the rapid clearance of nanoparticles by immune and excretory systems after administration. Another limitation of using MSNs in clinical applications is that upon administration of MSNs in the body and exposure to blood, protein corona could form on the surface of the MSNs, which can eventually block the pores and reduce the release of drugs from the pores of MSNs. Therefore, the detailed in vivo analysis of pharmacokinetic and pharmacodynamic experiments, possible immunogenicity, and rigorous biodistribution of MSN-based systems ought to be utilized before aiming to translate clinically [79].

6.4. Mechanism of Cell Death Induced by Tin-Based Nanomaterials

The results of published articles indicate that when Sn-based nanomaterials (SnO2 NPs or SnNPs) pass through the cell membranes, cell death is initiated by several mechanisms. One of the toxicological processes proposed is ROS generation [27][28][30]. Sn-based nanomaterials could also induce apoptosis in breast cancer cells by mitigation of mitochondrial membrane potential, deactivation of catalase and superoxide dismutase activity, downregulation of PI3K/AKT/mTOR, overexpression of Bax/Bcl-2 signaling pathway [27], LDH leakage, as well as by the accumulation of cells in the sub-G1 phase [28]. Consequently, it could be speculated that Sn-based nanomaterials hinder the expression of cytokines or signaling transduction pathways based on activating PI3K, which could mitigate the downstream AKT kinase function and relevant reactions stimulated by AKT. Inactivation of the PI3K/AKT/mTOR pathway leads to overexpression of proteins, including Bax, and down-expression of Bcl-2, and finally leads to apoptosis [27][52].

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Subjects: Oncology
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