BC is one of the most well-known cancer types, having various pathological subtypes and clinical outcomes. BC may be caused by a mutation that results from the aging process and risk factors associated with a healthy lifestyle [27]. The most promising strategy for cancer treatment is to disrupt the three phases of carcinogenesis—initiation, promotion, and progression—and alter the carcinogenesis signaling pathways [4]. BC treatment may be quite successful, mainly when the illness is detected early and has a favorable prognosis (Figure 2) [28,29].

Cancer develops through a series of molecular processes, namely mutations in DNA molecules that code for proteins that initiate cell division, proliferation, and growth. As a result, damage to DNA or proteins that regulate the cell cycle can result in uncontrolled cell division and proliferation, referred to as cancer. Cancer causes dysregulation of apoptosis, proliferation, angiogenesis, and metastasis [4].

BC is molecularly classified into estrogen receptor (ER) and progesterone receptor (PR) expression and human epidermal growth factor receptor (HER2) amplification [4]. Approximately 60–70% of early BC patients are hormone-sensitive, showing positive estrogen receptor (ER+), positive progesterone receptor (PR+), or both. About 15–20% of BC patients exhibit a triple-negative phenotype due to the absence of ER, PR, and HER2 amplification. Approximately 20% of BC cases show HER2 overexpression, resulting in aggressive disease and reduced survival [36,37].

BRCA1 is a human tumor-suppressor gene responsible for repairing damaged DNA or destroying cells if the DNA cannot be repaired. BC 1 (BCA1) and BC 2 (BCA2) are essential for genome stability. Mutations in genes give the risk of BC up to 15–20 times [38,39,40].

The tumor suppressor TP53 gene encodes the protein p53, which regulates the cell cycle, induces apoptosis, maintains genome integrity, and prevents tumor development. Mutations in the TP53 gene increase the risk of BC [4]. When stress occurs, phosphorylation of p53 interferes with binding to protein MDM2, resulting in p53 accumulation and subsequent transcription of several genes, including the gene encoding the protein cyclin-dependent kinase inhibitor (CKI) p21. P21 interacts with and inactivates the G1/S-Cdk complex, reprogramming cells to G1 for DNA repair [41,42].

BC treatment protects genomic stability by avoiding DNA damage, delaying the cell cycle or inducing apoptotic cell death, and influencing aberrant cell proliferation pathways [4]. Chemotherapy can inactivate normal cell p53 and induce apoptosis in regularly developing cells/tissues, such as bone marrow, lymphoid organs, hair follicles, and small intestinal epithelium [2,43,44].

Overexpression of MDR1 is one of the main reasons for multidrug resistance to chemotherapeutic drugs [45]. The expression of P-glycoprotein encoded by the multidrug resistance (MDR1) gene is associated with the emergence of the MDR phenotype in cancer cells [46]. P-glycoprotein (P-gp) is a well-identified membrane transporter with the capability to efflux drug molecules out of the cancer cell, leading to the reduced efficiency of chemotherapy [47]. MDR mechanisms fall into different categories: (1) enhance the efflux of drugs across membrane carriers, using ATP binding cassette (ABC) carriers as major carriers; (2) diminished uptake of drugs via influx carriers, such as solvent carriers; (3) enhanced metabolic drugs, including the removal of S-transferase glutathione and P450 cytochrome enzyme; and (4) inhibiting of apoptotic pathways [48,49,50,51].

Cytotoxicity refers to a poisonous agent’s toxic effect on cells. Cytotoxic agents inhibit cell growth and can occasionally result in cell death [52]. Exposure of cells to cytotoxic substances can result in various cell-death consequences [53,54,55]. Following that, cells may initiate a program of programmed cell death (apoptosis) or necrosis [56,57]. Cells that undergo fast necrosis in vitro lack the time and energy necessary to activate apoptotic pathways and do not exhibit apoptotic markers. Secondary necrosis occurs when apoptotic cells in culture experience apoptosis [58]. The causes of cytotoxicity are divided into the following: (1) Chemical cytotoxic agents—the primary goal for cytotoxic drugs, or cytostatic agents, is to prevent the growth of cancer cells, often accomplished by targeting processes that directly disrupt DNA replication or transcription interfering with critical cell processes during mitosis [59]. (2) Biological cytotoxic agents—biological cytotoxic agents are commonly defined as harmful compounds produced from viruses, bacteria, fungus, plants, or animals. The most well-known compounds in this category are bacterial endo-/exotoxins and antibiotics [58,60]. (3) Physical cytotoxic agents—heat, ultrasonic vibrations, and radiation are all examples of physical agents that are cytotoxic. It has been discovered that using ultrasonic microbubbles enhances the cytotoxicity of chemotherapy medicines on tumor cells. Numerous research studies on radiation’s cytotoxicity may be found in the literature [59].

Cell death is a type of cellular suicide that is regulated by an intracellular program and acts as an innate method to maintain the balance of cell survival. In humans, cells undergo three stages of aging, namely (1) proliferation for a certain number of cycles; (2) loss of replicative ability, and then inactivity for a certain period of time; and (3) then they dying and death [61]. Many stimuli cause cell death, and the mode of cell death will follow one of two general patterns. The first is necrosis; oncotic necrosis is most often the result of a severe metabolic disorder and is characterized by cellular swelling, leading to the rupture of the plasma membrane with the release of intracellular contents. The second pattern is apoptosis, a form of programmed cell death. Apoptosis causes regular resorption of individual cells initiated by a well-defined pathway involving the activation of proteases called caspases [62].

Apoptosis is essential for maintaining tissue homeostasis in balance with cell proliferation and death. Unwanted, old, damaged, and altered cells of an organism must be removed by apoptosis [63]. Apoptosis also protects cells in disease states or harmful chemicals, for example, in immunological reactions [64]. Moreover, p53 is a cellular stress sensor and a major pathway activator. The extrinsic pathway begins outside the cell when it is determined in the extracellular environment that the cell must be killed [65,66]. Clearing damaged organelles is necessary for autophagy to support cell survival. Cell death and cell survival are represented by apoptosis. Induction of caspases or degradation of endogenous apoptosis inhibitors can be preceded or enhanced by autophagy [67]

In contrast to necrotic cell death, which usually occurs due to adenosine triphosphate (ATP) depletion, apoptosis is an ATP-requiring process. Different organelles (plasma membrane, mitochondria, nucleus, endoplasmic reticulum, and lysosomes) elicit cell-death signals. In particular, mitochondrial permeabilization and dysfunction usually develop in necrosis and apoptosis. In some cases, apoptosis and necrosis share a signaling pathway, resulting in programmed necrosis called necroptosis. In this way, apoptosis and necrosis may represent extreme endpoints on the phenotypic continuum of lost cell viability [68].