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Topic Review
Proteins Related to Human Neurodegenerative Diseases inYeast Cells
A characteristic feature of neurodegenerative diseases (NDs) is the formation of protein aggregates (inclusion bodies) in cells of the nervous system, formed as a result of the misfolding of proteins. Based on the reviewed results of studies on NDs and related protein aggregation, as well as viral protein aggregation, a new experimental model system for the study of human NDs is proposed. The core of the proposed system is a comparative transcriptomic analysis of changes in signaling pathways during the expression of viral capsid proteins in yeast cells.
  • 424
  • 12 Dec 2023
Topic Review
Regenerative Potential (RP) of MSCEVs
Mesenchymal stem cell extracellular vesicles (MSCEVs) obtained from MSCs can have numerous therapeutic applications via regeneration of various body tissues. MSCEV action can be potentiated by modifying the mesenchymal stem cells culturing methodology and bioengineering extracellular vesicles (EVs). 
  • 418
  • 11 Sep 2023
Topic Review
Protective Genes against Cancer
Richard Peto’s paradox, first described in 1975 from an epidemiological perspective, established an inverse correlation between the probability of developing cancer in multicellular organisms and the number of cells. Larger animals exhibit fewer tumors compared to smaller ones, though exceptions exist. Mice are more susceptible to cancer than humans, while elephants and whales demonstrate significantly lower cancer prevalence rates than humans. How nature and evolution have addressed the issue of cancer in the animal kingdom remains largely unexplored. In the field of medicine, much attention has been devoted to cancer-predisposing genes, as they offer avenues for intervention, including blocking, downregulating, early diagnosis, and targeted treatment. Predisposing genes also tend to manifest clinically earlier and more aggressively, making them easier to identify. 
  • 416
  • 01 Feb 2024
Topic Review
Aberrant MET Receptor Tyrosine Kinase Signaling in Glioblastoma
Despite therapeutic advances, the treatment of brain tumors, including glioblastoma (GBM), an aggressive primary brain tumor associated with poor prognosis and resistance to therapy, remains a significant challenge. Receptor tyrosine kinases (RTKs) are critical during development and in adulthood. Dysregulation of RTKs through activating mutations and gene amplification contributes to many human cancers and provides attractive therapeutic targets for treatment. Under physiological conditions, the Met RTK, the hepatocyte growth factor/scatter factor (HGF/SF) receptor, promotes fundamental signaling cascades that modulate epithelial-to-mesenchymal transition (EMT) involved in tissue repair and embryogenesis. In cancer, increased Met activity promotes tumor growth and metastasis by providing signals for proliferation, survival, and migration/invasion. Recent clinical genomic studies have unveiled multiple mechanisms by which MET is genetically altered in GBM, including focal amplification, chromosomal rearrangements generating gene fusions, and a splicing variant mutation (exon 14 skipping, METex14del). Notably, MET overexpression contributes to chemotherapy resistance in GBM by promoting the survival of cancer stem-like cells. This is linked to distinctive Met-induced pathways, such as the upregulation of DNA repair mechanisms, which can protect tumor cells from the cytotoxic effects of chemotherapy. 
  • 412
  • 11 Mar 2024
Topic Review
Tumor-Derived Extracellular Vesicles in Anti-Cancer Therapies
The infiltration of primary tumors and metastasis formation at distant sites strongly impact the prognosis and the quality of life of cancer patients. Current therapies including surgery, radiotherapy, and chemotherapy are limited in targeting the complex cell migration mechanisms responsible for cancer cell invasiveness and metastasis. Extracellular vesicles (EVs) are lipid-enveloped particles involved in inter-tissue and inter-cell communication. Tumor-derived extracellular vesicles (TDEVs) impact cancer cell migration. They can not only be considered as a target for cancer therapy but can also be used for the development of anti-tumor therapeutic strategies.
  • 410
  • 26 Sep 2023
Topic Review
Emerging Roles of Ubiquitination in Biomolecular Condensates
Biomolecular condensates are dynamic non-membrane-bound macromolecular high-order assemblies that participate in a growing list of cellular processes, such as transcription, the cell cycle, etc. Disturbed dynamics of biomolecular condensates are associated with many diseases, including cancer and neurodegeneration. Extensive efforts have been devoted to uncovering the molecular and biochemical grammar governing the dynamics of biomolecular condensates and establishing the critical roles of protein posttranslational modifications (PTMs) in this process.
  • 403
  • 23 Oct 2023
Topic Review
Wound Repair of the Cell Membrane
The cell membrane is frequently subjected to damage, either through physical or chemical means. The swift restoration of the cell membrane’s integrity is crucial to prevent the leakage of intracellular materials and the uncontrolled influx of extracellular ions. Consequently, wound repair plays a vital role in cell survival, akin to the importance of DNA repair.
  • 398
  • 22 Feb 2024
Topic Review
Canonical and Non-Canonical Inflammasome Pathway in Ehrlichiosis
Ehrlichia is an obligately intracellular bacterium which is responsible for causing human monocytic ehrlichiosis (HME), a potentially lethal disease similar to toxic shock syndrome and septic shock syndrome. Several studies have indicated that canonical and non-canonical inflammasome activation is a crucial pathogenic mechanism that induces dysregulated inflammation and host cellular death in the pathophysiology of HME. Mechanistically, the activation of canonical and non-canonical inflammasome pathways affected by virulent Ehrlichia infection is due to a block in autophagy. 
  • 396
  • 27 Nov 2023
Topic Review
Mass Spectrometry Investigation of ATP-Binding Cassette Proteins
Drug resistance remains one of the main causes of poor outcome in cancer therapy. It is also becoming evident that drug resistance to both chemotherapy and to antibiotics is driven by more than one mechanism. So far, there are at least eight recognized mechanisms behind such resistance. In normal tissues, ATP-binding cassette (ABC)  transporters protect the cells from the toxic effects of xenobiotics, whereas in tumor cells, they reduce the intracellular concentrations of anticancer drugs, which ultimately leads to the emergence of multidrug resistance (MDR). A deeper understanding of the structures and the biology of these proteins is central to current efforts to circumvent resistance to both chemotherapy, targeted therapy, and antibiotics. 
  • 388
  • 04 Feb 2024
Topic Review
PARP1 in Homeostasis and Tumorigenesis
Detailing the connection between homeostatic functions of enzymatic families and eventual progression into tumorigenesis is crucial to the understanding of anti-cancer therapies. One key enzyme group involved in this process is the Poly (ADP-ribose) polymerase (PARP) family, responsible for an expansive number of cellular functions, featuring members well established as regulators of DNA repair, genomic stability and beyond. Several PARP inhibitors (PARPi) have been approved for clinical use in a range of cancers, with many more still in trials. Unfortunately, the occurrence of resistance to PARPi therapy is growing in prevalence and requires the introduction of novel counter-resistance mechanisms to maintain efficacy.
  • 381
  • 22 Aug 2023
Topic Review
Regulation of NcRNAs on Ferroptosis
Ferroptosis is a non-apoptotic mode of cell death driven by membrane lipid peroxidation and is characterized by elevated intracellular levels of Fe2+, ROS, and lipid peroxidation. Studies have shown that ferroptosis is related to the development of multiple diseases, such as cancer, neurodegenerative diseases, and acute myeloid leukemia. Ferroptosis plays a dual role in the occurrence and development of these diseases. Ferroptosis mainly involves iron metabolism, ROS, and lipid metabolism. Various mechanisms, including epigenetic regulation, have been reported to be deeply involved in ferroptosis. Abnormal epigenetic modifications have been reported to promote tumor onset or other diseases and resistance to chemotherapy drugs. 
  • 356
  • 12 Mar 2024
Topic Review
Gene Silencing Interrogating Essential Aspects of Cell Biology
The development of small-interfering RNA-mediated gene-silencing strategies has made it possible to study the function(s) of essential gene products in human cells. In these functional studies, a certain target gene is transiently silenced in the cell type of choice with two different siRNAs that are directed at the same mRNA. Routinely, we employ one siRNA targeting the coding region and another one targeting the non-coding or untranslated region (UTR) of the respective mRNA and compare the phenotypes of these two cell pools with cells, which were treated with a non-targeting siRNA. The first aim always is to optimize gene-silencing conditions in a way that leads to 90% depletion of the protein of interest without affecting the three cellular parameters, growth, viability, and morphology. Since our major interest are proteins of the human endoplasmic reticulum (ER), we analyze as functional read-outs the effect of the silencing on i) the biogenesis of secretory- and membrane proteins, ii) the differential cellular proteome iii) the differential ensemble structure of ER membrane proteins, iv) cellular calcium homeostasis, v) cellular energy homeostasis, vi) cellular migratory potential, and vii) cellular invasive potential. The silencing with an UTR-siRNA allows subsequent cDNA-based complementation as gold-standard for demonstrating specificity of the observed effects and carries the additional benefit of facilitating analysis of the consequences of disease-linked mutant variants.
  • 34
  • 15 Dec 2025
Topic Review Peer Reviewed
Mismatch Repair Deficiency and Microsatellite Instability
Mismatch repair deficiency (MMRd) is caused by the biallelic inactivation of an MMR gene, which can be attributed either to an inherited or an acquired pathway. MMRd is characterized by the inability of cells to repair spontaneous mutations in microsatellites that occur during replication. Microsatellites are repetitive nucleotide sequences composed of one to six base pairs. Mutations in microsatellites lead to deletions or insertions of sequence units that are designated as microsatellite instability (MSI). MMRd is diagnosed by immunochemistry and is characterized by loss of nuclear immunostaining for at least one of the four MMR proteins that are routinely examined, i.e., MSH2, MSH6, MLH1 and PMS2. Available tests for MSI are PCR and next generation sequencing. MMRd and MSI predispose to tumor initiation and progression, increase tumor mutational burden as well as tumor immunogenicity, facilitate the activation of the programmed cell death protein 1/programmed cell death ligand 1 (PD-1/PD-L1) immune checkpoint pathway and serve as prognostic and predictive biomarkers in solid tumors.
  • 19
  • 29 Apr 2026
Topic Review Peer Reviewed
Interleukin-33 and Obesity-Related Inflammation and Cancer
Interleukin-33 (IL-33) is a cytokine belonging to the IL-1 family. It is primarily associated with type 2 immune responses. It interacts with a receptor complex on immune cells in reaction to tissue damage or cellular injury. IL-33 is crucial in immune responses and is involved in various autoimmune and inflammatory diseases. Obesity is marked by chronic inflammation and is a known risk factor for several types of cancer. Recent studies have shown that IL-33 and its receptor complex are expressed in adipose (fat) tissue, suggesting they may play a role in obesity. While inflammation connects obesity and cancer, it is not yet clear whether IL-33 contributes to cancer associated with obesity. Depending on the cellular context, inflammatory environment, expression levels, and bioactivity, IL-33 can exhibit both protumorigenic and antitumorigenic effects. This review will explore the various functions of IL-33 in the inflammation linked to obesity and its relationship with cancer.
  • 12
  • 29 Apr 2026
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