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| also known as Prx Peroxiredoxins are endogenous antioxidants and redox sensors. Properties of the peroxiredoxins make them suitable as markers of oxidative stress. Peroxiredoxins (Prxs) are a family of antioxidant enzymes that play a crucial role in cellular redox signaling and the detoxification of reactive oxygen species (ROS). They are involved in various cellular processes, including cell proliferation, differentiation, and apoptosis. Prx isoforms (such as Prx1 and Prx4) are often overexpressed. This overexpression can help cancer cells cope with increased levels of reactive oxygen species (ROS) generated during rapid cell division and metabolic changes. Elevated Prx levels have been linked to resistance against chemotherapy and radiation therapy. For example, Prx2 and Prx3 have been implicated in protecting cancer cells from oxidative damage caused by these treatments. Some Prxs, such as Prx3, can act as tumor suppressors. Their downregulation or loss of function has been associated with increased tumorigenesis and poor prognosis in certain cancers. PRDX family comprises several isoforms (for example, PRDX1, PRDX2, PRDX3, etc.) that function as antioxidant enzymes to reduce reactive oxygen species (ROS) and maintain redox balance. PRDX family—especially key isoforms like PRDX1 and PRDX2—are often upregulated in various cancers, correlating with worse prognosis and enhanced tumor cell survival. Through their ROS-detoxifying capabilities, these proteins generally play protumorigenic roles by protecting malignant cells from oxidative stress and supporting resistance to apoptosis and therapy. |
| Cyclooxygenase (COX)-2 overexpression has been noted in various cancers.
PI3Ks/AKT pathways are over-activated in several types of cancers. EGFR altered activity has been noted in various pathological conditions. However, its regulation is an important step in the inhibition of cancer. In this regard, EGCG shows a pivotal role in the inhibition of EGFR activity. Activating protein-1 transcription factor has been associated with pathogenesis including cancer. Activation of the sonic hedgehog (Shh) pathway is required for the growth of numerous tissues and organs and recent evidence indicates that this pathway is often recruited to stimulate growth of cancer stem cells (CSCs) and to orchestrate the reprogramming of cancer cells via epithelial mesenchymal transition (EMT). Increased expression of Nanog has been associated with the aggressive nature of certain cancers, highlighting its role in promoting cancer stem cell characteristics. The aberrant hedgehog (Hh)/GLI signaling pathway causes the formation and progression of a variety of tumors. The process of cell apoptosis is often accompanied by the destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis. Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses50. Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers [23–25]. The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell. Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure. Heat shock proteins (HSPs) are normally induced under environmental stress to serve as chaperones for maintenance of correct protein folding but they are often overexpressed in many cancers, including breast cancer. Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research. Since increased Nrf2 gene expression is one of the main mechanisms of cancer cells in resisting chemotherapeutic drugs and survival in oxidative conditions; finding compounds with the ability to suppress Nrf2 gene expression with minimum side effects can be considered an important strategy for increasing the sensitivity of cancer cells to chemotherapy. Overexpression of c-met stimulates proliferation, migration and invasion in various types of cancer including prostate cancer. Overexpression of TGFα and EGFR by many carcinomas correlates with the development of cancer metastasis, resistance to chemotherapy and poor prognosis. More than 50% of human cancers have a mutated nonfunctional p53. |
| 5470- | AF, | Exploring a Therapeutic Gold Mine: The Antifungal Potential of the Gold-Based Antirheumatic Drug Auranofin |
| - | Review, | Var, | NA |
| 3160- | Ash, | Withaferin A: A Pleiotropic Anticancer Agent from the Indian Medicinal Plant Withania somnifera (L.) Dunal |
| - | Review, | Var, | NA |
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