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| P-glycoprotein (P-gp), also known as multidrug resistance protein 1 (MDR1), is a membrane protein that plays a crucial role in the transport of various substances across cellular membranes. It is part of the ATP-binding cassette (ABC) transporter family. P-glycoprotein is often overexpressed in a variety of cancers, including breast cancer, lung cancer, leukemia, and ovarian cancer. - The overexpression of P-glycoprotein (P-gp), is widely considered as an important reason for the MDR (multidrug resistance). ABCB1 - ATP-Binding Cassette Subfamily B Member 1 / P-Glycoprotein Abbreviation: ABCB1, P-gp, P-glycoprotein, MDR1 Type: ATP-dependent membrane efflux transporter / multidrug resistance protein Function: ABCB1 encodes P-glycoprotein, an ATP-binding cassette transporter that exports a broad range of drugs, xenobiotics, lipids, and other substrates across cellular membranes. It is highly expressed in barrier tissues including the intestine, liver, kidney, placenta, and blood-brain barrier, where it limits tissue accumulation of potentially harmful compounds. Cancer: ↑ Frequently overexpressed or functionally activated in drug-resistant tumors. Increased ABCB1 lowers intracellular concentrations of many anticancer agents by actively transporting them out of cancer cells, producing multidrug resistance and reducing chemotherapy effectiveness. Alzheimer's Disease: ↓ Reduced ABCB1/P-glycoprotein expression or transport activity at the blood-brain barrier is associated with impaired amyloid-β clearance from the brain. Lower P-gp function correlates with increased cerebral Aβ accumulation and may contribute to Alzheimer's disease progression. |
| -Cyclooxygenase cox2 overexpression has been noted in various cancers. -PIK3s /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. -AP1 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 responses. -Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers. -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. 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. -CBS, and/or CSE and/or 3-MST is overexpressed in many forms of cancer -Methionine addiction is a fundamental and general metabolic hallmark of cancer, known as the Hoffman effect. Methionine addiction is targeted in cancer by methionine restriction, including recombinant methioninase (rMETase) -Reliance on aerobic glycolysis is one of the hallmarks of cancer. (PKM2-inhibit) is a key mediator of glycolysis in cancer cells |
| 5856- | CAP, | Potential of capsaicin as a combinatorial agent to overcome chemoresistance and to improve outcomes of cancer therapy |
| - | Review, | Var, | NA |
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