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| ATG16L1 - Autophagy Related 16 Like 1 Abbreviation: ATG16L1, ATG16 Type: Autophagy-related protein / ATG12-ATG5-ATG16L1 complex component / LC3 lipidation regulator Function: ATG16L1 forms a complex with ATG12-conjugated ATG5 and directs LC3/ATG8 lipidation to autophagic membranes. It is required for phagophore expansion and autophagosome formation and also participates in noncanonical autophagy processes such as LC3-associated phagocytosis and conjugation of ATG8 proteins to single membranes. Cancer: ↕ Context-dependent. Normal ATG16L1-dependent autophagy can suppress tumor initiation by removing damaged proteins and organelles and limiting genomic stress. In established tumors, however, ATG16L1-dependent autophagy can support survival during hypoxia, nutrient deprivation, metabolic stress, and anticancer treatment. Favorable Direction in Cancer: Context-dependent. ↓ ATG16L1/autophagy may be favorable in tumors that depend on autophagy for survival, whereas loss of ATG16L1-mediated quality control can promote tumor initiation in other settings. Interpretation Note: When a paper refers simply to mammalian “ATG16,” ATG16L1 is usually the intended target. ATG16L2 is a distinct human paralog and should be recorded separately when specifically measured. |
| -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 |
| 8235- | LCA, | Anticancer effects of licochalcones: A review of the mechanisms |
| - | Review, | Var, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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