| Source: HalifaxProj(block) CGL-CF TCGA |
| Type: |
| Notch signaling pathway is a regulator of self-renewal and differentiation in several tissues and cell types.; Notch hyperactivation has been implicated as oncogenic in several cancers including breast cancer and T-cell acute lymphoblastic leukemia (T-ALL). Due to its dual roles, NOTCH signaling is being explored as a therapeutic target. Inhibitors of NOTCH signaling are being investigated in clinical trials for various cancers, particularly those with aberrant NOTCH activation. The abnormal activation of the NOTCH pathway has been linked to increased cancer cell growth, survival, invasion, and resistance to chemotherapy and radiation therapy. On the other hand, blocking the NOTCH pathway has been shown to trigger cancer cell differentiation and cell death, and it makes them more responsive to therapy. Hence, inhibiting the NOTCH pathway has become a promising approach for treating cancer, and various NOTCH pathway inhibitors are currently under development for cancer treatment. |
| 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. |
| 3160- | Ash, | Withaferin A: A Pleiotropic Anticancer Agent from the Indian Medicinal Plant Withania somnifera (L.) Dunal |
| - | Review, | Var, | NA |
| 2617- | Ba, | Potential of baicalein in the prevention and treatment of cancer: A scientometric analyses based review |
| - | Review, | Var, | NA |
| 5888- | CAR, | Therapeutic application of carvacrol: A comprehensive review |
| - | Review, | Var, | NA | - | Review, | Stroke, | NA | - | Review, | Diabetic, | NA | - | Review, | Park, | NA |
| 5893- | CAR, | TV, | Thymol and Carvacrol: Molecular Mechanisms, Therapeutic Potential, and Synergy With Conventional Therapies in Cancer Management |
| - | Review, | Var, | NA |
| 6009- | CGA, | Chlorogenic Acid: An In-Depth Review of Its Effectiveness in Cancer Treatment |
| - | Review, | Var, | NA |
| 3861- | CUR, | Curcumin as a novel therapeutic candidate for cancer: can this natural compound revolutionize cancer treatment? |
| - | Review, | Var, | NA |
| 1605- | EA, | Ellagic Acid and Cancer Hallmarks: Insights from Experimental Evidence |
| - | Review, | Var, | NA |
| 1621- | EA, | The multifaceted mechanisms of ellagic acid in the treatment of tumors: State-of-the-art |
| - | Review, | Var, | NA |
| 2916- | LT, | Antioxidative and Anticancer Potential of Luteolin: A Comprehensive Approach Against Wide Range of Human Malignancies |
| - | Review, | Var, | NA | - | Review, | AD, | NA | - | Review, | Park, | NA |
| 1803- | NarG, | Naringin and naringenin as anticancer agents and adjuvants in cancer combination therapy: Efficacy and molecular mechanisms of action, a comprehensive narrative review |
| - | Review, | Var, | NA |
| 5253- | NCL, | Niclosamide: Beyond an antihelminthic drug |
| - | Review, | Var, | NA |
| 5254- | NCL, | The magic bullet: Niclosamide |
| - | Review, | Var, | NA |
| 4701- | PTS, | RES, | Targeting cancer stem cells and signaling pathways by resveratrol and pterostilbene |
| - | Review, | Var, | NA |
| 3360- | QC, | Role of Flavonoids as Epigenetic Modulators in Cancer Prevention and Therapy |
| - | Review, | Var, | NA |
| 4667- | RES, | CUR, | SFN, | Physiological modulation of cancer stem cells by natural compounds: Insights from preclinical models |
| - | Review, | Var, | NA |
| 4663- | RES, | Exploring resveratrol’s inhibitory potential on lung cancer stem cells: a scoping review of mechanistic pathways across cancer models |
| - | Review, | Var, | NA |
| 1730- | SFN, | Sulforaphane: An emergent anti-cancer stem cell agent |
| - | Review, | Var, | NA |
| 2084- | TQ, | Thymoquinone, as an anticancer molecule: from basic research to clinical investigation |
| - | 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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