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| – Some studies have reported upregulated expression of certain GABA receptor subunits (e.g., GABA_A receptor subunits) in breast tumors. – Increased expression has been associated with enhanced cell proliferation and migration, with some reports linking this to a poorer prognosis. -GABAergic transmission is deficient in anxiety. -Neurons expressing GABAA α1 receptors can mediate sedation, -while those expressing GABAA α2 receptors mediate anxiolytic. -In addition, extra-synaptic GABAA α5 receptors can also regulate the activity of hippocampal pyramidal cells, thereby affecting associative temporal and spatial memory Gamma-aminobutyric acid — Gamma-aminobutyric acid is an endogenous non-protein amino acid, inhibitory neurotransmitter, metabolic intermediate, and signaling ligand commonly abbreviated GABA. As a database target, it represents changes in GABA concentration, synthesis, secretion, uptake, extracellular accumulation, or GABA-shunt utilization rather than modulation of a specific GABA receptor. GABA is synthesized from glutamate by GAD1/GAD67 and GAD2/GAD65, transported by GABA transporters, and metabolized primarily by ABAT/GABA transaminase. In cancer, GABA may be produced by tumor, neural, stromal, or immune cells and can influence proliferation, invasion, mitochondrial metabolism, β-catenin signaling, and antitumor immunity. Its biological direction is strongly tumor-, receptor-, concentration-, and compartment-dependent. Typical cancer modulation: Variable/context-dependent. GABA production, secretion, extracellular accumulation, uptake, or GABA-shunt utilization may be ↑ in tumors that exploit GABA for metabolic adaptation, β-catenin activation, growth, invasion, or immune evasion. GABA signaling may instead suppress proliferation or migration in tumors expressing inhibitory GABA receptor configurations. Normal-cell relevance: GABA generally reduces neuronal excitability through GABA receptor signaling and also regulates pancreatic, immune, gastrointestinal, vascular, and endocrine functions. In Alzheimer’s disease, reduced phasic inhibition and excessive astrocyte-derived tonic GABA may coexist in different circuits; therefore total GABA direction alone may not indicate whether GABAergic function is beneficial or pathological. Target classification: Neurotransmitter; amino-acid metabolite; signaling ligand; tumor-microenvironment mediator; metabolic substrate. |
| 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. -CBS, and/or CSE and/or 3-MST is overexpressed in many forms of cancer |
| 6135- | CHr, | Chrysin as a Multifunctional Therapeutic Flavonoid: Emerging Insights in Pathogenesis Management: A Narrative Review |
| - | Review, | Var, | NA | - | Review, | AD, | NA |
| 6201- | Cuc, | Cucurbitacin B and Its Derivatives: A Review of Progress in Biological Activities |
| - | Review, | Var, | NA | - | Review, | AD, | NA |
| 3930- | PTS, | A Review of Pterostilbene Antioxidant Activity and Disease Modification |
| - | Review, | Var, | NA | - | Review, | adrenal, | NA | - | Review, | Stroke, | NA |
| 3401- | TQ, | Molecular mechanisms and signaling pathways of black cumin (Nigella sativa) and its active constituent, thymoquinone: a review |
| - | 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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:26 Cells:% prod#:% Target#:1205 State#:% Dir#:2
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