| Features: |
| Usnic Acid Recommended Abbreviation: UA Type: Natural product / lichen secondary metabolite / dibenzofuran derivative Source: Usnic acid is a secondary metabolite produced by several lichen genera, including Usnea, Cladonia, Lecanora, and related species. It occurs naturally as (+)- and (-)-usnic acid enantiomers. Function: Usnic acid exhibits antimicrobial, anti-inflammatory, antioxidant, antiviral, antiparasitic, photoprotective, and experimental anticancer activities. Its biological effects involve mitochondrial function, oxidative stress, apoptosis, inflammatory signaling, and cellular metabolism. Cancer: Usnic acid has demonstrated preclinical anticancer activity in multiple cancer models, including proliferation ↓, tumor-cell viability ↓, apoptosis ↑, mitochondrial dysfunction ↑, and modulation of oxidative-stress and survival pathways. Its anticancer activity remains predominantly experimental, and toxicity may limit systemic therapeutic use. Neuroprotection: Experimental studies indicate antioxidant and neuroprotective activity, including Nrf2-associated cytoprotective responses and protection against oxidative and ischemic neuronal injury. Direct evidence for Alzheimer's disease is not sufficiently established to assign a specific Alzheimer's disease direction. Safety: Usnic acid has a significant hepatotoxicity concern, particularly with systemic or oral exposure at higher doses. Human cases of severe liver injury, including acute liver failure requiring transplantation, have been reported with usnic-acid-containing weight-loss supplements. Mitochondrial dysfunction and oxidative stress are important mechanisms implicated in its hepatotoxicity. |
| Source: CGL-CS |
| Type: oncogene |
| Family of RAS proteins (KRAS, NRAS, and HRAS) have been well described to cause oncogenic transformation. - The expression and mutational status of RAS isoforms are critical in several cancers and are generally linked with a poorer prognosis when mutated. RAS is one of the most frequently activated oncogenic drivers in human cancer. Mutations lock RAS in its GTP-bound active state, making signaling: -Constitutive -Growth-factor independent -Resistant to normal feedback control Key framing: RAS is a true driver oncogene, not just an amplifier. Core Oncogenic Pathways Downstream of RAS RAS sits at the apex of multiple essential signaling cascades: a. MAPK Pathway (RAF–MEK–ERK) -Drives proliferation -Induces cell-cycle genes (Cyclin D, MYC, FOS/AP-1) -Supports invasion and differentiation blockade b. PI3K–AKT–mTOR -Promotes survival and metabolic reprogramming -Enhances resistance to apoptosis -Supports protein synthesis and growth c. RAL-GDS and Others -Cytoskeletal remodeling -Vesicle trafficking -Metastatic behavior Together, these create a multi-axis growth and survival program. |
| 8159- | UsA, | Usnic acid suppresses cervical cancer cell proliferation by inhibiting PD-L1 expression and enhancing T-lymphocyte tumor-killing activity |
| - | in-vitro, | Cerv, | HeLa |
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:% Cells:% prod#:481 Target#:269 State#:% Dir#:1
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