| Features: Anti-oxidant, anti-tumor | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Thymoquinone is a bioactive compound found in the seeds of Nigella sativa, commonly known as black seed or black cumin. Pathways: -Cell cycle arrest, apoptosis induction, ROS generation in cancer cells -inhibit the activation of NF-κB, Suppress the PI3K/Akt signaling cascade -Inhibit angiogenic factors such as VEGF, MMPs -Inhibit HDACs, UHRF1, and DNMTs -Note half-life 3-6hrs. BioAv low oral bioavailability due to its lipophilic nature. Note refridgeration of Black seed oil improves the stability of TQ. DIY: ~1 part lecithin : 2–3 parts black seed oil : 4–5 parts warm water. (chat ai) Pathways: - usually induce ROS production in Cancer cells, and lowers ROS in normal cells - ROS↑ related: MMP↓(ΔΨm), ER Stress↑, GRP78↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx, - May Low AntiOxidant defense in Cancer Cells: NRF2↓(usually contrary), GSH↓ HO1↓(contrary), GPx↓ - Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑, - lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓ - inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, VEGF↓, FAK↓, NF-κB↓, CXCR4↓, TGF-β↓, ERK↓ - reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMTs↓, EZH2↓, P53↑, HSP↓, Sp proteins↓, TET↑ - cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓, - inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓, - inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PDKs↓, GRP78↑, GlucoseCon↓ - inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, EGFR↓, Integrins↓, - Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, α↓, ERK↓, JNK, - Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective, - Selectivity: Cancer Cells vs Normal Cells
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| 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. |
| 2127- | TQ, | Therapeutic Potential of Thymoquinone in Glioblastoma Treatment: Targeting Major Gliomagenesis Signaling Pathways |
| - | Review, | GBM, | 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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