| Source: HalifaxProj(inhibit) CGL-CS |
| Type: |
| Phosphatidylinositol 3-kinase (PtdIns3K or PI3K) is a family of enzymes that play a crucial role in cell signaling pathways, particularly in the regulation of cell growth, survival, and metabolism. The PI3K pathway is one of the most frequently altered pathways in human cancer.
Inhibition of the PI3K pathway has been explored as a therapeutic strategy for cancer treatment. Several PI3K inhibitors have been developed and are currently being tested in clinical trials. These inhibitors can target specific components of the pathway, such as PI3K, AKT, or mTOR. Class I phosphoinositide 3-kinase (PI3K) Class III PtdIns3K In contrast to the class III PtdIns3K as a positive regulator of autophagy, class I PI3K-AKT signaling has an opposing effect on the initiation of autophagy. PI3K inhibitors include: -Idelalisib , Copanlisib, Alpelisib -LY294002? -Wortmannin: potent PI3K inhibitor, has some associated toxicity. -Quercetin: -Curcumin -Resveratrol -Epigallocatechin Gallate (EGCG) |
| Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression. TP53 is the most commonly mutated gene in human cancer. HH↑, GLI-1↑, SHH↑ P53↓ The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca. It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma. Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer. It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress. Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC. |
| 240- | Api, | The flavonoid apigenin reduces prostate cancer CD44(+) stem cell survival and migration through PI3K/Akt/NF-κB signaling |
| - | in-vitro, | Pca, | PC3 | - | in-vitro, | Pca, | CD44+ |
| 2792- | CHr, | Chrysin induces death of prostate cancer cells by inducing ROS and ER stress |
| - | in-vitro, | Pca, | DU145 | - | in-vitro, | Pca, | PC3 |
| 61- | QC, | Midkine downregulation increases the efficacy of quercetin on prostate cancer stem cell survival and migration through PI3K/AKT and MAPK/ERK pathway |
| - | in-vitro, | Pca, | PC3 | - | in-vitro, | Pca, | LNCaP | - | in-vitro, | Pca, | ARPE-19 |
| 63- | QC, | Quercetin facilitates cell death and chemosensitivity through RAGE/PI3K/AKT/mTOR axis in human pancreatic cancer cells |
| - | in-vitro, | Pca, | NA |
| 66- | QC, | Emerging impact of quercetin in the treatment of prostate cancer |
| - | Review, | Pca, | NA |
| 86- | QC, | PacT, | Quercetin regulates insulin like growth factor signaling and induces intrinsic and extrinsic pathway mediated apoptosis in androgen independent prostate cancer cells (PC-3) |
| - | vitro+vivo, | Pca, | PC3 |
| 3369- | QC, | Pharmacological basis and new insights of quercetin action in respect to its anti-cancer effects |
| - | Review, | Pca, | NA |
| 1469- | SFN, | Sulforaphane enhances the therapeutic potential of TRAIL in prostate cancer orthotopic model through regulation of apoptosis, metastasis, and angiogenesis |
| - | in-vitro, | Pca, | PC3 | - | in-vitro, | Pca, | LNCaP | - | in-vivo, | Pca, | 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:22 Cells:% prod#:% Target#:252 State#:% Dir#:1
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