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| The PI3K/Akt/mTOR signaling pathway is a critical regulator of cell growth, proliferation, survival, and metabolism. In many cancers (such as breast, colorectal, lung, and endometrial cancers), the PI3K/Akt/mTOR pathway is often hyperactivated. – This hyperactivation is frequently due to gene mutations (e.g., in PIK3CA), loss of PTEN, and amplification events that enhance the pathway’s activity. – Increased activity is also observed via elevated levels of phosphorylated Akt and mTOR in tumors compared to normal tissues. |
| 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. |
| 124- | CUR, | Curcumin-Gene Expression Response in Hormone Dependent and Independent Metastatic Prostate Cancer Cells |
| - | in-vitro, | Pca, | LNCaP | - | in-vitro, | Pca, | C4-2B |
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#:254 State#:% Dir#:1
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