| Source: HalifaxProj(inhibit) CGL-CS TCGA |
| Type: |
| 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 responses. Anti-inflammatory cytokine. In normal tissues, TGF-β plays an essential role in cell cycle regulation, immune function, and tissue remodeling. - In early carcinogenesis, TGF-β typically acts as a tumor suppressor by inhibiting cell proliferation and inducing apoptosis. In advanced cancers, cells frequently become resistant to the growth-inhibitory effects of TGF-β. - TGF-β then switches roles and promotes tumor progression by stimulating epithelial-to-mesenchymal transition (EMT), cell invasion, metastasis, and immune evasion. Non-canonical (Smad-independent) pathways, such as MAPK, PI3K/Akt, and Rho signaling, also contribute to TGF-β-mediated responses. Elevated levels of TGF-β have been detected in many advanced-stage cancers, including breast, lung, colorectal, pancreatic, and prostate cancers. - The switch from a tumor-suppressive to a tumor-promoting role is often associated with increased TGF-β production and activation in the tumor microenvironment. High TGF-β expression or signaling activity is frequently correlated with aggressive disease features, resistance to therapy, increased metastasis, and poorer overall survival in many cancer types. |
| 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. |
| 238- | Api, | Apigenin inhibits TGF-β-induced VEGF expression in human prostate carcinoma cells via a Smad2/3- and Src-dependent mechanism |
| - | in-vitro, | Pca, | PC3 | - | in-vitro, | Pca, | LNCaP | - | in-vitro, | Pca, | C4-2B |
| 153- | CUR, | Curcumin Inhibits Prostate Cancer Bone Metastasis by Up-Regulating Bone Morphogenic Protein-7 in Vivo |
| - | in-vivo, | Pca, | C4-2B |
| 123- | CUR, | Synthesis of novel 4-Boc-piperidone chalcones and evaluation of their cytotoxic activity against highly-metastatic cancer cells |
| - | in-vitro, | Colon, | LoVo | - | in-vitro, | Colon, | COLO205 | - | in-vitro, | Pca, | PC3 | - | in-vitro, | Pca, | 22Rv1 |
| 124- | CUR, | Curcumin-Gene Expression Response in Hormone Dependent and Independent Metastatic Prostate Cancer Cells |
| - | in-vitro, | Pca, | LNCaP | - | in-vitro, | Pca, | C4-2B |
| 26- | EGCG, | QC, | docx, | Green tea and quercetin sensitize PC-3 xenograft prostate tumors to docetaxel chemotherapy |
| - | vitro+vivo, | Pca, | PC3 |
| 3369- | QC, | Pharmacological basis and new insights of quercetin action in respect to its anti-cancer effects |
| - | Review, | Pca, | NA |
| 1138- | TQ, | Thymoquinone inhibits epithelial-mesenchymal transition in prostate cancer cells by negatively regulating the TGF-β/Smad2/3 signaling pathway |
| - | in-vitro, | Pca, | DU145 | - | in-vitro, | Pca, | PC3 |
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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