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| TRIB3 overexpression is significantly linked to malignant progression and unfavorable prognosis in diverse solid tumors. TRIB3 encodes a pseudokinase—a kinase-like protein lacking catalytic activity but acting as a scaffold and signaling modulator. TRIB3 is strongly induced by cellular stress, particularly ER stress, nutrient deprivation, hypoxia, and oxidative stress, via ATF4/CHOP-dependent pathways. Functionally UPREGULATED in many cancers, particularly in aggressive, hypoxic, or metabolically stressed tumors. -Rarely mutated -Induced by the tumor microenvironment -Maintained by chronic stress signaling TRIB3 is best viewed as a stress-selected dependency, not a classical oncogene. High TRIB3 expression correlates with: -EMT and invasive behavior -Metastatic competence -Poor prognosis in multiple solid tumors (e.g., breast, lung, colorectal, liver) TRIB3 reports whether a tumor has entered a stress-adapted, survival-biased state. It is not used to choose a specific drug today. TRIB3 is used as a clinical biomarker for Stress Adaptation |
| 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. |
| 150- | NRF, | CUR, | docx, | Subverting ER-Stress towards Apoptosis by Nelfinavir and Curcumin Coexposure Augments Docetaxel Efficacy in Castration Resistant Prostate Cancer Cells |
| - | in-vitro, | Pca, | C4-2B |
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