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| JNK acts synergistically with NF-κB, JAK/STAT, and other signaling molecules to exert a survival function. Janus signaling promotes cancer cell survival. JNK, or c-Jun N-terminal kinase, is a member of the mitogen-activated protein kinase (MAPK) family. It plays a crucial role in various cellular processes, including cell proliferation, differentiation, and apoptosis (programmed cell death). JNK is activated in response to various stress signals, such as UV radiation, oxidative stress, and inflammatory cytokines. JNK activation can promote apoptosis in cancer cells, acting as a tumor suppressor. However, in other contexts, it can promote cell survival and proliferation, contributing to tumor progression. JNK is often unregulated in cancers, leading to increased cancer cell proliferation, survival, and resistance to apoptosis. This activation is typically associated with poor prognosis and aggressive tumor behavior. |
| 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. |
| 3442- | ALA, | α‑lipoic acid modulates prostate cancer cell growth and bone cell differentiation |
| - | in-vitro, | Pca, | 22Rv1 | - | in-vitro, | Pca, | C4-2B | - | in-vitro, | Nor, | 3T3 |
| 277- | ALA, | α-lipoic acid modulates prostate cancer cell growth and bone cell differentiation |
| - | in-vitro, | Pca, | 22Rv1 | - | in-vitro, | Pca, | C4-2B |
| 1390- | BBR, | Rad, | Berberine Inhibited Radioresistant Effects and Enhanced Anti-Tumor Effects in the Irradiated-Human Prostate Cancer Cells |
| - | in-vitro, | Pca, | PC3 |
| 167- | CUR, | Curcumin-induced apoptosis in PC3 prostate carcinoma cells is caspase-independent and involves cellular ceramide accumulation and damage to mitochondria |
| - | in-vitro, | Pca, | PC3 |
| 1958- | GamB, | Gambogenic acid induces apoptosis and autophagy through ROS-mediated endoplasmic reticulum stress via JNK pathway in prostate cancer cells |
| - | in-vitro, | Pca, | NA | - | in-vivo, | NA, | NA |
| 2060- | GamB, | Gambogenic acid induces apoptosis and autophagy through ROS-mediated endoplasmic reticulum stress via JNK pathway in prostate cancer cells |
| - | in-vitro, | 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#:168 State#:% Dir#:2
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