| Source: HalifaxProj(activate) |
| Type: |
| Autophagy genes, including Atg3, Atg5, Atg6, Atg7, Atg10, Atg12, and Atg17. Tumor autophagy refers to the process by which cancer cells degrade and recycle cellular components through autophagy, a cellular mechanism that helps maintain homeostasis and respond to stress. Autophagy can have dual roles in cancer, acting as both a tumor suppressor and a promoter, depending on the context. Authophagy is the process used by cancer cells to “self-eat” to survive. Authophagy can be both good and bad. If authophagy is prolonged this will become a lethal process to cancer. On the other hand, for a short while (e.g. during chemotheraphy, radiotheraphy, etc.) authophagy is used by cancer cells to survive. For example, Chloroquine is a blocker of autophagy and has been used in a lab setting to dramatically enhance tumor response to radiotherapy, chemotherapy. |
| 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. |
| 318- | AgNPs, | Silver nanoparticles regulate autophagy through lysosome injury and cell hypoxia in prostate cancer cells |
| - | in-vitro, | Pca, | PC3 |
| 1563- | Api, | MET, | Metformin-induced ROS upregulation as amplified by apigenin causes profound anticancer activity while sparing normal cells |
| - | in-vitro, | Nor, | HDFa | - | in-vitro, | PC, | AsPC-1 | - | in-vitro, | PC, | MIA PaCa-2 | - | in-vitro, | Pca, | DU145 | - | in-vitro, | Pca, | LNCaP | - | in-vivo, | NA, | NA |
| 1580- | Citrate, | Citrate activates autophagic death of prostate cancer cells via downregulation CaMKII/AKT/mTOR pathway |
| - | in-vitro, | Pca, | PC3 | - | in-vivo, | PC, | NA | - | in-vitro, | Pca, | LNCaP | - | in-vitro, | Pca, | WPMY-1 |
| 132- | CUR, | Targeting multiple pro-apoptotic signaling pathways with curcumin in prostate cancer cells |
| - | in-vitro, | Pca, | PC3 |
| 159- | CUR, | Crosstalk from survival to necrotic death coexists in DU-145 cells by curcumin treatment |
| - | in-vitro, | Pca, | DU145 |
| 1869- | DCA, | Dichloroacetate induces autophagy in colorectal cancer cells and tumours |
| - | in-vitro, | CRC, | HT-29 | - | in-vitro, | CRC, | HCT116 | - | in-vitro, | Pca, | PC3 | - | in-vitro, | CRC, | HT-29 |
| 5931- | EGCG, | BTZ, | EGCG antagonizes Bortezomib cytotoxicity in prostate cancer cells by an autophagic mechanism |
| - | 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 |
| 4946- | PEITC, | Phenethyl Isothiocyanate Inhibits Oxidative Phosphorylation to Trigger Reactive Oxygen Species-mediated Death of Human Prostate Cancer Cells |
| - | in-vitro, | Pca, | LNCaP | - | in-vitro, | Pca, | PC3 |
| 63- | QC, | Quercetin facilitates cell death and chemosensitivity through RAGE/PI3K/AKT/mTOR axis in human pancreatic cancer cells |
| - | in-vitro, | Pca, | NA |
| 5105- | SSE, | Sodium selenite induces apoptosis by generation of superoxide via the mitochondrial-dependent pathway in human prostate cancer cells |
| - | in-vitro, | Pca, | LNCaP |
| 1824- | VitK2, | Vitamin K and its analogs: Potential avenues for prostate cancer management |
| - | Review, | Pca, | NA |
| 1837- | VitK3, | VitC, | Alpha-Tocopheryl Succinate Inhibits Autophagic Survival of Prostate Cancer Cells Induced by Vitamin K3 and Ascorbate to Trigger Cell Death |
| - | 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
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