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| The caspase family of proteases are essential to initiate and execute apoptotic cell death. Targeting caspase pathways by gene therapy or endogenous inhibitors represents a promising therapeutic strategy for cancer. Caspases are divided into two groups: the initiator caspases (caspase-2, -8, -9 and -10), which are the first to be activated in response to a signal, and the executioner caspases (caspase-3, -6, and -7) that carry out the demolition phase of apoptosis. Caspases are a cysteine protease that speed up a chemical reaction via pointing their target substrates following an aspartic acid residue.1 They are grouped into apoptotic (caspase-2, 3, 6, 7, 8, 9 and 10) and inflammatory (caspase-1, 4, 5, 11 and 12) mediated caspases. |
| 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 |
| 282- | ALA, | Alpha-lipoic acid induced apoptosis of PC3 prostate cancer cells through an alteration on mitochondrial membrane depolarization and MMP-9 mRNA expression |
| - | in-vitro, | Pca, | PC3 |
| 1564- | Api, | Apigenin-induced prostate cancer cell death is initiated by reactive oxygen species and p53 activation |
| - | in-vitro, | Pca, | 22Rv1 | - | in-vivo, | NA, | NA |
| 2754- | BetA, | Betulinic acid inhibits prostate cancer growth through inhibition of specificity protein transcription factors |
| - | in-vitro, | Pca, | LNCaP |
| - | in-vitro, | Pca, | DU145 |
| 135- | CUR, | Curcumin induces apoptosis and protective autophagy in castration-resistant prostate cancer cells through iron chelation |
| - | in-vitro, | Pca, | DU145 | - | in-vitro, | Pca, | PC3 |
| 1955- | GamB, | Gambogic acid inhibits thioredoxin activity and induces ROS-mediated cell death in castration-resistant prostate cancer |
| - | in-vitro, | Pca, | PC3 | - | in-vitro, | Pca, | LNCaP | - | in-vitro, | Pca, | DU145 |
| 4639- | HT, | Hydroxytyrosol Induces Apoptosis, Cell Cycle Arrest and Suppresses Multiple Oncogenic Signaling Pathways in 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#:443 State#:% Dir#:2
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