| Source: |
| Type: |
| Also known as Cadherin2 (CDH2). N-cadherin is a type of cell adhesion molecule that plays a crucial role in the development and maintenance of tissue structure. In the context of cancer, N-cadherin has been implicated in the progression and metastasis of various types of tumors. N-cadherin expression is increased in various types of cancer. Normally, N-cadherin is expressed in mesenchymal cells, such as fibroblasts and smooth muscle cells. However, in cancer cells, N-cadherin expression is often upregulated, which can contribute to the epithelial-to-mesenchymal transition (EMT). EMT is a process by which epithelial cells acquire a more mesenchymal phenotype, which is characterized by increased motility, invasiveness, and resistance to apoptosis. The expression of N-cadherin in cancer cells is closely associated with tumorigenesis and metastasis. Additionally, the soluble N-cadherin level in the serum of cancer patients is much higher than that in the serum of healthy patients, revealing a positive relation with poor prognosis. |
| 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. |
| 4816- | ASTX, | Potent carotenoid astaxanthin expands the anti-cancer activity of cisplatin in human prostate cancer cells |
| - | in-vitro, | Pca, | NA |
| 1121- | JG, | Juglone suppresses epithelial-mesenchymal transition in prostate cancer cells via the protein kinase B/glycogen synthase kinase-3β/Snail signaling pathway |
| - | in-vitro, | Pca, | LNCaP |
| 95- | QC, | Quercetin, a natural dietary flavonoid, acts as a chemopreventive agent |
| - | in-vitro, | Pca, | PC3 |
| 99- | QC, | Quercetin Inhibits Epithelial-to-Mesenchymal Transition (EMT) Process and Promotes Apoptosis in Prostate Cancer via Downregulating lncRNA MALAT1 |
| - | in-vitro, | Pca, | PC3 |
| 80- | QC, | Quercetin reverses EGF-induced epithelial to mesenchymal transition and invasiveness in prostate cancer (PC-3) cell line via EGFR/PI3K/Akt pathway |
| - | in-vitro, | Pca, | PC3 |
| 3078- | RES, | The Effects of Resveratrol on Prostate Cancer through Targeting the Tumor Microenvironment |
| - | Review, | Pca, | NA |
| 105- | RES, | QC, | The Effect of Resveratrol and Quercetin on Epithelial-Mesenchymal Transition in Pancreatic Cancer Stem Cell |
| - | in-vitro, | Pca, | PANC1 |
| 1137- | Taur, | Taurine Attenuates Epithelial-Mesenchymal Transition-Related Genes in Human 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#:355 State#:% Dir#:1
wNotes=0 sortOrder:rid,rpid