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| MCP-1 (Monocyte Chemoattractant Protein-1, also known as CCL2) MCP-1/CCL2 is a chemokine involved in recruiting monocytes, memory T cells, and dendritic cells to sites of inflammation. – It plays a key role in mediating immune cell trafficking, inflammation, and tissue remodeling. MCP-1 is pivotal in inflammatory responses and can modulate immune cell infiltration into tissues. – It also influences the polarization of macrophages, which may adopt pro-inflammatory (M1) or anti-inflammatory/pro-tumoral (M2) roles. Many cancers (such as breast, prostate, ovarian, lung, and colon cancers) exhibit increased levels of MCP-1. – Both tumor cells and associated stromal cells (e.g., cancer-associated fibroblasts, infiltrating immune cells) can produce MCP-1, contributing to an inflammatory milieu. • Inducers of MCP-1: – Hypoxia, oncogenic pathways, and cytokine-rich environments (e.g., IL-1β, TNF-α) can drive increased MCP-1 expression. – This upregulation often correlates with an ongoing inflammatory response in the tumor microenvironment. |
| 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. |
| 5951- | Cela, | Celastrol Suppresses Tumor Cell Growth through Targeting an AR-ERG-NF-κB Pathway in TMPRSS2/ERG Fusion Gene Expressing Prostate Cancer |
| - | vitro+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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:22 Cells:% prod#:% Target#:990 State#:% Dir#:1
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