AI Article Synopsis
- Angiogenesis, the formation of new blood vessels, is crucial for tumor growth and spread, and calcium signaling plays a significant role in this process, specifically in non-small cell lung cancer (NSCLC).
- Researchers used various methods, including small interfering RNA and assays, to study the impact of TRPV3, a calcium-permeable channel, on angiogenesis by checking effects on calcium levels and the migration and proliferation of endothelial cells.
- The findings showed that inhibiting TRPV3 reduced crucial proteins (VEGF and HIF-1α) associated with angiogenesis, indicating that TRPV3 is vital for NSCLC angiogenesis and suggesting that targeting this channel could offer new treatment strategies.
Article Abstract
Background: Angiogenesis is an essential physiological process in the growth and metastasis of primary tumors. Ca signaling is crucial for tumor angiogenesis. The purpose of this study was to detect the potential role of Ca permeable transient receptor potential vanilloid-3 (TRPV3) in the angiogenesis of non-small cell lung cancer (NSCLC).
Methods: Small interfering RNA was used to down-regulate TRPV3 expression in A549 cells. A laser scanning confocal microscope was used to examine intracellular calcium concentration ([Ca]i). Human umbilical vein endothelial cells (HUVECs) tube formation and migration assay, Western blot, MTT and ELISA were performed to detect the potential mechanisms of TRPV3 in tumor angiogenesis. A mouse tumor xenograft model was performed to expound the effects of TRPV3 on tumor cell growth.
Results: Inhibition of TRPV3 reduced [Ca]i and protein expressions of VEGF and HIF-1α in A549 cells. Moreover, HIF-1α depletion decreased the secretion and expression of VEGF. Depletion of TRPV3 inhibited HUVECs proliferation, tube formation and migration induced by conditioned medium. And TRPV3 inhibition could decrease the volume of xenograft tumors and MVD of CD34 cells. The expression levels of HIF-1α, VEGF and p-CaMKП in the xenograft tumors in RuR and siTRPV3 groups was reduced.
Conclusions: TRPV3 calcium channel protein may play a key role in NSCLC angiogenesis. TRPV3 could promote the angiogenesis through HIF-1α-VEGF signaling pathway. Targeting TRPV3 channel protein by novel approaches would be useful for reversing NSCLC angiogenesis.
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| http://dx.doi.org/10.1016/j.acthis.2022.151955 | DOI Listing |
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