4.7 Article

Carbonic Anhydrase VIII (CAVIII) Gene Mediated Colorectal Cancer Growth and Angiogenesis through Mediated miRNA 16-5p

期刊

BIOMEDICINES
卷 10, 期 5, 页码 -

出版社

MDPI
DOI: 10.3390/biomedicines10051030

关键词

carbonic anhydrase VIII; vascular endothelial growth factor; angiogenesis; miR-16-5p

资金

  1. Taiwan's Ministry of Science and Technology [MOST 106-2632-B-029-001, 106-2320-B-029-002, 104-2632-B-029-001, 105-2632-B-029-001]

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Research has shown that CAVIII is overexpressed in colorectal cancer tissues and more aggressive cancer cells. It may facilitate the release of VEGF by inhibiting miRNA16-5p. The CAVIII/miR-16-5p signaling pathway appears to function as a metastasis suppressor in CRC.
Carbonic anhydrase VIII (CAVIII) is a member of the CA family, while CA8 is the oncogene. Here we observed increased expression of CAVIII with high expression in colorectal cancer tissues. CAVIII is also expressed in more aggressive types of human colorectal cancer cells. Upregulated CAVIII expression in SW480 cell lines increased vascular endothelial growth factor (VEGF) and reduced miRNA16-5p. Conversely, knockdown of the CAVIII results in VEGF decline by up-regulated miRNA16-5p. Moreover, the collection of different grades of CAVIII expression CRC cells supernatant co-culture with endothelial progenitor cells (EPCs) promotes the ability of tube formation in soft agar and migration in the Transwell experiment, indicating that CAVIII might facilitate cancer-cell-released VEGF via the inhibition of miRNA16-5p signaling. Furthermore, in the xenograft tumor angiogenesis model, knockdown of CAVIII significantly reduced tumor growth and tumor-associated angiogenesis. Taken together, our results prove that the CAVIII/miR-16-5p signaling pathway might function as a metastasis suppressor in CRC. Targeting CAVIII/miR-16-5p may provide a strategy for blocking its metastasis.

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