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

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 expressi...

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Main Authors: Mingli Hsieh, Pei-Ju Huang, Pei-Yu Chou, Shih-Wei Wang, Hsi-Chi Lu, Wei-Wen Su, Yuan-Chiang Chung, Min-Huan Wu
Format: Article
Language:English
Published: MDPI AG 2022-04-01
Series:Biomedicines
Subjects:
Online Access:https://www.mdpi.com/2227-9059/10/5/1030
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author Mingli Hsieh
Pei-Ju Huang
Pei-Yu Chou
Shih-Wei Wang
Hsi-Chi Lu
Wei-Wen Su
Yuan-Chiang Chung
Min-Huan Wu
author_facet Mingli Hsieh
Pei-Ju Huang
Pei-Yu Chou
Shih-Wei Wang
Hsi-Chi Lu
Wei-Wen Su
Yuan-Chiang Chung
Min-Huan Wu
author_sort Mingli Hsieh
collection DOAJ
description 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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spelling doaj.art-968d3857e18c4de7ba6cdf213a7b07682023-11-23T10:10:04ZengMDPI AGBiomedicines2227-90592022-04-01105103010.3390/biomedicines10051030Carbonic Anhydrase VIII (CAVIII) Gene Mediated Colorectal Cancer Growth and Angiogenesis through Mediated miRNA 16-5pMingli Hsieh0Pei-Ju Huang1Pei-Yu Chou2Shih-Wei Wang3Hsi-Chi Lu4Wei-Wen Su5Yuan-Chiang Chung6Min-Huan Wu7Department of Life Science, Tunghai University, No. 1727, Sec. 4, Taiwan Boulevard, Taichung 407, TaiwanDepartment of Family Medicine, Changhua Christian Hospital, Changhua 500, TaiwanLife Science Research Center, Tunghai University, No. 1727, Sec. 4, Taiwan Boulevard, Taichung 407, TaiwanGraduate Institute of Natural Products, College of Pharmacy, Kaohsiung Medical University, Kaohsiung 807, TaiwanLife Science Research Center, Tunghai University, No. 1727, Sec. 4, Taiwan Boulevard, Taichung 407, TaiwanDepartment of Gastroenterology and Hepatology, Changhua Christian Hospital, Changhua 500, TaiwanDepartment of Surgery, Cheng-Ching General Hospital, Taichung 407, TaiwanLife Science Research Center, Tunghai University, No. 1727, Sec. 4, Taiwan Boulevard, Taichung 407, TaiwanCarbonic 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.https://www.mdpi.com/2227-9059/10/5/1030carbonic anhydrase VIIIvascular endothelial growth factorangiogenesismiR-16-5p
spellingShingle Mingli Hsieh
Pei-Ju Huang
Pei-Yu Chou
Shih-Wei Wang
Hsi-Chi Lu
Wei-Wen Su
Yuan-Chiang Chung
Min-Huan Wu
Carbonic Anhydrase VIII (CAVIII) Gene Mediated Colorectal Cancer Growth and Angiogenesis through Mediated miRNA 16-5p
Biomedicines
carbonic anhydrase VIII
vascular endothelial growth factor
angiogenesis
miR-16-5p
title Carbonic Anhydrase VIII (CAVIII) Gene Mediated Colorectal Cancer Growth and Angiogenesis through Mediated miRNA 16-5p
title_full Carbonic Anhydrase VIII (CAVIII) Gene Mediated Colorectal Cancer Growth and Angiogenesis through Mediated miRNA 16-5p
title_fullStr Carbonic Anhydrase VIII (CAVIII) Gene Mediated Colorectal Cancer Growth and Angiogenesis through Mediated miRNA 16-5p
title_full_unstemmed Carbonic Anhydrase VIII (CAVIII) Gene Mediated Colorectal Cancer Growth and Angiogenesis through Mediated miRNA 16-5p
title_short Carbonic Anhydrase VIII (CAVIII) Gene Mediated Colorectal Cancer Growth and Angiogenesis through Mediated miRNA 16-5p
title_sort carbonic anhydrase viii caviii gene mediated colorectal cancer growth and angiogenesis through mediated mirna 16 5p
topic carbonic anhydrase VIII
vascular endothelial growth factor
angiogenesis
miR-16-5p
url https://www.mdpi.com/2227-9059/10/5/1030
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