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Research Paper|Volume 12, Issue 21|pp 21674—21686

Circular RNA circSEMA5A promotes bladder cancer progression by upregulating ENO1 and SEMA5A expression

Lei Wang1, Haoran Li2, Qingdong Qiao1, Yukun Ge1, Ling Ma1, Qiang Wang3
  • 1Department of Urology, Xinxiang Central Hospital, Xinxiang, Henan, China
  • 2School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, Henan, China
  • 3Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing, China
Received: April 16, 2020Accepted: July 30, 2020Published: November 7, 2020
https://doi.org/10.18632/aging.103971

Copyright: © 2020 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Bladder cancer (BC) is one of the most commonly diagnosed urologic carcinomas, with high recurrence and death rates. Circular RNAs (circRNAs) are a class of noncoding RNAs which are anomalously expressed in cancers and involved in the progression of cancers. In this study, we found that circSEMA5A was upregulated in BC tissues and cell lines. The overexpressed circSEMA5A was correlated with malignant characteristics of BC. In vitro data indicated that circSEMA5A promoted proliferation, suppressed apoptosis, facilitated migration, accelerated invasion, enhanced angiogenesis and promotes glycolysis of BC. Mechanistically, circSEMA5A served as a miRNA sponge for miR-330-5p to upregulates Enolase 1 (ENO1) expression and facilitated the activation of Akt and β-catenin signaling pathways. Then, we showed that circSEMA5A exerted its biological functions partially via miR-330-5p/ENO1 signaling. Moreover, circSEMA5A raised SEMA5A expression by recruiting EIF4A3 to enhance the mRNA stability of SEMA5A, and thereby accelerated BC angiogenesis. To sum up, circSEMA5A is upregulated in BC and facilitates BC progression by mediating miR-330-5p/ENO1 signaling and upregulating SEMA5A expression.