1. Academic Validation
  2. circRNA-SMO upregulates CEP85 to promote proliferation and migration of glioblastoma via sponging miR-326

circRNA-SMO upregulates CEP85 to promote proliferation and migration of glioblastoma via sponging miR-326

  • Histol Histopathol. 2023 Jan 18;18587. doi: 10.14670/HH-18-587.
Bin Wu 1 2 3 4 Liang Xia 2 3 4 Shuyuan Zhang 2 3 4 Kai Jin 2 3 Liwen Li 2 3 Caixing Sun 2 3 5 Ting Xia 3 6 Gao Chen 7
Affiliations

Affiliations

  • 1 Department of Neurosurgery, The second Affiliated Hospital of Medical College of Zhejiang University, Hangzhou, Zhejiang Province, China.
  • 2 Department of Neurosurgery, Zhejiang Cancer Hospital, Hangzhou, Zhejiang Province, China.
  • 3 Institute of Basic Medicine and Cancer (IBMC), Chinese Academy of Sciences, Hangzhou, Zhejiang Province, China.
  • 4 Key Laboratory of Head and Neck Cancer Translational Research of Zhejiang Province, Hangzhou, Zhejiang Province, China.
  • 5 Key Laboratory of Head and Neck Cancer Translational Research of Zhejiang Province, Hangzhou, Zhejiang Province, China. [email protected].
  • 6 Department of Gynecologic Oncology, Zhejiang Cancer Hospital, Hangzhou, Zhejiang Province, China. [email protected].
  • 7 Department of Neurosurgery, The second Affiliated Hospital of Medical College of Zhejiang University, Hangzhou, Zhejiang Province, China. [email protected].
Abstract

Circular RNAs (circRNAs) play an important role in Cancer development by sponging MicroRNAs (miRNAs) to regulate the signaling axis. However, more comprehensive mechanisms of circRNAs in glioblastoma need to be elucidated. RT-qPCR was used to detect the expression levels of circRNA-SMO and miR-326. Dual-luciferase reporter assays were conducted to verify the interaction among circRNA-SMO, miR-326, and CEP85. Flow cytometric analysis was performed to detect Apoptosis. Western blotting was used to determine the protein levels of the different molecules. Animal xenograft experiments were performed to evaluate the role of circRNA-SMO in vivo. CircRNA-SMO was upregulated in glioblastoma tissues and glioblastoma cells. CircRNA-SMO downregulation inhibited the viability and colony-forming ability of the glioblastoma cells. In addition, miR-326 was downregulated in glioblastoma cells, which was verified to Sponge circRNA-SMO and interact with CEP85. Moreover, circRNA-SMO inhibition induced the elevation of miR-326 and Apoptosis, accompanied by a decrease in CEP85. CircRNA-SMO knockdown-mediated tumor inhibition was prevented by an miR-326 inhibitor. Furthermore, circRNA-SMO inhibition inhibited tumor growth in vivo, accompanied by an increase in miR-326 and a decline in CEP85 in tumor tissues. Conclusions. CircRNA-SMO sponges miR-326 to promote glioblastoma proliferation and migration by upregulating CEP85 expression. This study clarified the role of circRNA-SMO in the development of glioblastoma, providing novel insights for its treatment.

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