Table of Content

Open Access iconOpen Access

ARTICLE

Inhibition of Long Noncoding RNA CRNDE Increases Chemosensitivity of Medulloblastoma Cells by Targeting miR-29c-3p

by

* Medical Department, Qingdao Infectious Disease Hospital, Qingdao, Shandong, P.R. China
† Department of Anesthesia, Qingdao Women and Children’s Hospital, Qingdao, Shandong, P.R. China
‡ Department of Pediatric Neurosurgery, Qingdao Women and Children’s Hospital, Qingdao, Shandong, P.R. China

Oncology Research 2020, 28(1), 95-102. https://doi.org/10.3727/096504019X15742472027401

Abstract

Long noncoding RNA CRNDE (CRNDE) recently emerged as a carcinogenic promoter in various cancers including medulloblastoma. However, the functions and molecular mechanisms of CRNDE to the acquired drug resistance of medulloblastoma are still unclear. The transcript levels of CRNDE were examined in four medulloblastoma cell lines exposed to cisplatin treatment, and IC50 values were calculated. Effects of CRNDE knockdown or miR-29c-3p overexpression on cell viability, colony formation, apoptosis, migration, and invasion were assessed using the CCK-8, colony formation assay, flow cytometry, and Transwell assays, respectively. RNA pulldown and RNA-binding protein immunoprecipitation (RIP) were performed to confirm the molecular interactions between CRNDE and miR-29c-3p involved in medulloblastoma cells. The in vivo role of CRNDE knockdown or miR-29c-3p overexpression on tumor growth and apoptosis was evaluated in a xenograft mouse model of human medulloblastoma. The transcript levels of lncRNA CRNDE were significantly higher in cisplatin-treated tumor cells with higher IC50 values. Depletion of CRNDE inhibited tumor cell proliferation and colony formation, induced cell apoptosis, and suppressed migration and invasion in medulloblastoma cells. Moreover, overexpression of miR-29c-3p inhibited tumor cell proliferation and colony formation, migration, and invasion, and enhanced apoptosis and chemosensitivity to cisplatin. In addition, CRNDE was found to act as a miR-29c-3p sponge. Furthermore, in vivo experiments showed the CRNDE/miR-29c-3p interactions involved in medulloblastoma. Our study demonstrates that CRNDE acts as a critical mediator of proliferation, apoptosis, migration, invasion, and resistance to chemotherapeutics via binding to and negatively regulating miR-29c-3p in medulloblastoma cells. These results provide novel molecular targets for treatment of medulloblastoma.

Keywords


Cite This Article

APA Style
Sun, X., Fan, W., An, Z., Sun, Y. (2020). Inhibition of long noncoding RNA CRNDE increases chemosensitivity of medulloblastoma cells by targeting mir-29c-3p. Oncology Research, 28(1), 95-102. https://doi.org/10.3727/096504019X15742472027401
Vancouver Style
Sun X, Fan W, An Z, Sun Y. Inhibition of long noncoding RNA CRNDE increases chemosensitivity of medulloblastoma cells by targeting mir-29c-3p. Oncol Res. 2020;28(1):95-102 https://doi.org/10.3727/096504019X15742472027401
IEEE Style
X. Sun, W. Fan, Z. An, and Y. Sun, “Inhibition of Long Noncoding RNA CRNDE Increases Chemosensitivity of Medulloblastoma Cells by Targeting miR-29c-3p,” Oncol. Res., vol. 28, no. 1, pp. 95-102, 2020. https://doi.org/10.3727/096504019X15742472027401



cc Copyright © 2020 The Author(s). Published by Tech Science Press.
This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
  • 776

    View

  • 531

    Download

  • 0

    Like

Share Link