In:
Frontiers in Oncology, Frontiers Media SA, Vol. 11 ( 2021-4-14)
Kurzfassung:
Background: Colorectal cancer (CRC), the most commonly diagnosed cancer in the world, has a high mortality rate. In recent decades, long non-coding RNAs (lncRNAs) have been proven to exert an important effect on CRC growth. However, the CTBP1-AS2 expression and function in CRC are largely unknown. Materials and Methods: The CTBP1-AS2 and miR-93-5p expression in CRC and para-cancerous tissues was detected by reverse transcription-PCR. The expression of CTBP1-AS2, miR-93-5p and the transforming growth factor-beta (TGF-β)/small mothers against decapentaplegic 2/3 (SMAD2/3) pathway was selectively regulated to study the correlation between CTBP1-AS2 expression and prognosis of patients with CRC. CRC cell proliferation, apoptosis, and invasion were measured in vivo and in vitro . In addition, bioinformatics was applied to explore the targeting relationship between CTBP1-AS2 and miR-93-5p. The targeting binding sites between CTBP1-AS2 and miR-93-5p, as well as between miR-93-5p and TGF-β, were verified by the dual-luciferase reporter assay and the RNA immunoprecipitation experiment. Results: Compared with normal para-cancerous tissues, CTBP1-AS2 was considerably overexpressed in CRC tissues and was closely associated with worse survival of patients with CRC. Functionally, gain and loss in experiments illustrated that CTBP1-AS2 accelerated CRC cell proliferation and invasion and inhibited cell apoptosis. Mechanistically, CTBP1-AS2 regulated the malignant phenotype of tumor cells through the TGF-β/SMAD2/3 pathway. Moreover, miR-93-5p, as an endogenous competitive RNA of CTBP1-AS2, attenuated the oncogenic effects mediated by CTBP1-AS2. Conclusion: CTBP1-AS2 promotes the TGF-β/SMAD2/3 pathway activation by inhibiting miR-93-5p, thereby accelerating CRC development.
Materialart:
Online-Ressource
ISSN:
2234-943X
DOI:
10.3389/fonc.2021.626620
DOI:
10.3389/fonc.2021.626620.s001
DOI:
10.3389/fonc.2021.626620.s002
DOI:
10.3389/fonc.2021.626620.s003
Sprache:
Unbekannt
Verlag:
Frontiers Media SA
Publikationsdatum:
2021
ZDB Id:
2649216-7
