circBANP promotes colorectal cancer growth and metastasis via sponging let-7d-5p to modulate HMGA1/Wnt/β-catenin signaling.

Mol Ther Oncolytics

Department of General Surgery, The Second Affiliated Hospital, Nanjing Medical University, Nanjing 210000, Jiangsu Province, P.R. China.

Published: June 2021

Colorectal cancer (CRC) is one of the most common and deadly cancers, and the incidence of CRC is on the rise. Due to the lack of early diagnosis method and high metastasis of the disease, the prognosis of CRC remains very poor. Exploring the underlying molecular mechanisms of CRC is very necessary for effective therapy. In this study, we investigated the function of circBANP in CRC. The results showed that circBANP was elevated in both CRC tissues and cells and its level positively correlated with the stage of CRC. Knockdown of circBANP greatly suppressed the epithelial-mesenchymal transition (EMT) process and CRC cell proliferation, migration, and invasion. In addition, knockdown of circBANP inhibited CRC tumor growth and metastasis . Further, circBANP directly bound to let-7d-5p and regulated CRC development via acting as a let-7d-5p sponge. Let-7d-5p directly targeted HMGA1 and thus circBANP/let-7d-5p regulated Wnt/β-catenin signaling via HMGA1. Collectively, circBANP promotes CRC development and metastasis via acting as a let-7d-5p sponge to regulate HMGA1/Wnt/β-catenin signaling, providing a potential biomarker and therapeutic target for the management of CRC.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8079336PMC
http://dx.doi.org/10.1016/j.omto.2021.03.012DOI Listing

Publication Analysis

Top Keywords

crc
12
circbanp promotes
8
colorectal cancer
8
growth metastasis
8
hmga1/wnt/β-catenin signaling
8
knockdown circbanp
8
crc development
8
acting let-7d-5p
8
let-7d-5p sponge
8
circbanp
7

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!