LincROR promotes tumor growth of colorectal cancer through the miR-145/WNT2B/WNT10A/Wnt/β-catenin regulatory axis

• Published in: PloS one Vol. 19; no. 11; p. e0312417
• Main Authors: Deng, Li-Qiang, Li, Shi-Ying, Xie, Tian, Zeng, Wei-Qiang, Wang, Yu-Yan, Shi, Chuan-Jian, Jin-Fang, Zhang
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 01.11.2024; Public Library of Science (PLoS)
• Subjects: Animals; Apoptosis; beta Catenin - genetics; beta Catenin - metabolism; Binding sites; Bioinformatics; Cancer; Carcinogenesis - genetics; Cell cycle; Cell growth; Cell Line, Tumor; Cell Proliferation - genetics; Cell viability; Colorectal cancer; Colorectal carcinoma; Colorectal Neoplasms - genetics; Colorectal Neoplasms - metabolism; Colorectal Neoplasms - pathology; Female; Gene Expression Regulation, Neoplastic; Glycoproteins; Humans; In vivo methods and tests; Liver cancer; Male; Medical prognosis; Mice; Mice, Inbred BALB C; Mice, Nude; MicroRNAs; MicroRNAs - genetics; MicroRNAs - metabolism; miRNA; Molecular modelling; Plasmids; Protein expression; Proteins; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; Stem cells; Therapeutic targets; Tumorigenesis; Tumors; Wnt protein; Wnt Proteins - genetics; Wnt Proteins - metabolism; Wnt Signaling Pathway - genetics; β-Catenin
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0312417

Colorectal cancer (CRC) is a prevalent form of malignant tumor, and the current clinical treatments are far from satisfactory. Identifying new therapeutic targets is therefore essential for clinical practices. The long intergenic non-protein coding RNA lincROR has been shown to play a significant role in the tumorigenesis of various cancers. However, the molecular mechanism underlying lincROR-mediated CRC tumorigenesis remains unclear. In the present study, we found that knockdown of lincROR significantly inhibited cell viability in vitro , while its overexpression promoted tumor growth in vivo . Mechanistically, lincROR acted as a miRNA sponge for miR-145, thereby elevating the expression of the target genes WNT2B and WNT10A. The overexpression of WNT2B and WNT10A definitely activated the Wnt/β-catenin pathway, thus led to promoting tumorigenesis in CRC. In summary, our findings identified lincROR as a novel activator of the Wnt/β-catenin pathway by serving as a miRNA sponge for miR-145 and facilitating tumorigenesis, which suggests that lincROR may be a potential therapeutic target for CRC patients.