MiR-130a-3p Suppresses Colorectal Cancer Growth by Targeting Wnt Family Member 1 (WNT1)
Overview
Authors
Affiliations
The microRNA miR-130a-3p (miR-130a-3p) has anti-tumor activity against numerous cancer types. Further, miR-130a-3p may target Wnt signaling, which is a critical pathway regulating tumorigenesis. Functions of miR-130a-3p in colorectal cancer (CRC) and contributions of Wnt1 pathway modulation, however, have not been examined, hence the exploration on these two aspects. In this study, in comparison with normal controls, both CRC tissue and multiple CRC cell lines showed downregulated miR-130a-3p. MiR-130a-3p overexpression contributed to a decrease in CRC cell proliferation. Additionally, its overexpression also caused reduced expression of WNT Family Member 1 (WNT1) and downstream WNT pathway factors c-myc and cyclin D1. Dual-luciferase assay revealed WNT1 as a direct target of miR-130a-3p, and further the inhibitory effect of miR-130a-3p on c-myc and cyclin D1 was proved to be reversed by overexpressed WNT1. Collectively, miR-130a-3p inhibits CRC growth by directly targeting WNT1, and miR-130a-3p and WNT1 pathway-associated factors are defined as potential targets for CRC treatment.
Wang X, Qu Z, Zhao S, Luo L, Yan L Mol Med. 2024; 30(1):193.
PMID: 39468464 PMC: 11520425. DOI: 10.1186/s10020-024-00957-x.
The expression and biological role of complement C1s in esophageal squamous cell carcinoma.
Ge R, Luan Z, Guo T, Xia S, Ye J, Xu J Open Life Sci. 2024; 19(1):20220915.
PMID: 39071493 PMC: 11282917. DOI: 10.1515/biol-2022-0915.
Exploring the Key Signaling Pathways and ncRNAs in Colorectal Cancer.
Lee Y, Kim W, Park E, Lee D, Kim J, Shin H Int J Mol Sci. 2024; 25(8).
PMID: 38674135 PMC: 11050203. DOI: 10.3390/ijms25084548.
KLF3 promotes colorectal cancer growth by activating WNT1.
Shen W, Yuan L, Hao B, Xiang J, Cheng F, Wu Z Aging (Albany NY). 2024; 16(3):2475-2493.
PMID: 38305787 PMC: 10911342. DOI: 10.18632/aging.205494.
Saffar K, Larypoor M, Torbati M Mol Biol Rep. 2024; 51(1):122.
PMID: 38227272 DOI: 10.1007/s11033-023-09008-w.