Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2019 Aug;8(4):1097–1108. doi: 10.21037/tcr.2019.06.20

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

2019 Translational Cancer Research. All rights reserved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

PMC Copyright notice

Wnt/β-catenin signaling is responsible for the oncogenic role of MIR17HG-miR-17/miR-18a axis in colon cancer. (A,B) Depletion of MIR17HG in colon cancer cells caused the suppression of Wnt/β-catenin signaling, whereas miR-17 or miR-18a overexpression abrogated this effect. (C) The downstream target genes of Wnt/β-catenin signaling in sh-NC/sh-MIR17HG colon cancer cells were detected by qRT-PCR after treated with 10 µmol/L CHIR99021 for 36 hours. (D,E) Depletion of MIR17HG decreased the proliferative and invasive abilities of colon cancer cells, and these effects were rescued by activating Wnt/β-catenin signaling. *P<0.05; **P<0.01; ***P<0.001.