The roles of long non-coding RNAs (lncRNAs) have been discussed and analysed in previous studies. The messenger RNAs (mRNAs) are frequently reported to be regulated by lncRNAsin colorectal cancer (CRC).Here,we elucidated the role of themRNAactin gamma 2 (ACTG2) in CRC progression using SW837 and LOVO cells. Gene expression was detected by real-time quantitative polymerase chain reaction (RT-qPCR) and subcellular localization was assessed using subcellular fractionation assay. Cell counting kit-8 (CCK-8), colony formation, and Transwell assayswere performed to detectCRCcell phenotypes.RNApulldown, luciferase reporter, andRNAimmunoprecipitation (RIP) assays were conducted to reveal the interactionsamongmicroRNA-3918 (miR-3918), lncRNAmir-497-195 cluster host gene (MIR497HG) andACTG2.The ACTG2 level was downregulated in CRC cells and samples. ACTG2 overexpression suppressed CRC cell proliferation, migration, and invasion. Additionally, miR-3918 inhibition increased the level of ACTG2 and the interaction between miR-3918 and ACTG2 was verified. MIR497HG was markedly downregulated in CRC cells and samples. Overexpression of MIR497HG decreased miR-3918 expression while increased ACTG2 expression. Further, the inhibitory effects exerted by MIR497HG overexpression on malignant phenotypes of CRC cells were reversed by ACTG2 knockdown.MIR497HGexerts inhibitory effects on CRC progression by the miR-3918/ACTG2 axis.Our study conducted a systematic analysis of the biological roles of ACTG2, miR-3918 and MIR497HG, and the relationship among them in CRC progression. ACTG2 and MIR497HG were found to be tumour suppressors in CRC cell growth. More importantly, a novel ceRNA network, with MIR497HG as a ceRNA to regulate the miR-3918/ACTG2 axis, was found to play a key role in CRC cell proliferation, migration and invasion.

The published figure 1, h&j and figure 4, e&g showing the Transwell assays were given incorrectly. We now provide the correct images. The replacement of the images does not affect the scientific conclusions of the article. We deeply regret theinconvenience.