Long noncoding RNAs (lncRNAs) play a critical role in the development of lung carcinoma. The mechanism of MALAT1 in lung carcinoma development is not understood very well. This study aimed to investigate the role of MALAT1 in lung carcinoma progression and the mechanism underlying the role of miR-491-5p in the MALAT1 mediated regulation of UBE2C expression. The results indicated that the expression of MALAT1 was often augmented in lung carcinoma cells. Suppression of MALAT1 blocked the proliferation, invasion and migration ability of cancer cells and inhibited the expression of UBE2C. UBE2C restoration attenuated the MALAT1 knockdown-induced anti-cancer effects. Moreover, UBE2C and MALAT1 were indicated as targets of miR-491-5p and inhibition of miR-491-5p restored the MALAT1 knockdown-induced inhibition of the progression of lung carcinoma. Furthermore, MALAT1 sponged miR-491-5p to upregulate UBE2C expression, causing it to act as a competing endogenous RNA. Collectively, MALAT1 downregulation suppressed lung carcinoma progression by regulating the miR-491-5p/UBE2C axis. These results indicate that MALAT1 could be a molecular target for lung carcinoma treatment and prognosis.
In the article titled “UBE2C Induces Cisplatin Resistance via ZEB1/2-Dependent Upregulation of ABCG2 and ERCC1 in NSCLC Cells” [1], there is a concern of figure issue. In Figure 5(c), the wound healing images of PBS treatment were unintentionally misused for the control, siUBE2C, siUBE2C + ZEB1, and UBE2C treatments in the groups of 0 h. In addition, the wound healing image of siUBE2C treatment was unintentionally misused for the UBE2C + siZEB1 treatment in the groups of 36 h. The only change is in the panel of Figure 5(c), and the rest of the figure is identical to the published version. This unintentional error also has no bearing on the work’s scientific conclusions in any way. The authors apologize to the Editor of Journal of Oncology and to the readership for any inconvenience caused. The corrected figure and legend are presented here.