lncRNA HOTAIRM1 regulates cell proliferation and the metastasis of thyroid cancer by targeting Wnt10b
Authors: Chenyao Li
Xinxin Chen
Guang Chen
Tao Liu
Journal: Oncology Reports (2020)
Discipline: CLINICAL MEDICINE
Keywords: papillary thyroid cancer; lncRNA HOTAIRM1; miR-148a; Wnt10b.
Affiliations: Department of Colorectal and Anal Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China., Department of Burn Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China., Department of Thyroid Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.

Abstract:  Long non‑coding RNAs play a role in a variety of malignancies, such as thyroid cancer (TC). However, the effects and function of lincRNA HOTAIRM1 (LINC HOTAIRM1) in TC remains obscure. In the present study, the expression of HOTAIRM1 was evaluated in TC tissues and cells by RT‑qPCR and the association between the lncRNA and disease progression was assessed. In vitro, the biological function of HOTAIRM1 was assessed in TC. Moreover, changes in the expression of Wnt10b were measured by western blot analysis. In addition, MTT assay, bioinformatics analysis and luciferase assays were performed to determine the target binding effect between LINC HOTAIRM1 and miR‑148a, as well as that between Wnt10b and miR‑148a. The changes in the metastatic ability of TPC‑1 and BCPAP cells were evaluated by Transwell assay. The pronounced upregulated expression of HOTAIRM1 was evident in TC cells and tissues, and was associated with TNM stage and lymph node metastasis. When HOTAIRM1 was knocked down, this inhibited the proliferative and invasive abilities of TPC‑1 and BCPAP cells in vitro. The knockdown of this lncRNA also increased the expression of microRNA‑148a (miR‑148a) and decreased Wnt10b expression in these cells, whereas transfection with miR‑148a inhibitor was sufficient to overcome this Wnt10b downregulation. In line with these results, the overexpression of miR‑148a markedly suppressed Wnt10b expression, whereas miR‑148a inhibition resulted in the opposite effects. The overexpression of Wnt10b was also sufficient to overcome the effects of miR‑148a mimics on TPC‑1 and BCPAP cells. Taken together, these results suggest that miR‑148a and Wnt10b are downstream effectors of the HOTAIRM1 signaling pathway in TC. This HOTAIRM1/miR‑148a/Wnt10 axis may thus be amenable to therapeutic targeting in order to improve disease outcomes in patients with TC. 

Retracted: No

PubPeer comments:
 Figure 6. Some WB results were repeated at the edge of the figure. It seems to be a careless mistake happened during figure processing. ![file] , 
 Fig 1B.  TC patient survival curves for individuals exhibiting low or high levels of HOTAIRM1 expression (n=52) ![file] Patient survival was evidently followed for 5 years after recruitment. It is hard to reconcile this with the note that  A total of 52 pairs clinical tissues were obtained from patients with TC at the First Hospital of Jilin University from **March 2019 to November 2019** . Was a time machine involved? , 
 Thank you for your attention to this article. First of all, In the first picture, the two pictures are not duplicated, they are obviously different, but the strips are slanted when running. The time in the second figure, which is the time of the patient tissue used, if this patient was lost five years ago, of course, he would not be included, so there would be no need to test for HOMAD. That is to say, we identify the patients that can be contacted, and then test their indicators, and screen them out for statistics. ,