miR-429 promotes the proliferation of non-small cell lung cancer cells via targeting DLC-1
Authors: Wenliang Liu
Hui Zhou
Peng Xiao
Journal: Oncology Letters (2016)
Discipline: CLINICAL MEDICINE
Keywords: deleted in liver cancer 1; microRNA; non-small cell lung cancer; proliferation.
Affiliations: Department of Thoracic Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, P.R. China., Department of Thoracic Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, P.R. China., Department of Medical Oncology, Tumor Hospital of Hunan, Changsha, Hunan 410000, P.R. China; State Key Laboratory of Medical Genetics, Central South University, Changsha, Hunan 410078, P.R. China.

Abstract:  The microRNA (miR)-200 family has been demonstrated to be associated with the tumorigenesis and progression of multiple types of human cancer, including non-small cell lung cancer (NSCLC). As a member of the miR-200 family, miR-429 was recently identified to have an oncogenic role in NSCLC. However, the role of miR-429 in NSCLC growth as well as the underlying mechanism remains to be fully elucidated. In the present study, NSCLC cell line H1229 was transfected with miR-429 mimic or inhibitor, respectively. It was observed that overexpression of miR-429 led to a significant increase in NSCLC cell proliferation, while knockdown of miR-429 suppressed the proliferation of H1229 cells. Bioinformatic prediction suggested that deleted in liver cancer 1 (DLC-1), a tumor suppressor in NSCLC, was a putative target gene of miR-429. Therefore, a luciferase reporter assay was performed and confirmed that miR-429 was able to bind the 3'-untranslated region of DLC-1 mRNA in H1229 cells. Furthermore, overexpression of miR-429 inhibited the protein expression of DLC-1, while knockdown of miR-429 promoted the protein expression of DLC-1 in NSCLC H1229 cells. In addition, overexpression of DLC-1 not only inhibited H1229 cell proliferation, but also additionally reversed the promoting effect of miR-429 overexpression on H1229 cell proliferation. Based on these findings, the present study suggests that miR-429 may have an oncogenic role in the regulation of cell proliferation via direct inhibition of DLC-1 protein expression in NSCLC cells. Therefore, miR-429 may present a putative therapeutic target for the treatment of NSCLC growth. 

Retracted: Yes

PubPeer comments:
 *[right]* Fig 3B.  western blotting assays were performed to examine the ... protein levels of DLCu20111 in H1229 cells transfected with DLCu20111 plasmid or blank vector . *[left]* Fig 7 from [Shi et al (2015)] .  Western blot assay was performed to determine the protein levels of E-cadherin and N-cadherin in Saos-2 cells transfected with miR-204 mimics or Sirt1 siRNA, respectively . Unexpected similarity after 180-deg flip.  , 
 *[above[* Fig 4A.  Western blotting was performed to examine the protein level of DLCu20111 in H1229 cells transfected with miRu2011429 mimic, or cou2011transfected with miRu2011429 mimic and DLCu20111 plasmid, respectively . *[below]* Fig 4B from [Lei et al (2014)] .  Western blotting data revealing that miR-145 significantly inhibited the protein expression of MMP2 and MMP9 in KHOS and U2OS cell invasion, which was reversed by ROCK1 overexpression . Unexpected similarity of two bands (after 180-deg flip).  , 
 Retracted [May 24 2021] .  Following the publication of this paper, it was drawn to the Editorsu2019 attention by a concerned reader that certain of the western blotting data in the article (featured in Figs. 3B and 4A) were strikingly similar to data appearing in different form in a pair of other articles by different authors (which were already under consideration for publication or had already been published elsewhere at the time of the present articleu2019s submission. Owing to the fact that the contentious data in the above article had already appeared in different form in other articles prior to its submission to Oncology Letters, the Editor has decided that this paper should be retracted from the Journal. The authors agreed with the retraction of the paper. The Editor apologizes to the readership for any inconvenience caused. ---------------------------------- Background [here] . ,