Retracted: microRNA-130a Promotes Human Keratinocyte Viability and Migration and Inhibits Apoptosis Through Direct Regulation of STK40-Mediated NF-κB Pathway and Indirect Regulation of SOX9-Meditated JNK/MAPK Pathway: A Potential Role in Psoriasis
Authors: Yongliang Zhao
Liqian Liu
Leihong Lu
Ying Xiong
Hongxiao Chen
Fujun Tian
Zongshan Wang
Journal: DNA and Cell Biology (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: JNK/MAPK; NF-κB; microRNA-130a; psoriasis; serine/threonine kinase 40
Affiliations: Department of Dermatology, Linyi People's Hospital, Linyi, China.

Abstract:  Psoriasis is a chronic inflammatory skin disorder. The aim of this study was to determine a potential role of microRNA (miR)-130a in psoriasis, and underlying mechanism. Expression levels of miR-130a in psoriasis specimens and normal skin tissues were analyzed. MiR-130a mimic, inhibitor, miR-control, small interfering RNA (siRNA) specific serine/threonine kinase 40 (STK40), or sex-determining region Y chromosome-box 9 (SOX9) were transfected to human keratinocyte HaCaT cells, respectively. After transfection, the cell viability, apoptosis, and migration were determined. Luciferase reporter assay, quantitative reverse transcription-polymerase chain reaction, and western blot were performed to explore whether STK40 was a target of miR-130a. The effects of aberrant expressions of miR-130a, STK40, or SOX9 on key proteins of NF-κB and c-Jun N-terminal kinase (JNK)/mitogen-activated protein kinase (MAPK) pathway were assessed. The miR-130a levels were significantly higher in patients with psoriasis compared to the healthy controls (p &lt; 0.01). Overexpressing miR-130a strikingly promoted HaCaT cell viability and migration and inhibited apoptosis (p &lt; 0.01 or p &lt; 0.05). We confirmed that STK40 was a direct target of miR-130a, and STK40 was involved in miR-130a-induced cell functions. Overexpressing miR-130a significantly upregulated NF-κB p65, SOX9, p-c-Jun, p-JNK, and p-p38MAPK proteins and silencing miR-130a downregulated them. In addition, silencing STK40 alleviated the effects of anti-miR-130a on SOX9 expression. Furthermore, silencing SOX9 also decreased levels of p-c-Jun, p-JNK, and p-p38MAPK proteins. MiR-130a regulates human keratinocyte HaCaT viability, migration and apoptosis might be by direct regulation of STK40-mediated NF-κB pathway and by indirect regulation of SOX9-mediated downstream JNK/MAPK signaling pathway. 

Retracted: Yes

PubPeer comments:
 Western blots populated with tadpoles.... apoptosis flow-cytometry scatterplots reminiscent of mandolins... This paper has all the hallmarks of a product of the  Tadpoles papermill discussed here: - https: scienceintegritydigest.com 2020 02 21 the-tadpole-paper-mill - https: forbetterscience.com 2020 01 24 the-full-service-paper-mill-and-its-chinese-customers ![file] ![file] , 
 2021 retraction. https: www.liebertpub.com doi 10.1089 dna.2016.3517.retract DNA and Cell Biology officially retracts the article entitled, u201cmicroRNA-130a Promotes Human Keratinocyte Viability and Migration and Inhibits Apoptosis Through Direct Regulation of STK40-Mediated NF-u03baB Pathway and Indirect Regulation of SOX9-Meditated JNK MAPK Pathway: A Potential Role in Psoriasis,u201d by Ying Xiong, Hongxiao Chen, Liqian Liu, Leihong Lu, Zongshan Wang, Fujun Tian, and Yongliang Zhao (DNA Cell Biol 2017;36(3):219u2013226; doi: 10.1089 dna.2016.3517). A serious concern was brought to the attention of Dr. Carol Reiss, the Editor-in-Chief of DNA and Cell Biology, regarding the supporting data underlying the study. Dr. Reiss contacted the authors to request that all original uncropped scans of membranes used for Western blot analysis be supplied for further assessment, however the authors did not respond within the 2-week timeframe supplied. Dr. Reiss contacted the authors again, indicating that their failure to reply was indicative of their acknowledgement of misconduct. DNA and Cell Biology and its editorial leadership treat these reports of possible scientific misconduct very seriously and therefore officially retracts this article from the scientific literature. ,