MicroRNA‑34a directly targets high‑mobility group box 1 and inhibits the cancer cell proliferation, migration and invasion in cutaneous squamous cell carcinoma Retraction in /10.3892/etm.2021.10692

Li,Shanshan; Luo,Chengqun; Zhou,Jun; Zhang,Yong

doi:10.3892/etm.2017.5245

MicroRNA‑34a directly targets high‑mobility group box 1 and inhibits the cancer cell proliferation, migration and invasion in cutaneous squamous cell carcinoma

Retraction in: /10.3892/etm.2021.10692

Authors:
- Shanshan Li
- Chengqun Luo
- Jun Zhou
- Yong Zhang
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Affiliations: Department of Plastic and Reconstructive Surgery, Plastic Surgery Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100144, P.R. China, Department of Burns, The Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, P.R. China, Department of Neurology, The Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, P.R. China, Department of Cosmetic and Plastic Surgery, The Third People's Hospital of Huaihua, Huaihua, Hunan 418000, P.R. China
Published online on: October 2, 2017 https://doi.org/10.3892/etm.2017.5245
Pages: 5611-5618

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Abstract

Cutaneous squamous cell carcinoma (CSCC) is the second most common type of skin cancer with increasing incidence. In recent years, several microRNAs (miRs) have been demonstrated to serve an oncogenic or tumor suppressive role in CSCC. However, the exact role of miR‑34a in CSCC and the underlying regulatory mechanism remain unclear. The present study aimed to investigate the regulatory mechanism of miR‑34a in the malignant phenotypes of CSCC cells using MTT assay, wound healing assay and transwell assay. It was observed that miR‑34a was significantly downregulated in CSCC tissues and cell lines, and low miR‑34a expression was associated with the aggressive progression of CSCC. Restoration of miR‑34a significantly suppressed the proliferation, migration and invasion of CSCC SCL‑1 cells. High‑mobility group box 1 (HMGB1) was then identified as a target gene of miR‑34a in SCL‑1 cells using bioinformatics prediction. The expression of HMGB1 was significantly upregulated in the CSCC tissues and cell lines. Furthermore, the protein expression of HMGB1 was negatively regulated by miR‑34a in SCL‑1 cells, while overexpression of HMGB1 impaired the inhibitory effects of miR‑34a on SCL‑1 cells. These findings suggest that miR‑34a represses the malignant phenotypes of CSCC cells, at least partly, via the inhibition of HMGB1. Therefore, miR‑34a may be used as a promising therapeutic candidate for CSCC.

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