MicroRNA‑152 inhibits cell proliferation, migration and invasion by directly targeting MAFB in nasopharyngeal carcinoma Retraction in /10.3892/mmr.2023.12960

Li,Yan; Min,Daliu; Wang,Kai; Yin,Shankai; Zheng,Hongliang; Liu,Liangfa

doi:10.3892/mmr.2016.6059

MicroRNA‑152 inhibits cell proliferation, migration and invasion by directly targeting MAFB in nasopharyngeal carcinoma

Retraction in: /10.3892/mmr.2023.12960

Authors:
- Yan Li
- Daliu Min
- Kai Wang
- Shankai Yin
- Hongliang Zheng
- Liangfa Liu
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Affiliations: Department of Otolaryngology, Affiliated Sixth People's Hospital of Shanghai Jiao Tong University, Shanghai 200233, P.R. China, Department of Otolaryngology Head Neck Surgery, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, P.R. China, Department of Otolaryngology, Zhabei Central Hospital, Shanghai 200070, P.R. China, Department of Otorhinolaryngology Head and Neck Surgery, Changhai Hospital, Second Military Medical University, Beijing 200433, P.R. China
Published online on: December 19, 2016 https://doi.org/10.3892/mmr.2016.6059
Pages: 948-956

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Abstract

Aberrant expression of microRNAs (miRs) has been reported to be involved in nasopharyngeal carcinoma (NPC) carcinogenesis and development. The expression and functions of miR‑152 have previously been studied in several types of cancer. However, to the best of our knowledge, no previous studies have investigated the effects of miR‑152 on NPC. The present study aimed to explore the expression, functions and molecular mechanisms of miR‑152 in NPC. The expression levels of miR‑152 were detected in NPC tissues and cell lines using quantitative polymerase chain reaction (qPCR). Cell proliferation, migration and invasion were measured by MTT, cell migration and invasion assays, respectively. Dual‑luciferase reporter assay was used to determine whether V‑maf avian musculoaponeurotic fibrosarcoma oncogene homolog B (MAFB) was a direct target gene of miR‑152. qPCR and western blotting were used to detect the mRNA and protein expression levels of MAFB. In addition, functional assays were performed to explore the effects of endogenous MAFB on NPC. The results of the present study demonstrated that miR‑152 was significantly downregulated in NPC tissues and cell lines. Furthermore, ectopic expression of miR‑152 suppressed cell proliferation, migration and invasion of NPC cells. Dual‑luciferase reporter assay demonstrated that MAFB was a direct target gene of miR‑152, and qPCR and western blotting indicated that miR‑152 negatively regulated MAFB expression at the mRNA and protein level. Knockdown of MAFB expression markedly suppressed NPC cell proliferation, migration and invasion. These findings suggested that miR‑152 may target MAFB to regulate NPC initiation and progression; therefore, it may be investigated as a target for the treatment of NPC.

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