Publications by authors named "Bufeng Zhuang"

2 Publications

  • Page 1 of 1

MicroRNA‑92a promotes non‑small cell lung cancer cell growth by targeting tumor suppressor gene FBXW7.

Mol Med Rep 2020 Oct 28;22(4):2817-2825. Epub 2020 Jul 28.

Department of Thoracic Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai 201999, P.R. China.

MicroRNA (miRNA/miR)‑92a has been identified as being significantly downregulated in non‑small cell lung cancer (NSCLC) tissues using a miRNA array. However, its biological function and molecular mechanisms in NSCLC have not been fully elucidated. The aim of the present study was to determine the role of miR‑92a in NSCLC and the mechanisms by which it affects NSCLC cells. The expression levels of miR‑92a in NSCLC tissues and cell lines were analyzed using reverse transcription‑quantitative PCR. Cell viability and cell apoptosis were determined using an MTT assay and flow cytometry, respectively. It was observed that miR‑92a was significantly upregulated in NSCLC tissues and cell lines. Inhibition of miR‑92a significantly suppressed viability of NSCLC cells, with concomitant downregulation of key proliferative genes, such as proliferating cell nuclear antigen and Ki‑67. miR‑92a downregulation induced apoptosis of NSCLC cells, as evidenced by flow cytometry and apoptosis‑related protein detection. Luciferase assays confirmed that miR‑92a could directly bind to the 3'‑untranslated region of tumor suppressor F‑box/WD repeat‑containing protein 7 (FBXW7) and suppress its translation. Furthermore, small interfering RNA‑mediated FBXW7 inhibition partially attenuated the tumor suppressive effect of an miR‑92a inhibitor on NSCLC cells. Collectively, these findings demonstrated that miR‑92a might function as an oncogene in NSCLC by regulating FBXW7. In conclusion, miR‑92a could serve as a potential therapeutic target in NSCLC treatment.
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http://dx.doi.org/10.3892/mmr.2020.11373DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7453619PMC
October 2020

MicroRNA‑629 inhibition suppresses the viability and invasion of non‑small cell lung cancer cells by directly targeting RUNX3.

Mol Med Rep 2019 May 27;19(5):3933-3940. Epub 2019 Feb 27.

Department of Thoracic Surgery, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 201900, P.R. China.

Dysregulated microRNAs (miRNAs/miRs) directly modulate the biological functions of non‑small cell lung cancer (NSCLC) cells and contribute to the initiation and progression of NSCLC; however, the specific roles and underlying mechanisms of the dysregulated miRNAs in NSCLC require further investigation. The present study reported that miRNA‑629‑5p (miR‑629) was upregulated in NSCLC tissues and cell lines. High miR‑629 expression levels were significantly associated with tumour size, clinical stage and lymph node metastasis in patients with NSCLC. Functional experiments indicated that miR‑629 inhibition suppressed the viability and invasion NSCLC cells in vitro. Furthermore, bioinformatics prediction, luciferase reporter assay, reverse transcription‑quantitative polymerase chain reaction and western blot analysis demonstrated that runt‑related transcription factor 3 (RUNX3) was a direct target gene of miR‑629 in NSCLC. Restoration of RUNX3 expression suppressed the effects of miR‑629 inhibition in NSCLC cells. Rescue experiments revealed that RUNX3 knockdown partially abrogated the effects of miR‑629 inhibition on NSCLC cells. In summary, miR‑629 directly targeted RUNX3 to inhibit the progression of NSCLC, suggesting that this miRNA may be considered as a diagnostic and therapeutic target for patients with NSCLC.
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http://dx.doi.org/10.3892/mmr.2019.9990DOI Listing
May 2019
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