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miR‑4636 inhibits tumor cell proliferation, migration and invasion, and serves as a candidate clinical biomarker for gastric cancer
Author(s) -
Jiaying Tang,
Ying Hu,
Chunjie Zhang,
Cuixue Gong
Publication year - 2020
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2020.12294
Subject(s) - oncogene , microrna , cancer , gene knockdown , biomarker , cell cycle , cancer research , biology , cell growth , medicine , cell culture , gene , genetics , biochemistry
Gastric cancer (GC) is one of the most common malignancies with a high worldwide incidence rate. The association between microRNAs (miRs) and malignancy has been widely studied in recent years. The aim of the present study was to assess the clinical value of miR-4636 in patients with GC and its effect on the proliferation, migration and invasion of GC cells. Reverse transcription-quantitative PCR was used to detect the expression of miR-4636. Receiver operating characteristics curve, Kaplan-Meier survival curve and Cox regression analyses were used to evaluate the diagnostic and prognostic value of miR-4636. Transwell migration and MTT assays were used to assess the regulatory effects of miR-4636 expression on the biological function of GC. The results demonstrated that the expression of miR-4636 was significantly downregulated in GC serum and tissue samples, as well as in GC cell lines. The aberrant miR-4636 expression was closely associated with lymph node metastasis and TNM stage, and had considerable diagnostic and prognostic significance in patients with GC. Cellular experiments revealed that the overexpression of miR-4636 inhibited GC cell proliferation, migration and invasion, while the knockdown of miR-4636 led to opposite effects on the biological function of GC. In summary, decreased miR-4636 expression may serve as a biomarker for the diagnosis and prognosis of GC. Furthermore, miR-4636 overexpression significantly inhibited GC cell proliferation, migration and invasion, indicating the potential of miR-4636 as a therapeutic target for GC treatment.

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