microRNA‑144 inhibits cell proliferation and invasion by directly targeting TIGAR in esophageal carcinoma
- Yushu Mu
- Qifei Wang
- Lei Tan
- Lin Lin
- Benhua Zhang
Affiliations: Department of Thoracic Surgery, Affiliated Hospital of Taishan Medical University, Tai'an, Shandong 271000, P.R. China, Department of Thoracic Surgery, Tai'an City Central Hospital, Tai'an, Shandong 271000, P.R. China, Department of Digestive Medicine, Tai'an City Central Hospital, Tai'an, Shandong 271000, P.R. China, Department of Oncology, Affiliated Hospital of Taishan Medical University, Tai'an, Shandong 271000, P.R. China
- Published online on: February 24, 2020 http://doi.org/10.3892/ol.2020.11420
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microRNAs (miRNAs) have been identified to play vital roles in the development and progression of numerous different types of human malignancy, including esophageal squamous cell carcinoma (ESCC). In the present study, the biological function of microRNA‑144 (miR‑144) was investigated, as well as its underlying molecular mechanism in ESCC. The results revealed that miR‑144 expression was significantly decreased, whereas the expression of TP53‑inducible glycolysis and apoptosis regulator (TIGAR) was significantly increased in human ESCC tissues when compared with adjacent non‑tumor tissues. An increase in TIGAR was significantly associated with tumor size and Tumor‑Node‑Metastasis staging in patients. Functional analysis revealed that the overexpression of miR‑144 using lentivirus particles significantly inhibited cell proliferation and tumor colony formation, and induced cell apoptosis in EC9706 and EC109 cells. The autophagy activity was also enhanced by miR‑144 activity. In addition, overexpression of miR‑144 significantly inhibited tumor growth in vivo. In the present study, TIGAR was confirmed to be the downstream target of miR‑144 in ESCC. siRNA‑mediated downregulation of TIGAR inversely regulated the inhibition effect of miR‑144 on ESCC cells. To conclude, the present study demonstrated that miR‑144 inhibits proliferation and invasion in esophageal cancer by directly targeting TIGAR.