TUFM-knockdown inhibits the migration and proliferation of gastrointestinal stromal tumor cells

Gastrointestinal stromal tumors (GISTs) are the most common pathologic type of mesenchymal tumor in the digestive tract. Patients with GIST face the risk of metastasis, postoperative recurrence and imatinib mesylate (IM) resistance. Mitochondrial Tu translation elongation factor (TUFM) is highly expressed in GISTs, and is associated with oncogenesis, progression and prognosis. There is evidence that TUFM is involved in tumor invasion and metastasis. However, the effect of TUFM on GIST-T1 cells and the IM-resistant GIST-IR cell line remains unclear. The present study aimed to evaluate the effects of TUFM on the proliferation, migration and apoptosis of GIST cells in vitro. TUFM short hairpin (sh)RNA expression plasmids were transfected into GIST-T1 and GIST-IR cells by electroporation. The expression levels of enhanced green fluorescent protein were observed by fluorescence microscopy to evaluate the electroporation efficiency. The expression levels of TUFM were detected by western blot analysis and reverse transcription-quantitative PCR. Cell proliferation was assessed by counting cells and using a Cell Counting Kit-8 assay. Cell migration was analyzed using wound healing and Transwell migration assays. Cell cycle distribution and late apoptosis were assessed by flow cytometry. TUFM shRNA expression plasmids were successfully transfected into the GIST cell line by electroporation. The transfection efficiency was >75%, and the TUFM gene silencing efficiency was 73.2±1.4%. TUFM-knockdown decreased the proliferation and migration capacity of GIST-T1 and GIST-IR cells. The proportion of cells in the pre-G1 stage was increased without change in the proportions of cells in the G(1), S and G(2)/M stages after TUFM silencing in GIST-T1 and GIST-IR cells. TUFM may be related to GIST infiltration and metastatic recurrence, suggesting that TUFM may be an effective target for preventing the progression and metastasis of GISTs.