Zonglin Chen1, Yong Xie1, Weidong Chen1, Tiegang Li1, Xianyu Chen2, Bo Liu1. 1. Department of General Surgery, The Second Xiangya Hospital, Central South University, Changsha 410008, Hunan, China. 2. Department of General Surgery, The Second Xiangya Hospital, Central South University, Changsha 410008, Hunan, China. Electronic address: chenxianyu6692@163.com.
Abstract
OBJECTIVE: Exosomes (Exos) are known to transfer microRNAs (miRNAs) to participate in human diseases. We aim to identify the role of human umbilical cord mesenchymal stem cells (HUCMSCs)-derived Exos (HUCMSC-Exos) conveying miR-6785-5p in gastric cancer (GC). METHODS: MiR-6785-5p and inhibin subunit beta A (INHBA) expression in GC tissues and cells were determined. GC cells were transfected with the vectors that altered miR-6785-5p or INHBA expression. HUCMSCs were transfected with altered miR-6785-5p or INHBA vectors, and the HUCMSC-Exos were extracted. Then, HUCMSC-Exos were co-cultured with GC cells. The proliferation, migration, invasion, apoptosis and angiogenesis of GC cells were assessed. The binding relationship between miR-6785-5p and INHBA was verified. RESULTS: MiR-6785-5p was down-regulated and INHBA was up-regulated in GC tissues and cells. Elevation of miR-6785-5p or inhibition of INHBA restricted the malignant development of GC cells. HUCMSC-Exos suppressed malignant episodes of GC cells, which could be further enhanced by up-regulated miR-6785-5p or down-regulated INHBA. Elevated INHBA abolished the impacts of up-regulated miR-6785-5p in HUCMSC-Exos on GC cells. INHBA was confirmed as a target gene of miR-6785-5p. CONCLUSION: HUCMSC-Exos containing elevated miR-6785-5p suppress angiogenesis and metastasis in GC via inhibiting INHBA. This study may further the understanding on molecular mechanisms of GC.
OBJECTIVE: Exosomes (Exos) are known to transfer microRNAs (miRNAs) to participate in human diseases. We aim to identify the role of human umbilical cord mesenchymal stem cells (HUCMSCs)-derived Exos (HUCMSC-Exos) conveying miR-6785-5p in gastric cancer (GC). METHODS:MiR-6785-5p and inhibin subunit beta A (INHBA) expression in GC tissues and cells were determined. GC cells were transfected with the vectors that altered miR-6785-5p or INHBA expression. HUCMSCs were transfected with altered miR-6785-5p or INHBA vectors, and the HUCMSC-Exos were extracted. Then, HUCMSC-Exos were co-cultured with GC cells. The proliferation, migration, invasion, apoptosis and angiogenesis of GC cells were assessed. The binding relationship between miR-6785-5p and INHBA was verified. RESULTS:MiR-6785-5p was down-regulated and INHBA was up-regulated in GC tissues and cells. Elevation of miR-6785-5p or inhibition of INHBA restricted the malignant development of GC cells. HUCMSC-Exos suppressed malignant episodes of GC cells, which could be further enhanced by up-regulated miR-6785-5p or down-regulated INHBA. Elevated INHBA abolished the impacts of up-regulated miR-6785-5p in HUCMSC-Exos on GC cells. INHBA was confirmed as a target gene of miR-6785-5p. CONCLUSION: HUCMSC-Exos containing elevated miR-6785-5p suppress angiogenesis and metastasis in GC via inhibiting INHBA. This study may further the understanding on molecular mechanisms of GC.