Yang Gao1, Fan Yang2. 1. General Practice Center, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu 610000, China gaoyangcaicai@163.com. 2. General Practice Center, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu 610000, China.
Abstract
OBJECTIVE: To investigate the effect of miR-26b on the invasion and migration of lung cancer cell and to explore its mechanism. Methods: qPCR was used to detect the expression of miR-26b in lung cancer. Luciferase reporter gene was used to detect interaction between miR-26b and hENT1. Transwell assay was used to detect invasion ability after treatment of miR-26b mimics. Scratch assay was used to detect migration ability after treatment of miR-26b mimics. The expressions of hENT1, ROCK-1 and RhoA were detected by Western blot. The changes of cytoskeleton after miR-26b mimics treatment with phalloidin were observed. The effect of miR-26b mimics on the tumor size and volume of lung cancer was determined by subcutaneous tumor formation in nude mice. Results: MiR-26b expression was significantly reduced in lung cancer. With the progress of lung cancer, the expression of miR-26b was reduced. With the progress in differentiation of lung cancer, the expression of miR-26b was decreased. Decrease of miR-26b was associated with lung cancer lymph node metastasis. HENT1 was the direct target of miR-26b; miR-26b regulated the invasion and migration ability of human lung carcinoma A549 cells. MiR-26b regulated the expression of hENT1, ROCK-1 and RhoA. After the treatment with miR-26b mimics, the F-actin staining was significantly reduced, whereas the formation of wrinkles and the formation of pseudopodia were significantly reduced. Subcutaneous tumor formation in nude mice showed that miR-26b mimics treatment significantly reduced the tumor size and mass. Conclusion: MiR-26b plays a role in tumor suppression in lung cancer. miR-26b can regulate the invasion and migration ability of lung carcinoma A549 cells by targeting hENT1 depending on the RhoA/ROCK-1 pathway.
OBJECTIVE: To investigate the effect of miR-26b on the invasion and migration of lung cancer cell and to explore its mechanism. Methods: qPCR was used to detect the expression of miR-26b in lung cancer. Luciferase reporter gene was used to detect interaction between miR-26b and hENT1. Transwell assay was used to detect invasion ability after treatment of miR-26b mimics. Scratch assay was used to detect migration ability after treatment of miR-26b mimics. The expressions of hENT1, ROCK-1 and RhoA were detected by Western blot. The changes of cytoskeleton after miR-26b mimics treatment with phalloidin were observed. The effect of miR-26b mimics on the tumor size and volume of lung cancer was determined by subcutaneous tumor formation in nude mice. Results:MiR-26b expression was significantly reduced in lung cancer. With the progress of lung cancer, the expression of miR-26b was reduced. With the progress in differentiation of lung cancer, the expression of miR-26b was decreased. Decrease of miR-26b was associated with lung cancer lymph node metastasis. HENT1 was the direct target of miR-26b; miR-26b regulated the invasion and migration ability of humanlung carcinoma A549 cells. MiR-26b regulated the expression of hENT1, ROCK-1 and RhoA. After the treatment with miR-26b mimics, the F-actin staining was significantly reduced, whereas the formation of wrinkles and the formation of pseudopodia were significantly reduced. Subcutaneous tumor formation in nude mice showed that miR-26b mimics treatment significantly reduced the tumor size and mass. Conclusion:MiR-26b plays a role in tumor suppression in lung cancer. miR-26b can regulate the invasion and migration ability of lung carcinoma A549 cells by targeting hENT1 depending on the RhoA/ROCK-1 pathway.