Guixiang Lv1, Mingjuan Wu2, Meijie Wang1, Xiaochen Jiang1, Jingli Du3, Kaili Zhang1, Dongliang Li1, Ning Ma1, Yahui Peng1, Lujing Wang1, Lingyun Zhou1, Weiming Zhao1, Yufei Jiao4, Xu Gao1, Zheng Hu1,5. 1. Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China. 2. Academy of Traditional Chinese Medicines, Harbin, China. 3. Department of Pathology, General Hospital of PLA, Beijing, China. 4. Department of Pathology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China. 5. Laboratory of Sono- and Photo-theranostic Technologies, Harbin Institute of Technology, Harbin, China.
Abstract
BACKGROUND & AIMS: Several studies have shown that miR-320a induces apoptosis, inhibits cell proliferation, and affects cell cycle progression as a tumour suppressor in many cancers. However, the involvement of miR-320a in the invasion and metastasis of hepatocellular carcinoma (HCC) is still unknown. METHODS: Endogenous miR-320a and high mobility group box 1 (HMGB1) expressions were assayed by real-time PCR. Luciferase activities were measured using a dual-luciferase reporter assay system. Western blots were used to determine the protein expressions of HMGB1, MMP2, and MMP9. Invasion and metastasis of tumour cells were, respectively, evaluated by the transwell invasion assay and the wound healing assay. RESULTS: The expression of miR-320a was significantly decreased in 24 of 32 (75%) HCC tissues and associated with the invasion and metastasis of HCC. Furthermore, we demonstrated that HMGB1 was a direct target of miR-320a and there was a significant negative correlation between miR-320a and HMGB1 expression in HCC. Ectopic expression or inhibition of miR-320a potently regulated the invasion and metastasis of HCC cells in HMGB1-dependent manner. CONCLUSIONS: Our results showed that miR-320a was involved in the invasion and metastasis by targeting HMGB1 and had an anti-metastasis effect in HCC.
BACKGROUND & AIMS: Several studies have shown that miR-320a induces apoptosis, inhibits cell proliferation, and affects cell cycle progression as a tumour suppressor in many cancers. However, the involvement of miR-320a in the invasion and metastasis of hepatocellular carcinoma (HCC) is still unknown. METHODS: Endogenous miR-320a and high mobility group box 1 (HMGB1) expressions were assayed by real-time PCR. Luciferase activities were measured using a dual-luciferase reporter assay system. Western blots were used to determine the protein expressions of HMGB1, MMP2, and MMP9. Invasion and metastasis of tumour cells were, respectively, evaluated by the transwell invasion assay and the wound healing assay. RESULTS: The expression of miR-320a was significantly decreased in 24 of 32 (75%) HCC tissues and associated with the invasion and metastasis of HCC. Furthermore, we demonstrated that HMGB1 was a direct target of miR-320a and there was a significant negative correlation between miR-320a and HMGB1 expression in HCC. Ectopic expression or inhibition of miR-320a potently regulated the invasion and metastasis of HCC cells in HMGB1-dependent manner. CONCLUSIONS: Our results showed that miR-320a was involved in the invasion and metastasis by targeting HMGB1 and had an anti-metastasis effect in HCC.