Zongguo Yang1, Yuquan Tao2, Xin Xu2, Feng Cai3, Yongchun Yu4, Lifang Ma5. 1. Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200071, PR China; Department of Integrative Medicine, Shanghai Public Health Clinical Center, Fudan University, Shanghai, 201508, PR China. 2. Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200071, PR China. 3. Department of Clinical Laboratory Medicine, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200071, PR China. 4. Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200071, PR China; Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, 200030, PR China. Electronic address: yueyongchun88@163.com. 5. Department of Clinical Laboratory Medicine, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200071, PR China. Electronic address: malifang0606118@126.com.
Abstract
OBJECTIVE: This study aimed to evaluate functions of APOBEC3F gene in biological process of hepatocellular carcinoma (HCC) and anti-tumor mechanisms of bufalin. METHODS: Effect of APOBEC3F and bufalin on cell proliferation and migration abilities were evaluated by CCK-8, wounding healing tests and transwell assays in SK-Hep1 and Bel-7404 cells. Bioinformatic analysis were also used to compare APOBEC3F expression levels, detect coexpressed genes and enrichment of pathways. RESULTS: APOBEC3F was overexpressed in tumor tissues compared to adjacent tissues in HCC patients. And, APOBEC3F promotes cell proliferation and migration in SK-Hep1 and Bel-7404 cells. Bufalin inhibits cell proliferation and migration and reduces APOBEC3F expression. GO and KEGG enrichment of APOBEC3F-coexpressed genes revealed that APOBEC3F might active intestinal immune network for IgA production signaling pathway, leading to malignant biological behaviors of HCC cells. Additionally, siAPOBEC3F could decrease pIgR, CCR9, CCR10 and CXCR4 protein levels. And, bufalin inhibits the pIgR, CCR9, CCR10 and CXCR4 protein expressions. CONCLUSIONS: Bufalin inhibits cell proliferation and migration of HCC cells via APOBEC3F induced intestinal immune network for IgA production signaling pathway.
OBJECTIVE: This study aimed to evaluate functions of APOBEC3F gene in biological process of hepatocellular carcinoma (HCC) and anti-tumor mechanisms of bufalin. METHODS: Effect of APOBEC3F and bufalin on cell proliferation and migration abilities were evaluated by CCK-8, wounding healing tests and transwell assays in SK-Hep1 and Bel-7404 cells. Bioinformatic analysis were also used to compare APOBEC3F expression levels, detect coexpressed genes and enrichment of pathways. RESULTS:APOBEC3F was overexpressed in tumor tissues compared to adjacent tissues in HCC patients. And, APOBEC3F promotes cell proliferation and migration in SK-Hep1 and Bel-7404 cells. Bufalin inhibits cell proliferation and migration and reduces APOBEC3F expression. GO and KEGG enrichment of APOBEC3F-coexpressed genes revealed that APOBEC3F might active intestinal immune network for IgA production signaling pathway, leading to malignant biological behaviors of HCC cells. Additionally, siAPOBEC3F could decrease pIgR, CCR9, CCR10 and CXCR4 protein levels. And, bufalin inhibits the pIgR, CCR9, CCR10 and CXCR4 protein expressions. CONCLUSIONS:Bufalin inhibits cell proliferation and migration of HCC cells via APOBEC3F induced intestinal immune network for IgA production signaling pathway.