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44. Sodium Butyrate-Modulated Mitochondrial Function in High-Insulin Induced HepG2 Cell Dysfunction

Author

Zhao, Tingting, primary, Gu, Junling, additional, Zhang, Huixia, additional, Wang, Zhe, additional, Zhang, Wenqian, additional, Zhao, Yonghua, additional, Zheng, Ying, additional, Zhang, Wei, additional, Zhou, Hua, additional, Zhang, Guilin, additional, Sun, Qingmin, additional, Zhou, Enchao, additional, Liu, Zhilong, additional, and Xu, Youhua, additional

Published
2020
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46. Effect of Genistein on vasculogenic mimicry formation by human uveal melanoma cells

Author

Gu Haijuan, Yang Li, Sun Qingmin, Cong Rihong, Zeng Ying, and Wang Bin

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Vasculogenic mimicry (VM) was increasingly recognized as a form of aggressive melanoma acquiring blood supply. Genistein had attracted much attention as a potential anticancer agent. Therefore, we examined the effect of Genistein on VM in human uveal melanoma cells. Methods VM structure was detected by periodic acid-Schiff (PAS) staining for uveal melanoma C918 cells cultured on the three-dimensional type I collagen gels after exposed to Genistein. We used reverse transcription polymerase chain reaction (RT-PCR) and Western Blot analysis to examine the effect of Genistein on vascular endothelial cadherin (VE-cadherin) mRNA and protein expression. The nude mice models of human uveal melanoma C918 cells were established to assess the number of VM using immunohistochemical and PAS double-staining. Results Genistein inhibited the survival of C918 cells in vitro. The ectopic model study showed that VM in tumor tissue sections were significantly reduced by Genistein in vivo. In vitro, the VM structure was found in control, 25 and 50 μM Genistein-treatment groups but not in 100 and 200 μM. RT-PCR and Western Blot showed that 100 and 200 μM concentration of Genistein could significantly decrease VE-cadherin mRNA and protein expression of C918 cells compared with control (P < 0.05). However, the 25 and 50 μM Genistein slightly decreased the VE-cadherin level in vitro (P > 0.05). Conclusion Genistein inhibits VM formation of uveal melanoma cells in vivo and in vitro. One possible underlying molecular mechanism by which Genistein could inhibit VM formation of uveal melanoma is related to down-regulation of VE-cadherin.

Published
2009
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50. Hepatocyte growth factor alleviates hepatic insulin resistance and lipid accumulation in high‐fat diet‐fed mice.

Author

Jing, Yali, Sun, Qingmin, Xiong, Xiaolu, Meng, Ran, Tang, Sunyinyan, Cao, Shu, Bi, Yan, and Zhu, Dalong

Subjects
*HEPATOCYTE growth factor, *TYPE 2 diabetes, *FARNESOID X receptor, *INSULIN resistance, *LIPID metabolism
Abstract

Aims/Introduction: Type 2 diabetes mellitus is frequently accompanied by fatty liver disease. Lipid accumulation within the liver is considered as one of the risk factors for insulin resistance. Hepatocyte growth factor (HGF) is used to treat liver dysfunction; however, the effect and mechanism of HGF on hepatic lipid metabolism are still not fully understood. Materials and Methods: Male C57BL/6 mice were induced with a high‐fat diet for 12 weeks, followed by a 4‐week treatment of HGF or vehicle saline. The levels of fasting blood glucose, fasting insulin and homeostatic model assessment of insulin resistance were calculated for insulin sensitivity. Biochemical plasma parameters were also measured to assess the effect of HGF on lipid accumulation. Additionally, genes in the lipid metabolism pathway were evaluated in palmitic acid‐treated HepG2 cells and high‐fat diet mice. Results: HGF treatment significantly decreased the levels of fasting blood glucose, hepatic triglyceride and cholesterol contents. Additionally, HGF‐regulated expression levels of sterol regulatory element‐binding protein‐1c/fatty acid synthase, peroxidase proliferator‐activated receptor‐α, and upstream nuclear receptors, such as farnesoid X receptor and small heterodimer partner. Furthermore, c‐Met inhibitor could partially reverse the effects of HGF. Conclusions: HGF treatment can ameliorate hepatic insulin resistance and steatosis through regulation of lipid metabolism. These effects might occur through farnesoid X receptor–small heterodimer partner axis‐dependent transcriptional activity. HGF reduced the levels of fasting blood glucose, blood lipid level, and improved the HFD‐fed mice. HGF significantly regulated lipogenesis‐related genes SREBP‐1c/FAS as well as PPARα, and nuclear receptors such as FXR, SHP. HGF ameliorates hyperglycemia and by improving hepatic insulin resistance and steatosis in HFD‐fed C57BL/6 mice. [ABSTRACT FROM AUTHOR]

Published
2019
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