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Start Over Author "Wen, Huihong" Topic liver cancer
2 results on '"Wen, Huihong"'

1. miR-602 Mediates the RASSF1A/JNK Pathway, Thereby Promoting Postoperative Recurrence in Nude Mice with Liver Cancer

Author

Zhou, Cheng, Huang, Yajing, Chen, Yongxu, Xie, Yingjie, Wen, Huihong, Tan, Wei, and Wang, Changjun

Subjects
liver cancer, endocrine system, miR-602, postoperative recurrence, JNK, RASSF1A, OncoTargets and Therapy, Original Research
Abstract

Cheng Zhou,1,2 Yajing Huang,3 Yongxu Chen,1,2 Yingjie Xie,4 Huihong Wen,3 Wei Tan,2 Changjun Wang1,2 1School of Medicine, South China University of Technology, Guangzhou, People’s Republic of China; 2Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, Guangdong Geriatric Institute, Guangzhou, People’s Republic of China; 3Guangzhou University of Chinese Medicine, Guangzhou, People’s Republic of China; 4School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, People’s Republic of ChinaCorrespondence: Changjun WangGuangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, Guangdong Geriatric Institute, No. 106, Zhongshan Second Road, Guangzhou, People’s Republic of ChinaTel +86 20-83827812-70521Email gzwchj@126.comPurpose: At present, there are few studies on the mechanisms underlying postoperative recurrence of liver cancer, and the mechanism of action of miR-602 in postoperative recurrence of liver tumors is not clear. Our goals were to investigate the effects of miR-602 on the expression of the Ras-associated domain family 1A (RASSF1A) gene and the regulation of primary and recurrent hepatic tumors to clarify the molecular mechanisms of miR-602 in postoperative hepatocellular carcinoma.Methods: We constructed a mouse liver orthotopic tumor model and a mouse liver recurrent tumor model. We measured the expression levels of the RASSF1A gene and then analyzed the effects of miR-602 on the regulation of RASSF1A. We transiently transfected the miR-602 gene into cells that stably overexpressed RASSF1A and examined relevant indicators to elucidate the mechanisms by which miR-602 regulates the RASSF1A/c-Jun N-terminal kinase (JNK) pathway in recurrence and dormancy in liver cancer.Results: RASSF1A expression was inversely related to that of JNK, activating transcription factor 2 (ATF-2), and c-Jun in SMMC7721 cells stably transfected with the RASSF1A gene and in recurrent mouse tumor tissues. After transient transfection of cells with miR-602 mimic or miR-602 inhibitor, the expression of miR-602 was inversely related to that of RASSF1A.Conclusion: MiR-602 might inhibit the JNK signaling pathway by inhibiting the expression of RASSF1A, thereby promoting recurrence of liver cancer after surgery. The low expression levels of miR-602 in liver cancer tissues were closely related to postoperative recurrence; they could be used as a marker to judge the prognosis of patients with liver cancer.Keywords: miR-602, JNK, RASSF1A, liver cancer, postoperative recurrence

Published
2020

2. TNF-α derived from M2 tumor-associated macrophages promotes epithelial-mesenchymal transition and cancer stemness through the Wnt/β-catenin pathway in SMMC-7721 hepatocellular carcinoma cells.

Author

Chen, Yongxu, Wen, Huihong, Zhou, Cheng, Su, Qiao, Lin, Yongxin, Xie, Yingjie, Huang, Yajing, Qiu, Qixuan, Lin, Juze, Huang, Xuhui, Tan, Wei, Min, Cunyun, and Wang, Changjun

Subjects
*TUMOR necrosis factors, *MESENCHYMAL stem cells, *WNT signal transduction, *LIVER cancer, *CANCER cells
Abstract

Abstract M2-polarized tumor-associated macrophages (M2-TAMs) infiltrating the tumor microenvironment contribute to hepatocellular carcinoma (HCC) progression. It was reported that cancer cells undergoing EMT will acquire stemness characteristics. Here, the HCC SMMC-7721 cell line was co-cultured with M2-TAMs polarized from THP-1 cells in vitro. In in vivo studies, we used nude mice subcutaneous tumor model to test whether the growth of the tumor was affected by M2-TAMs. Subsequently, EMT, stemness and Wnt/β-catenin pathway related markers were detected in cells and subcutaneous tumor tissues. TNF-α was also assessed in both the co-culture system supernatants and in nude mice serum. We found that SMMC-7721 underwent EMT and acquired stemness after co-culture with M2-TAMs, and resulted in larger tumor size following subcutaneous injection of SMMC-7721 suspended in M2-TAMs supernatants compared with SMMC-7721 alone. Enzyme linked immunosorbent assay showed that TNF-α expression was elevated in supernatants of M2-TAMs and positively correlated with tumor size in the serum of nude mice. Furthermore, we found that the Wnt/β-catenin pathway was a downstream target of TNF-α and that the Wnt/β-catenin inhibitor ICG-001 partially reversed EMT and attenuated cancer stemness. Our results indicate that TNF-α derived from M2-TAMs promote EMT and cancer stemness cells via the Wnt/β-catenin pathway. [ABSTRACT FROM AUTHOR]

Published
2019
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