Xincheng Liu1, Yu Huang2, Chenglong Jiang3, Huohui Ou4, Botang Guo5, Hui Liao6, Xianghong Li7, Dinghua Yang8. 1. Department of Hepatobiliary Surgery, Nanfang Hospital Affiliated to Southern Medical University, Guangzhou 510515, Guangdong, China. Electronic address: liuxincheng321@163.com. 2. Department of Laboratory Medicine, Nanfang Hospital Affiliated to Southern Medical University, Guangzhou 510515, Guangdong, China. Electronic address: hy5810@yahoo.com. 3. Department of Hepatobiliary Surgery, Nanfang Hospital Affiliated to Southern Medical University, Guangzhou 510515, Guangdong, China. Electronic address: jiangclnf@139.com. 4. Department of Hepatobiliary Surgery, Nanfang Hospital Affiliated to Southern Medical University, Guangzhou 510515, Guangdong, China. Electronic address: ouhuohui@126.com. 5. Department of Hepatobiliary Surgery, Nanfang Hospital Affiliated to Southern Medical University, Guangzhou 510515, Guangdong, China. Electronic address: gbtkobe@163.com. 6. Department of Hepatobiliary Surgery, Nanfang Hospital Affiliated to Southern Medical University, Guangzhou 510515, Guangdong, China. Electronic address: jxliaohui@sina.com. 7. Department of Hepatobiliary Surgery, Nanfang Hospital Affiliated to Southern Medical University, Guangzhou 510515, Guangdong, China. Electronic address: lixhly@hotmail.com. 8. Department of Hepatobiliary Surgery, Nanfang Hospital Affiliated to Southern Medical University, Guangzhou 510515, Guangdong, China. Electronic address: dhyangyd@yahoo.com.
Abstract
BACKGROUND: Methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) is the key enzyme in the transformation of folic acid metabolites. MTHFD2 overexpression plays a key role in the progression of human cancers, and depletion of MTHFD2 has shown potential antitumor activities in several types of cancer. However, the role of MTHFD2 in hepatocellular carcinoma (HCC) has not been investigated. AIMS: To investigate the expression of MTHFD2 in HCC patients, and its associated clinical implications and possible functions in HCC. METHODS: Reverse transcription-polymerase chain reaction and immunohistochemical staining were used to detect MTHFD2 expression in liver tissues from HCC patients, then associations of MTHFD2 expression with demographic and clinicopathologic features were analysed. The effects of siRNA interference of MTHFD2 on cell proliferation, cell cycle, apoptosis, and migration were investigated in HCC cell lines. RESULTS: Significant overexpression of MTHFD2 was observed in HCC tissues, and overexpression of MTHFD2 was correlated with TNM stage, tumor microembolus, tumor metastasis, recurrence and the time of recurrence (P<0.05) in HCC patients. siRNA-mediated silencing of MTHFD2 inhibited migration, invasion and epithelial-mesenchymal transition progression in HCC cell lines, but no obvious effects on cell proliferation, apoptosis or cell cycle distribution were detected. CONCLUSIONS: MTHFD2 is overexpressed in HCC, and is associated with poor prognosis and cellular features connected to metastatic disease.
BACKGROUND:Methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) is the key enzyme in the transformation of folic acid metabolites. MTHFD2 overexpression plays a key role in the progression of humancancers, and depletion of MTHFD2 has shown potential antitumor activities in several types of cancer. However, the role of MTHFD2 in hepatocellular carcinoma (HCC) has not been investigated. AIMS: To investigate the expression of MTHFD2 in HCC patients, and its associated clinical implications and possible functions in HCC. METHODS: Reverse transcription-polymerase chain reaction and immunohistochemical staining were used to detect MTHFD2 expression in liver tissues from HCC patients, then associations of MTHFD2 expression with demographic and clinicopathologic features were analysed. The effects of siRNA interference of MTHFD2 on cell proliferation, cell cycle, apoptosis, and migration were investigated in HCC cell lines. RESULTS: Significant overexpression of MTHFD2 was observed in HCC tissues, and overexpression of MTHFD2 was correlated with TNM stage, tumor microembolus, tumor metastasis, recurrence and the time of recurrence (P<0.05) in HCC patients. siRNA-mediated silencing of MTHFD2 inhibited migration, invasion and epithelial-mesenchymal transition progression in HCC cell lines, but no obvious effects on cell proliferation, apoptosis or cell cycle distribution were detected. CONCLUSIONS:MTHFD2 is overexpressed in HCC, and is associated with poor prognosis and cellular features connected to metastatic disease.
Authors: Le-Yang Xiang; Huo-Hui Ou; Zhan-Jun Chen; Ying-Hao Fang; Yu Huang; Xiang-Hong Li; Ding-Hua Yang Journal: Nan Fang Yi Ke Da Xue Xue Bao Date: 2017-08-20
Authors: Sha Yao; Luogen Peng; Omar Elakad; Stefan Küffer; Marc Hinterthaner; Bernhard C Danner; Alexander von Hammerstein-Equord; Philipp Ströbel; Hanibal Bohnenberger Journal: Transl Lung Cancer Res Date: 2021-06