Article
Gastroenterology & Hepatology
Junfeng Wang, Yongchun Wang, Yifan Chu, Zhixiong Li, Xingjuan Yu, Zhijie Huang, Jing Xu, Limin Zheng
Summary: Tumor-infiltrating macrophages in human hepatocellular carcinoma exhibit higher proliferative capacity, less differentiation, and are induced by tumor cell-derived adenosine and autocrine granulocyte-macrophage colony-stimulating factor (GM-CSF). Local macrophage proliferation is an important mechanism for macrophage accumulation in HCC tissues and selective modulation at the source may offer a novel strategy for cancer therapy.
JOURNAL OF HEPATOLOGY
(2021)
Article
Oncology
Yabing Hu, Yongchu Huang, Xiaohang Xie, Longshan Li, Yong Zhang, Xiaochao Zhang
Summary: In this study, we found that high expression of ARF6 is associated with poor prognosis and promotes the proliferation of hepatocellular carcinoma (HCC). ARF6 was upregulated in HCC tissues and correlated with poor tumor differentiation, incomplete tumor encapsulation, advanced tumor TNM stage, and poor prognosis. ARF6 activated the STAT3 signaling pathway to enhance HCC cell proliferation and tumor growth. These findings suggest that ARF6 may serve as a potential prognostic and therapeutic target for HCC patients.
CANCER CELL INTERNATIONAL
(2023)
Article
Cell Biology
Honglei Cui, Danfeng Guo, Xiaodan Zhang, Yaohua Zhu, Zhihui Wang, Yang Jin, Wenzhi Guo, Shuijun Zhang
Summary: The study revealed that ENO3 is significantly down-regulated in HCC patients and is related to poor prognosis. Overexpression of ENO3 inhibited the proliferative, migratory, and invasive abilities of HCC cells, while also inhibiting the EMT process. ENO3 further modulated the transcription of genes associated with proliferation and metastasis capacity of HCC cells by suppressing the Wnt/beta-catenin signal.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Oncology
Jie Sun, Zheng Dong, Zhengyao Chang, Hongfei Liu, Qiyu Jiang, Deyuan Zhang, Shanshan Lu, Xiaodong Jia, Dawei Wu, Aaron Ge, Pan Zhao, Jing Wang, Yinying Lu
Summary: The study found that the expression of MARCH6 was elevated in human HCC samples and was associated with poor prognosis. Over-expression of MARCH6 promoted cell growth and migration of HCC cells, while its knockdown suppressed these functions. Additionally, MARCH6-mediated up-regulation of ATF2 contributed to HCC development, suggesting MARCH6 may be a promising target for HCC diagnosis and treatment.
Article
Cell Biology
Tianhao Zhou, Rui Qin, Susu Shi, Hua Zhang, Chuanling Niu, Gaoda Ju, Sen Miao
Summary: DTYMK is significantly upregulated in tumor tissue of HCC patients and is associated with worse overall survival. High expression of DTYMK correlates with poor relapse free survival and disease-specific survival, indicating its role in promoting tumor growth and proliferation through cell cycle regulation.
Article
Biochemistry & Molecular Biology
Tingting Zou, Yang Wang, Ling Dong, Tiantian Che, Huakan Zhao, Xiaohua Yan, Zhenghong Lin
Summary: This study reveals that the interaction between ubiquitin-specific peptidase 27 (USP27) and histone methyltransferase SETD3 promotes tumor cell growth and is positively correlated in hepatocellular carcinoma (HCC) tissues. Higher expression of USP27 and SETD3 predicts a worse survival in HCC patients.
CELLULAR AND MOLECULAR LIFE SCIENCES
(2022)
Article
Cell Biology
Jicheng Duan, Youwen Qian, Xiaohui Fu, Meiling Chen, Kai Liu, Hu Liu, Jiahe Yang, Chen Liu, Yanxin Chang
Summary: The study found that TMEM106C is overexpressed in HCC, and inhibition of TMEM106C can significantly suppress the proliferation and metastasis of HCC. Upregulation of TMEM106C is closely correlated with sex, tumor stage, tumor grade, and other indicators, affecting cell cycle signaling pathways and organelle fission through the regulation of CDK kinases.
Article
Biochemistry & Molecular Biology
Yu Jin Kim, Nayeong Yuk, Hee Jeong Shin, Hye Jin Jung
Summary: Violacein has shown promising therapeutic potential in effectively suppressing hepatocellular carcinoma (HCC) by inhibiting the proliferation and stemness of HCC cells. Its antiproliferative effect is attributed to cell cycle arrest at the sub-G1 phase and induction of apoptotic cell death.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Oncology
Federica Ragusa, Nadia Panera, Silvia Cardarelli, Marco Scarsella, Marzia Bianchi, Stefano Biagioni, Mauro Giorgi, Anna Alisi, Mara Massimi
Summary: The study found that PDE4D gene/protein were over-expressed in HCC samples compared to normal livers, and silencing or pharmacological inhibition of PDE4D activity showed anti-tumorigenic effects by reducing cell proliferation and increasing apoptosis. Over-expression of PDE4D in human HCCs correlated with up-regulated pro-oncogenic genes, suggesting a new potential molecular network for further investigation. PDE4D depletion/inhibition may serve as a novel biomarker for diagnosis and a potential adjuvant target for HCC therapy.
Article
Biochemistry & Molecular Biology
Luhao Li, Suxin Li, Haohao Wang, Lin Li, Peiju Wang, Dongqi Shen, Xiaowei Dang
Summary: The study revealed that GSG2 is overexpressed in HCC tissues, and knockdown of GSG2 can inhibit the progression of HCC, promote cell apoptosis, and potentially participate in the oncogenesis of HCC.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2022)
Article
Pharmacology & Pharmacy
Theresa H. Wirtz, Alena Saal, Irina Bergmann, Petra Fischer, Daniel Heinrichs, Elisa F. Brandt, Maria T. Koenen, Sonja Djudjaj, Kai M. Schneider, Peter Boor, Richard Bucala, Ralf Weiskirchen, Jurgen Bernhagen, Christian Trautwein, Marie-Luise Berres
Summary: The study identified a pro-tumorigenic role of MIF in the proliferation and therapy-induced apoptosis of HCC cells, mediated through the MIF cognate receptor CD74.
BRITISH JOURNAL OF PHARMACOLOGY
(2021)
Article
Cell Biology
Yening Xiao, Jiamei Ma, Chunliu Guo, Danni Liu, Jing Pan, Xiaoxi Huang
Summary: This study demonstrates that silencing of the CCNB2 gene can inhibit tumor formation and proliferation in nude mice. CCNB2 may accelerate the proliferation and metastasis of hepatocellular carcinoma cells by increasing JAG1 expression.
Article
Cell Biology
Rindert Missiaen, Nicole M. Anderson, Laura C. Kim, Bailey Nance, Michelle Burrows, Nicolas Skuli, Madeleine Carens, Romain Riscal, An Steensels, Fuming Li, M. Celeste Simon
Summary: Hepatocellular carcinoma (HCC) depends on exogenous arginine due to repression of urea cycle gene expression and unique dependence on cationic amino acid transporter SLC7A1. Arginine deprivation induces an integrated stress response, leading to HCC cell-cycle arrest and quiescence. Inhibiting GCN2 in arginine-deprived HCC cells promotes a senescent phenotype, making these cells vulnerable to senolytic compounds. Combined dietary arginine deprivation, GCN2 inhibition, and senotherapy show potential for HCC treatment.
Article
Oncology
Yunzheng Li, Binghua Li, Yanchao Xu, Liyuan Qian, Tiancheng Xu, Gang Meng, Huan Li, Ye Wang, Laizhu Zhang, Xiang Jiang, Qi Liu, Yuanyuan Xie, Chunxiao Cheng, Beicheng Sun, Decai Yu
Summary: The study reveals that low expression of GOT2 is associated with advanced progression and poor prognosis of HCC. Knock down of GOT2 promotes proliferation, migration, and invasion of HCC cells, and loss of GOT2 promotes tumor growth and metastasis in mouse models. Mechanistically, silencing of GOT2 reprograms glutamine metabolism to support the cellular antioxidant system and activates the PI3K/AKT/mTOR pathway, promoting HCC progression. HCC with low expression of GOT2 is highly sensitive to the glutaminase inhibitor CB-839.
Article
Cell Biology
Shu Hu, Jiancheng Liu, Shuying Feng, Yue Wang, Hongchao Liu
Summary: The study revealed that SUMO1P3 plays a crucial role in HCC progression, with its enhanced expression correlating with malignant features of liver cancer. Depletion of SUMO1P3 induces HCC cell apoptosis, suppresses cell migration and invasion, and ultimately delays tumor growth and metastasis.
