scholarly journals CXCR4 mediates matrix stiffness-induced downregulation of UBTD1 driving hepatocellular carcinoma progression via YAP signaling pathway

Theranostics ◽  
2020 ◽  
Vol 10 (13) ◽  
pp. 5790-5801 ◽  
Author(s):  
Nan Yang ◽  
Tianxiang Chen ◽  
Liang Wang ◽  
Runkun Liu ◽  
Yongshen Niu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Signaling Pathway ◽  
Matrix Stiffness

scholarly journals Higher Matrix Stiffness Upregulates Osteopontin Expression in Hepatocellular Carcinoma Cells Mediated by Integrin β1/GSK3β/β-Catenin Signaling Pathway

PLoS ONE ◽  
2015 ◽  
Vol 10 (8) ◽  
pp. e0134243 ◽  
Author(s):  
Yang You ◽  
Qiongdan Zheng ◽  
Yinying Dong ◽  
Yaohui Wang ◽  
Lan Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Signaling Pathway ◽  
Carcinoma Cells ◽  
Matrix Stiffness ◽  
Integrin Β1 ◽  
Hepatocellular Carcinoma Cells ◽  
Osteopontin Expression

microRNA-106b-5p Promotes Cell Growth and Sensitizes Chemosensitivity to Sorafenib by Targeting the BTG3/Bcl-xL/p27 Signaling Pathway in Hepatocellular Carcinoma

2020 ◽  
Author(s):  
Enkhnaran Bilegsaikhan ◽  
Ning-Ping Zhang ◽  
Guang-Cong Zhang ◽  
Hai-Ning Liu ◽  
Hao Wu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Growth ◽  
Signaling Pathway

Indazolo[3,2-b]quinazolinones Attack Hepatocellular Carcinoma Hep3B Cells by Inducing Mitochondrial-Dependent Apoptosis and Inhibition of Nrf2/ARE Signaling Pathway

2016 ◽  
Vol 16 (9) ◽  
pp. 820-828 ◽  
Author(s):  
Y. Zhang ◽  
R. Qiao ◽  
D. He ◽  
Z. Zhao ◽  
S. Yang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Signaling Pathway ◽  
Hep3b Cells

scholarly journals The effect of propofol on the proliferation and apoptosis of hepatocellular carcinoma cells through TGF-Β1/Smad2 signaling pathway

Bioengineered ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 4581-4592
Author(s):  
Zongchao Li ◽  
Honglei Liu ◽  
Yunxiao Zhang ◽  
Hongyu Tan
Keyword(s):  
Hepatocellular Carcinoma ◽  
Signaling Pathway ◽  
Carcinoma Cells ◽  
Hepatocellular Carcinoma Cells ◽  
Proliferation And Apoptosis ◽  
Tgf Β1

scholarly journals CircSOD2 induced epigenetic alteration drives hepatocellular carcinoma progression through activating JAK2/STAT3 signaling pathway

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Zhongwei Zhao ◽  
Jingjing Song ◽  
Bufu Tang ◽  
Shiji Fang ◽  
Dengke Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Migration ◽  
Real Time ◽  
Signaling Pathway ◽  
Molecular Mechanism ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Signaling Axis

Abstract Background Emerging evidence suggests that circular RNAs play critical roles in disease development especially in cancers. Previous genome-wide RNA-seq studies found that a circular RNA derived from SOD2 gene was highly upregulated in hepatocellular carcinoma (HCC), however, the role of circSOD2 in HCC remains largely unknown. Methods The expression profiling of circSOD2 and microRNA in HCC patients were assessed by Real-Time Quantitative Reverse Transcription PCR (qRT-PCR). SiRNA or CRISPR-CAS9 were used to silence gene expression. The biological function of circSOD2 in HCC was investigated using in vitro and in vivo studies including, trans-well cell migration, cell apoptosis, cell cycle, CCK8, siRNA interference, western blots, and xenograft mouse model. The underlying molecular mechanism was determined by Chromatin Immunoprecipitation quantitative real time PCR (ChIP-qPCR), bioinformatic analysis, biotin-pull down, RNA immunoprecipitation, 5-mc DNA pulldown and luciferase assays. Results In accordance with previous sequencing results, here, we demonstrated that circSOD2 was highly expressed in HCC tumor tissues compared with normal liver tissues. Mechanically, we showed that histone writer EP300 and WDR5 bind to circSOD2 promoter and trigger its promoter H3K27ac and H3K4me3 modification, respectively, which further activates circSOD2 expression. SiRNA mediated circSOD2 suppression impaired liver cancer cell growth, cell migration, prohibited cell cycle progression and in vivo tumor growth. By acting as a sponge, circSOD2 inhibits miR-502-5p expression and rescues miR-502-5p target gene DNMT3a expression. As a DNA methyltransferase, upregulated DNMA3a suppresses SOCS3 expression by increasing SOCS3 promoter DNA methylation. This event further accelerates SOCS3 downstream JAK2/STAT3 signaling pathway activation. In addition, we also found that activated STAT3 regulates circSOD2 expression in a feedback way. Conclusion The novel signaling axis circSOD2/miR-502-5p/DNMT3a/JAK2/STAT3/circSOD2 provides a better understanding of HCC tumorigenesis. The molecular mechanism underlying this signaling axis offers new prevention and treatment of HCC.

scholarly journals LINC00152 promotes proliferation in hepatocellular carcinoma by targeting EpCAM via the mTOR signaling pathway

Oncotarget ◽  
2015 ◽  
Vol 6 (40) ◽  
pp. 42813-42824 ◽  
Author(s):  
Jie Ji ◽  
Junwei Tang ◽  
Lei Deng ◽  
Yu Xie ◽  
Runqiu Jiang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway

scholarly journals MAPK/ERK Signaling Pathway in Hepatocellular Carcinoma

Cancers ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 3026
Author(s):  
Hyuk Moon ◽  
Simon-Weonsang Ro
Keyword(s):  
Hepatocellular Carcinoma ◽  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Therapeutic Strategies ◽  
Erk Signaling ◽  
Health Concern ◽  
Alternative Mechanism ◽  
Major Health ◽  
Activating Mutations ◽  
Genetic Events

Hepatocellular carcinoma (HCC) is a major health concern worldwide, and its incidence is increasing steadily. Recently, the MAPK/ERK signaling pathway in HCC has gained renewed attention from basic and clinical researchers. The MAPK/ERK signaling pathway is activated in more than 50% of human HCC cases; however, activating mutations in RAS and RAF genes are rarely found in HCC, which are major genetic events leading to the activation of the MAPK/ERK signaling pathway in other cancers. This suggests that there is an alternative mechanism behind the activation of the signaling pathway in HCC. Here, we will review recent advances in understanding the cellular and molecular mechanisms involved in the activation of the MAPK/ERK signaling pathway and discuss potential therapeutic strategies targeting the signaling pathway in the context of HCC.

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