scholarly journals Glycochenodeoxycholic acid induces stemness and chemoresistance via the STAT3 signaling pathway in hepatocellular carcinoma cells

Aging ◽  
2020 ◽  
Vol 12 (15) ◽  
pp. 15546-15555 ◽  
Author(s):  
Changying Shi ◽  
Jiamei Yang ◽  
Longmiao Hu ◽  
Boyi Liao ◽  
Liang Qiao ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Signaling Pathway ◽  
Carcinoma Cells ◽  
Hepatocellular Carcinoma Cells ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

scholarly journals Physagulide Q suppresses proliferation and induces apoptosis in human hepatocellular carcinoma cells by regulating the ROS-JAK2/Src-STAT3 signaling pathway

RSC Advances ◽  
2017 ◽  
Vol 7 (21) ◽  
pp. 12793-12804 ◽  
Author(s):  
Yan-Wei Yang ◽  
Lei Yang ◽  
Chao Zhang ◽  
Cai-Yun Gao ◽  
Ting Ma ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Signaling Pathway ◽  
Natural Compound ◽  
Carcinoma Cells ◽  
Human Hepatocellular Carcinoma ◽  
Hepatocellular Carcinoma Cells ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Physalis Angulata ◽  
Human Hepatocellular Carcinoma Cells

Physagulide Q (PQ), a new natural compound, was isolated from Physalis angulata L. in our laboratory.

Pyrimidine-2,4-dione Targets STAT3 Signaling Pathway to Induce Cytotoxicity in Hepatocellular Carcinoma Cells

2021 ◽  
pp. 128332
Author(s):  
Ayyiliath M Sajith ◽  
Kereyagalahally H. Narasimhamurthy ◽  
Muthu K. Shanmugam ◽  
Shobith Rangappa ◽  
S. Chandra Nayak ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Signaling Pathway ◽  
Carcinoma Cells ◽  
Hepatocellular Carcinoma Cells ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

scholarly journals Niclosamide Inhibits Cell Growth and Enhances Drug Sensitivity of Hepatocellular Carcinoma Cells via STAT3 Signaling Pathway

2018 ◽  
Vol 9 (22) ◽  
pp. 4150-4155 ◽  
Author(s):  
Chengzhi Wang ◽  
Xiaoqing Zhou ◽  
Hongjuan Xu ◽  
Xiaqing Shi ◽  
Jinfeng Zhao ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Growth ◽  
Signaling Pathway ◽  
Drug Sensitivity ◽  
Carcinoma Cells ◽  
Hepatocellular Carcinoma Cells ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

Vitexin abrogates invasion and survival of hepatocellular carcinoma cells through targeting STAT3 signaling pathway

Biochimie ◽  
2020 ◽  
Vol 175 ◽  
pp. 58-68 ◽  
Author(s):  
Jong Hyun Lee ◽  
Chakrabhavi Dhananjaya Mohan ◽  
Muthu K. Shanmugam ◽  
Shobith Rangappa ◽  
Gautam Sethi ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Signaling Pathway ◽  
Carcinoma Cells ◽  
Hepatocellular Carcinoma Cells ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

scholarly journals Sinomenine Suppresses Development of Hepatocellular Carcinoma Cells via Inhibiting MARCH1 and AMPK/STAT3 Signaling Pathway

2021 ◽  
Vol 8 ◽  
Author(s):  
Wei Yang ◽  
Qihua Feng ◽  
Minjing Li ◽  
Jiaqi Su ◽  
Peiyuan Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Signaling Pathway ◽  
Mechanism Of Action ◽  
Carcinoma Cells ◽  
Stat3 Signaling ◽  
Finger Protein ◽  
Novel Treatment ◽  
Stat3 Signaling Pathway ◽  
And Function ◽  
Hcc Cells

Promotion of apoptosis and suppression of proliferation in tumor cells are popular strategies for developing anticancer drugs. Sinomenine (SIN), a plant-derived alkaloid, displays antitumor activity. However, the mechanism of action of SIN against hepatocellular carcinoma (HCC) is unclear. Herein, several molecular technologies, such as Western Blotting, qRT-PCR, flow cytometry, and gene knockdown were applied to explore the role and mechanism of action of SIN in the treatment of HCC. It was found that SIN arrests HCC cell cycle at G0/G1 phase, induces apoptosis, and suppresses proliferation of HCC cells via down-regulating the expression of membrane-associated RING-CH finger protein 1 (MARCH1). Moreover, SIN induces cell death and growth inhibition through AMPK/STAT3 signaling pathway. MARCH1 expression was silenced by siRNA to explore its involvement in the regulation of AMPK/STAT3 signaling pathway. Silencing MARCH1 caused down-regulation of phosphorylation of AMPK, STAT3 and decreased cell viability and function. Our results suggested that SIN inhibits proliferation and promotes apoptosis of HCC cells by MARCH1-mediated AMPK/STAT3 signaling pathway. This study provides new support for SIN as a clinical anticancer drug and illustrates that targeting MARCH1 could be a novel treatment strategy in developing anticancer therapeutics.

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.

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