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 ◽  
...  
RSC Advances ◽  
2017 ◽  
Vol 7 (21) ◽  
pp. 12793-12804 ◽  
Author(s):  
Yan-Wei Yang ◽  
Lei Yang ◽  
Chao Zhang ◽  
Cai-Yun Gao ◽  
Ting Ma ◽  
...  

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


Author(s):  
Ayyiliath M Sajith ◽  
Kereyagalahally H. Narasimhamurthy ◽  
Muthu K. Shanmugam ◽  
Shobith Rangappa ◽  
S. Chandra Nayak ◽  
...  

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

Aging ◽  
2020 ◽  
Vol 12 (15) ◽  
pp. 15546-15555 ◽  
Author(s):  
Changying Shi ◽  
Jiamei Yang ◽  
Longmiao Hu ◽  
Boyi Liao ◽  
Liang Qiao ◽  
...  

2021 ◽  
Vol 8 ◽  
Author(s):  
Wei Yang ◽  
Qihua Feng ◽  
Minjing Li ◽  
Jiaqi Su ◽  
Peiyuan Wang ◽  
...  

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.


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