Effect of melanoma cells on proliferation and migration of activated hepatic stellate cells in vitro

2017 ◽  
Vol 213 (4) ◽  
pp. 400-404 ◽  
Author(s):  
Theresa Meyer ◽  
Andreas Koch ◽  
Eva-Vanessa Ebert ◽  
Barbara Czech ◽  
Martina Mueller ◽  
...  
Keyword(s):  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Melanoma Cells ◽  
Activated Hepatic Stellate Cells ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Nitrovasodilators inhibit platelet-derived growth factor-induced proliferation and migration of activated human hepatic stellate cells

2000 ◽  
Vol 119 (2) ◽  
pp. 479-492 ◽  
Author(s):  
Paola Failli ◽  
Raffaella M.S. DeFranco ◽  
Alessandra Caligiuri ◽  
Alessandra Gentilini ◽  
Roberto Giulio Romanelli ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Platelet Derived Growth Factor ◽  
And Migration ◽  
Proliferation And Migration

Comparison of the In Vitro Antifibrogenic Effects of Silymarin, Silybin A and 18α-Glycyrrhizin on Activated Hepatic Stellate Cells

2016 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Seyed Younes Hosseini ◽  
Kurosh Kalantar ◽  
Khashayar Shahin ◽  
Maryam Ghayour ◽  
Masoumeh Rajabi Bazl ◽  
...  
Keyword(s):  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Activated Hepatic Stellate Cells

Halofuginone inhibits in vitro migration and proliferation of activated hepatic stellate cells

2003 ◽  
Vol 124 (4) ◽  
pp. A765
Author(s):  
Yury Popov ◽  
eleonora Patsenker ◽  
Michael Bauer ◽  
Edith Niedobitek ◽  
Mark Pines ◽  
...  
Keyword(s):  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Activated Hepatic Stellate Cells

scholarly journals GJA1 promotes hepatocellular carcinoma progression by mediating TGF-β-induced activation and the epithelial–mesenchymal transition of hepatic stellate cells

Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 1459-1471
Author(s):  
Gengming Niu ◽  
Xiaotian Zhang ◽  
Runqi Hong ◽  
Ximin Yang ◽  
Jiawei Gu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Conditioned Medium ◽  
Hepatic Stellate Cells ◽  
Hepatic Cirrhosis ◽  
Epithelial Mesenchymal Transition ◽  
Stellate Cells ◽  
Gene Set Enrichment Analysis ◽  
Mesenchymal Transition ◽  
And Migration ◽  
Proliferation And Migration

Abstract Introduction Gap junction protein, alpha 1 (GJA1), which is correlated with recurrences and unfavorable prognoses in hepatocellular carcinomas (HCCs), is one of the specific proteins expressed by activated hepatic stellate cells (HSCs). Methods Expression of GJA1 was compared between HCCs and nontumor tissues (NTs), between hepatic cirrhosis and NTs, and between primary and metastatic HCCs using transcriptomic datasets from the Gene Expression Omnibus and the Integrative Molecular Database of Hepatocellular Carcinoma. The in vitro activities of GJA1 were investigated in cultured HSCs and HCC cells. The underlying mechanism was characterized using Gene Set Enrichment Analysis and validated by western blotting. Results The expression of GJA1 was significantly increased in HCCs and hepatic cirrhosis compared to that in NTs. GJA1 was also overexpressed in pulmonary metastases from HCCs when compared with HCCs without metastasis. Overexpression of GJA1 promoted while knockdown of GJA1 inhibited proliferation and transforming growth factor (TGF)-β-mediated activation and migration of cultured HSCs. Overexpression of GJA1 by lentivirus infection promoted proliferation and migration, while conditioned medium from HSCs overexpressing GJA1 promoted migration but inhibited proliferation of Hep3B and PLC-PRF-5 cells. Lentivirus infection with shGJA1 or conditioned medium from shGJA1-infected HSCs inhibited the proliferation and migration of HCCLM3 cells that had a high propensity toward lung metastasis. Mechanistically, GJA1 induced the epithelial–mesenchymal transition (EMT) in HSCs and HCCLM3 cells. Conclusion GJA1 promoted HCC progression by inducing HSC activation and the EMT in HSCs. GJA1 is potentially regulated by TGF-β and thus may be a therapeutic target to inhibit HCC progression.

scholarly journals Inhibiting IRE1α-endonuclease activity decreases tumor burden in a mouse model for hepatocellular carcinoma

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Nataša Pavlović ◽  
Carlemi Calitz ◽  
Kess Thanapirom ◽  
Guiseppe Mazza ◽  
Krista Rombouts ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Cells ◽  
Cell Activation ◽  
Stellate Cell ◽  
Stellate Cells ◽  
Tumor Burden ◽  
And Migration ◽  
Hcc Cells ◽  
Proliferation And Migration

Hepatocellular carcinoma (HCC) is a liver tumor that usually arises in patients with cirrhosis. Hepatic stellate cells are key players in the progression of HCC, as they create a fibrotic micro-environment and produce growth factors and cytokines that enhance tumor cell proliferation and migration. We assessed the role of endoplasmic reticulum (ER) stress in the cross-talk between stellate cells and HCC cells. Mice with a fibrotic HCC were treated with the IRE1α-inhibitor 4μ8C, which reduced tumor burden and collagen deposition. By co-culturing HCC-cells with stellate cells, we found that HCC-cells activate IREα in stellate cells, thereby contributing to their activation. Inhibiting IRE1α blocked stellate cell activation, which then decreased proliferation and migration of tumor cells in different in vitro 2D and 3D co-cultures. In addition, we also observed cell-line-specific direct effects of inhibiting IRE1α in tumor cells.

Interleukin-6 secreted by bipotential murine oval liver stem cells induces apoptosis of activated hepatic stellate cells by activating NF-κB-inducible nitric oxide synthase signaling

2017 ◽  
Vol 95 (2) ◽  
pp. 263-272 ◽  
Author(s):  
Palanivel Gajalakshmi ◽  
Syamantak Majumder ◽  
Cornelia S. Viebahn ◽  
Akila Swaminathan ◽  
George C. Yeoh ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Interleukin 6 ◽  
Hepatic Stellate Cells ◽  
Critical Role ◽  
In Vitro Study ◽  
Stellate Cells ◽  
Causative Factor ◽  
Activated Hepatic Stellate Cells ◽  
Induced Apoptosis

Liver fibrosis is now well recognized as the causative factor for increased mortality from complications associated with liver pathologies. Activated hepatic stellate cells (HSCs) play a critical role in the progression of liver fibrosis. Therefore, targeting these activated HSCs to prevent and (or) treat liver disease is a worthwhile approach to explore. In the present in vitro study, we investigated the use of bipotential murine oval liver cells (BMOL) in regulating the functions of activated HSCs to prevent progression of liver fibrosis. We used a conditioned medium-based approach to study the effect of BMOL cells on activated HSC survival and function. Our data showed that BMOL cells block the contraction of activated HSCs by inducing apoptosis of these cells. We demonstrated that BMOL cells secrete soluble factors, such as interleukin-6 (IL-6), which induced apoptosis of activated HSCs. Using both pharmacological and molecular inhibitor approaches, we further identified that IL-6-mediated activation of NF-κB–iNOS–NO–ROS signaling in activated HSCs plays a critical role in BMOL-cell-mediated apoptosis of activated HSCs. Thus, the present study provides an alternative cell-based therapeutic approach to treat liver fibrosis.

ERK5 differentially regulates PDGF-induced proliferation and migration of hepatic stellate cells

2008 ◽  
Vol 48 (1) ◽  
pp. 107-115 ◽  
Author(s):  
Elisabetta Rovida ◽  
Nadia Navari ◽  
Alessandra Caligiuri ◽  
Persio Dello Sbarba ◽  
Fabio Marra
Keyword(s):  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
And Migration ◽  
Proliferation And Migration
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