scholarly journals Opposite responses of normal hepatocytes and hepatocellular carcinoma cells to substrate viscoelasticity

2020 ◽  
Vol 8 (5) ◽  
pp. 1316-1328 ◽  
Author(s):  
Kalpana Mandal ◽  
Ze Gong ◽  
Alexis Rylander ◽  
Vivek B. Shenoy ◽  
Paul A. Janmey
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Morphology ◽  
Critical Role ◽  
Carcinoma Cells ◽  
Hepatocellular Carcinoma Cells ◽  
Substrate Interaction ◽  
Cell Substrate

Viscosity plays a critical role in cell morphology, dynamics and cell-substrate interaction.

HBx induces the proliferation of hepatocellular carcinoma cells via AP1 over-expressed as a result of ER stress

2015 ◽  
Vol 466 (1) ◽  
pp. 115-121 ◽  
Author(s):  
Hyun Kook Cho ◽  
So Young Kim ◽  
Yi Yi Kyaw ◽  
Aye Aye Win ◽  
Seung-Hoi Koo ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Transcription Factor ◽  
Er Stress ◽  
Critical Role ◽  
Carcinoma Cells ◽  
Hepatocellular Carcinoma Cells

HBx protein is encoded by HBV and plays a critical role in hepatocarcinogenesis. In the present study we show that HBx activates the expression of the CREBH transcription factor and interacts with the activated CREBH. CREBH activation by HBx may result in cell proliferation.

scholarly journals The Cell Surface GRP78 Facilitates the Invasion of Hepatocellular Carcinoma Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Xiu-Xiu Zhang ◽  
Hong-Dan Li ◽  
Song Zhao ◽  
Liang Zhao ◽  
Hui-Juan Song ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Surface ◽  
Critical Role ◽  
Carcinoma Cells ◽  
Hepatocellular Carcinoma Cells ◽  
Carcinoma Cell Lines ◽  
Cell Surface Grp78 ◽  
Adhesion And Invasion ◽  
E Cadherin

Invasion is a major characteristic of hepatocellular carcinoma and one of the main causes of refractory to treatment. We have previously reported that GRP78 promotes the invasion of hepatocellular carcinoma although the mechanism underlying this change remains uncertain. In this paper, we explored the role of the cell surface GRP78 in the regulation of cancer cell invasion in hepatocellular carcinoma cells. We found that neutralization of the endogenous cell surface GRP78 with the anti-GRP78 antibody inhibited the adhesion and invasion in hepatocellular carcinoma cell lines Mahlavu and SMMC7721. However, forced expression of the cell surface GRP78 facilitated the adhesion and invasion in SMMC7721. We further demonstrated that inhibition of the endogenous cell surface GRP78 specifically inhibited the secretion and activity of MMP-2 but did not affect the secretion and activity of MMP-9. We also found that inhibition of the cell surface GRP78 increased E-Cadherin expression and decreased N-Cadherin level. On the contrary, forced expression of the cell surface GRP78 increased N-Cadherin expression and decreased E-Cadherin level, suggesting that the cell surface GRP78 plays critical role in the regulation of EMT process. These findings suggest that the cell surface GRP78 plays a stimulatory role in the invasion process and may be a potential anti-invasion target for the treatment of hepatocellular carcinoma.

HIV-TAT-fused FHIT protein functions as a potential pro-apoptotic molecule in hepatocellular carcinoma cells

2012 ◽  
Vol 32 (3) ◽  
pp. 271-279 ◽  
Author(s):  
Gui-Rong Yu ◽  
Wei-Wei Qin ◽  
Ji-Peng Li ◽  
Wei Hua ◽  
Yan-Ling Meng ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cancer Cells ◽  
Large Fraction ◽  
Critical Role ◽  
Carcinoma Cells ◽  
Mechanistic Study ◽  
Hepatocellular Carcinoma Cells ◽  
Hiv Tat ◽  
Fhit Protein ◽  
Hcc Cells

Accumulating evidence has demonstrated that FHIT (fragile histidine triad) is a bona fide tumour suppressor gene in a large fraction of human tumours, including hepatocellular cancer. A virus-based delivery system has been developed to transfer the FHIT gene into many types of cancer cells to inhibit growth or even induce apoptosis. However, a protein-based replacement strategy for FHIT has not been performed in cancer cells. Here, we used HIV-TAT (transactivator of transcription)-derived peptide to transfer the purified FHIT protein into HCC (hepatocellular carcinoma) cells and determine the biological effect of this fusion protein in inducing apoptosis. Affinity chromatography was used to purify TAT peptide-fused human FHIT (TAT–FHIT) protein from BL21 Escherichia coli. Immunofluorescence staining and Western blot analysis were performed to identify the expression and internalization of TAT–FHIT in HCC cells compared with the purified FHIT protein. Our study showed that TAT–FHIT protein can translocate into cancer cells in 1 h after incubation at 37°C. Furthermore, the results of MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide] assay, Annexin-V staining and Western blotting demonstrated that TAT–FHIT can robustly inhibit growth and induce apoptosis of HCC cells in vitro. In addition, a mechanistic study showed that both exogenous and intrinsic apoptotic pathways were involved in TAT–FHIT-mediated apoptosis and this effect could be attenuated partially by a mitochondrial protector TAT-BH4, indicating that mitochondrion plays a critical role in TAT–FHIT-mediated pro-apoptotic effect in cancer cells. Taken together, our study suggests that TAT–FHIT is a potential pro-apoptotic molecule in HCC cells and strengthen the hypothesis of its therapeutic application against HCC.

scholarly journals The expression profiles and prognostic values of HSP70s in hepatocellular carcinoma

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ben Wang ◽  
Tian Lan ◽  
Han Xiao ◽  
Zhong-Huo Chen ◽  
Chao Wei ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Overall Survival ◽  
Survival Rate ◽  
Expression Profiles ◽  
Critical Role ◽  
Tumor Grade ◽  
Carcinoma Cells ◽  
Overall Survival Rate ◽  
Hepatocellular Carcinoma Cells ◽  
Hsp70 Family

Abstract Background The HSP70 family of heat shock protein plays a critical role in protein synthesis and transport to maintain protein homeostasis. Several studies have indicated that HSP70s are related to the development and occurrence of various cancers. Methods The relationship between the overall survival rate of hepatocellular carcinoma patients and the expression of 14 HSP70s from multiple databases, such as TCGA, ONCOMINE, cBioPortal was investigated. Western Blot and PCR were used to evaluate HSPA4 and HSPA14 expressions in various HCC cells to identify suitable cell lines for further experiments .Wound-healing assays, Transwell assays and EdU assays were used to verify the effects of HSPA4 and HSPA14 on the function of hepatocellular carcinoma cells, and statistical analysis was performed. Results Hepatocellular carcinoma tissues significantly expressed the 14 HSP70s compared to the normal samples. Besides, the high HSPA1A, HSPA1B, HSPA4, HSPA5, HSPA8, HSPA13, and HSPA14 expressions were inversely associated with the overall survival rate of patients, tumor grade, and cancer stage. A PPI regulatory network was constructed using the 14 HSP70s proteins with HSPA5 and HSPA8 at the network center. Univariate and multivariate analyses showed that HSPA4 and HSPA14 could be independent risk factors for the prognosis of hepatocellular carcinoma patients. Cell experiments have also confirmed that reducing HSPA4 and HSPA14 expressions can inhibit the invasion, metastasis, and proliferation of hepatocellular carcinoma cells. Conclusions Therefore, the HSP70s significantly influence the occurrence and development of hepatocellular carcinoma. For instance, HSPA4 and HSPA14 can be novel therapeutic targets and prognostic biomarkers for hepatocellular carcinoma.

HGF/SF downstream signaling in human hepatoblastoma and hepatocellular carcinoma cells

2004 ◽  
Vol 216 (03) ◽  
Author(s):  
S Grotegut ◽  
E Fasler-Kan ◽  
G Christofori ◽  
D von Schweinitz
Keyword(s):  
Hepatocellular Carcinoma ◽  
Carcinoma Cells ◽  
Hepatocellular Carcinoma Cells ◽  
Downstream Signaling
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