Abstract

Background: Glucose-regulated protein 78 (GRP78) plays an important role in embryonic development and cancer progression. However, there is little information regarding the regulation of GRP78 in hepatocellular carcinoma (HCC) metastasis. Methods: We used RNA silencing and cDNA expression vectors to manipulate target gene expression in HCC cells. The transwell migration assay and xCelligence biosensor system were applied to determine the proliferatory and migratory ability of the HCC cells. Results: In this study, we found that GRP78 silencing enhanced cell migration in both HepJ5 and Mahlavu cells. Overexpressed GRP78 in skHep1 cells suppressed the migratory ability. In the insight mechanism dissection for GRP78-mediated cancer migration, we found that downregulation of GRP78 caused the increase of vimentin expression on HCC cells. Suppressed vimentin expression also decreased the migratory ability on HCC, indicating that vimentin expression levels modulated the cell migratory ability. Conclusion: We found that silencing GRP78 in HCC cells may enhance cell migration through the increase of vimentin expression.

Original languageEnglish
Pages (from-to)S572-S579
JournalAnnals of Surgical Oncology
Volume19
Issue numberSUPPL. 3
DOIs
Publication statusPublished - Jul 2012

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Vimentin
Cell Movement
Hepatocellular Carcinoma
Up-Regulation
Biosensing Techniques
RNA Interference
glucose-regulated proteins
Embryonic Development
Dissection
Neoplasms
Down-Regulation
Complementary DNA
Neoplasm Metastasis
Gene Expression

ASJC Scopus subject areas

  • Surgery
  • Oncology

Cite this

@article{16241302230b41648fdf573b93cf930c,
title = "Silencing of glucose-regulated protein 78 (GRP78) enhances cell migration through the upregulation of vimentin in hepatocellular carcinoma cells",
abstract = "Background: Glucose-regulated protein 78 (GRP78) plays an important role in embryonic development and cancer progression. However, there is little information regarding the regulation of GRP78 in hepatocellular carcinoma (HCC) metastasis. Methods: We used RNA silencing and cDNA expression vectors to manipulate target gene expression in HCC cells. The transwell migration assay and xCelligence biosensor system were applied to determine the proliferatory and migratory ability of the HCC cells. Results: In this study, we found that GRP78 silencing enhanced cell migration in both HepJ5 and Mahlavu cells. Overexpressed GRP78 in skHep1 cells suppressed the migratory ability. In the insight mechanism dissection for GRP78-mediated cancer migration, we found that downregulation of GRP78 caused the increase of vimentin expression on HCC cells. Suppressed vimentin expression also decreased the migratory ability on HCC, indicating that vimentin expression levels modulated the cell migratory ability. Conclusion: We found that silencing GRP78 in HCC cells may enhance cell migration through the increase of vimentin expression.",
author = "Po-Li Wei and Li-Jen Kuo and Weu Wang and Feng-Yen Lin and Liu, {Hui Hsiung} and How Tseng and Yuan-Soon Ho and Ming-Te Huang and Chih-Hsiung Wu and Yu-Jia Chang",
year = "2012",
month = "7",
doi = "10.1245/s10434-011-2055-y",
language = "English",
volume = "19",
pages = "S572--S579",
journal = "Annals of Surgical Oncology",
issn = "1068-9265",
publisher = "Springer New York",
number = "SUPPL. 3",

}

TY - JOUR

T1 - Silencing of glucose-regulated protein 78 (GRP78) enhances cell migration through the upregulation of vimentin in hepatocellular carcinoma cells

AU - Wei, Po-Li

AU - Kuo, Li-Jen

AU - Wang, Weu

AU - Lin, Feng-Yen

AU - Liu, Hui Hsiung

AU - Tseng, How

AU - Ho, Yuan-Soon

AU - Huang, Ming-Te

AU - Wu, Chih-Hsiung

AU - Chang, Yu-Jia

PY - 2012/7

Y1 - 2012/7

N2 - Background: Glucose-regulated protein 78 (GRP78) plays an important role in embryonic development and cancer progression. However, there is little information regarding the regulation of GRP78 in hepatocellular carcinoma (HCC) metastasis. Methods: We used RNA silencing and cDNA expression vectors to manipulate target gene expression in HCC cells. The transwell migration assay and xCelligence biosensor system were applied to determine the proliferatory and migratory ability of the HCC cells. Results: In this study, we found that GRP78 silencing enhanced cell migration in both HepJ5 and Mahlavu cells. Overexpressed GRP78 in skHep1 cells suppressed the migratory ability. In the insight mechanism dissection for GRP78-mediated cancer migration, we found that downregulation of GRP78 caused the increase of vimentin expression on HCC cells. Suppressed vimentin expression also decreased the migratory ability on HCC, indicating that vimentin expression levels modulated the cell migratory ability. Conclusion: We found that silencing GRP78 in HCC cells may enhance cell migration through the increase of vimentin expression.

AB - Background: Glucose-regulated protein 78 (GRP78) plays an important role in embryonic development and cancer progression. However, there is little information regarding the regulation of GRP78 in hepatocellular carcinoma (HCC) metastasis. Methods: We used RNA silencing and cDNA expression vectors to manipulate target gene expression in HCC cells. The transwell migration assay and xCelligence biosensor system were applied to determine the proliferatory and migratory ability of the HCC cells. Results: In this study, we found that GRP78 silencing enhanced cell migration in both HepJ5 and Mahlavu cells. Overexpressed GRP78 in skHep1 cells suppressed the migratory ability. In the insight mechanism dissection for GRP78-mediated cancer migration, we found that downregulation of GRP78 caused the increase of vimentin expression on HCC cells. Suppressed vimentin expression also decreased the migratory ability on HCC, indicating that vimentin expression levels modulated the cell migratory ability. Conclusion: We found that silencing GRP78 in HCC cells may enhance cell migration through the increase of vimentin expression.

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U2 - 10.1245/s10434-011-2055-y

DO - 10.1245/s10434-011-2055-y

M3 - Article

VL - 19

SP - S572-S579

JO - Annals of Surgical Oncology

JF - Annals of Surgical Oncology

SN - 1068-9265

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