Molecular mechanism and function research of highly expressed PEG 10 gene in hepatocellular carcinoma

Yun Lin; Yun Li Zhang; Xin Hu; Qing Deng; Qi Li; Yong Gao; Xiao Mei Teng; Ze Guang Han; Jian Huang

doi:10.3781/j.issn.1000-7431.2013.01.005

Molecular mechanism and function research of highly expressed PEG 10 gene in hepatocellular carcinoma

Yun Lin, Yun Li Zhang, Xin Hu, Qing Deng, Qi Li, Yong Gao, Xiao Mei Teng, Ze Guang Han, Jian Huang

Research output: Contribution to journal › Article › peer-review

1 Scopus citations

Abstract

Objective: To study the molecular mechanism of dysregulation of PEG 10 (paternally expressed gene 10), an imprinted gene in HCC (hepatocellular carcinoma), and to analyze its effect on the growth of hepatocellular carcinoma cells. Methods: The expression level of PEG10 mRNA was detected by semi-quantitative RT-PCR in 30 paired HCC/adjacent non-cancerous tissues and 15 types of liver cancer cell lines. Methylation status of CpG islands at the promoter of PEG 10 gene in 17 paired HCC/adjacent noncancerous tissue samples in which the expression of PEG 10 gene in cancer tissues was significantly upregulated as compared with non-cancerous tissues was detected using MSP (methylation specific PCR). The PEG10 shRNA (short hairpin RNA) was used to silence the expression of PEG 10 gene in HCC QGY-7703 cells, and the colony-forming ability of QGY-7703 cells was detected by Western blotting and colony formation assay. Results: PEG10 mRNA expression level was significantly up-regulated in 67% (20/30) HCC tissues as compared with adjacent non-cancerous tissues. PEG 10 was expressed in 15 types of HCC cell lines. The methylation status of PEG 10 gene's CpG2 island was significantly decreased in 29.4% (5/17) HCC tissue samples, and the overall decreased methylation status of PEG 10 gene's CpG2 island in HCC tissues was verified using bisulfite sequencing. Interestingly, silencing the expression of PEG10 in HCC QGY-7703 cells using shRNA targeting PEG 10 gene markedly inhibited the colony-forming efficiency as compared with the HCC QGY-7703 cells transfected with negative control shRNA (P < 0.05). Conclusion: PEG 10, an imprinted gene, is up-regulated in HCC, and may be closely related with the decreased methylation status of CpG2 island at the promoter of PEG 10 gene. Silencing the expression of PEG10 can inhibit the growth of HCC cells, suggesting that PEG 10 gene may play an important role in the hepatocarcinogenesis, and it may be used as a new marker or a potential therapeutic target for HCC.

Original language	English (US)
Pages (from-to)	28-35
Number of pages	8
Journal	Tumor
Volume	33
Issue number	1
DOIs	https://doi.org/10.3781/j.issn.1000-7431.2013.01.005
State	Published - Jan 2013
Externally published	Yes

Keywords

DNA methylation
Liver neoplasms
PEG 10 gene

ASJC Scopus subject areas

Epidemiology
Oncology
Cancer Research

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10.3781/j.issn.1000-7431.2013.01.005

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@article{2d263207e0ef45fbac5c39dbd84c6bc9,

title = "Molecular mechanism and function research of highly expressed PEG 10 gene in hepatocellular carcinoma",

abstract = "Objective: To study the molecular mechanism of dysregulation of PEG 10 (paternally expressed gene 10), an imprinted gene in HCC (hepatocellular carcinoma), and to analyze its effect on the growth of hepatocellular carcinoma cells. Methods: The expression level of PEG10 mRNA was detected by semi-quantitative RT-PCR in 30 paired HCC/adjacent non-cancerous tissues and 15 types of liver cancer cell lines. Methylation status of CpG islands at the promoter of PEG 10 gene in 17 paired HCC/adjacent noncancerous tissue samples in which the expression of PEG 10 gene in cancer tissues was significantly upregulated as compared with non-cancerous tissues was detected using MSP (methylation specific PCR). The PEG10 shRNA (short hairpin RNA) was used to silence the expression of PEG 10 gene in HCC QGY-7703 cells, and the colony-forming ability of QGY-7703 cells was detected by Western blotting and colony formation assay. Results: PEG10 mRNA expression level was significantly up-regulated in 67% (20/30) HCC tissues as compared with adjacent non-cancerous tissues. PEG 10 was expressed in 15 types of HCC cell lines. The methylation status of PEG 10 gene's CpG2 island was significantly decreased in 29.4% (5/17) HCC tissue samples, and the overall decreased methylation status of PEG 10 gene's CpG2 island in HCC tissues was verified using bisulfite sequencing. Interestingly, silencing the expression of PEG10 in HCC QGY-7703 cells using shRNA targeting PEG 10 gene markedly inhibited the colony-forming efficiency as compared with the HCC QGY-7703 cells transfected with negative control shRNA (P < 0.05). Conclusion: PEG 10, an imprinted gene, is up-regulated in HCC, and may be closely related with the decreased methylation status of CpG2 island at the promoter of PEG 10 gene. Silencing the expression of PEG10 can inhibit the growth of HCC cells, suggesting that PEG 10 gene may play an important role in the hepatocarcinogenesis, and it may be used as a new marker or a potential therapeutic target for HCC.",

keywords = "DNA methylation, Liver neoplasms, PEG 10 gene",

author = "Yun Lin and Zhang, {Yun Li} and Xin Hu and Qing Deng and Qi Li and Yong Gao and Teng, {Xiao Mei} and Han, {Ze Guang} and Jian Huang",

year = "2013",

month = jan,

doi = "10.3781/j.issn.1000-7431.2013.01.005",

language = "English (US)",

volume = "33",

pages = "28--35",

journal = "Tumor",

issn = "1000-7431",

publisher = "Shanghai Jiao Tong University",

number = "1",

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TY - JOUR

T1 - Molecular mechanism and function research of highly expressed PEG 10 gene in hepatocellular carcinoma

AU - Lin, Yun

AU - Zhang, Yun Li

AU - Hu, Xin

AU - Deng, Qing

AU - Li, Qi

AU - Gao, Yong

AU - Teng, Xiao Mei

AU - Han, Ze Guang

AU - Huang, Jian

PY - 2013/1

Y1 - 2013/1

N2 - Objective: To study the molecular mechanism of dysregulation of PEG 10 (paternally expressed gene 10), an imprinted gene in HCC (hepatocellular carcinoma), and to analyze its effect on the growth of hepatocellular carcinoma cells. Methods: The expression level of PEG10 mRNA was detected by semi-quantitative RT-PCR in 30 paired HCC/adjacent non-cancerous tissues and 15 types of liver cancer cell lines. Methylation status of CpG islands at the promoter of PEG 10 gene in 17 paired HCC/adjacent noncancerous tissue samples in which the expression of PEG 10 gene in cancer tissues was significantly upregulated as compared with non-cancerous tissues was detected using MSP (methylation specific PCR). The PEG10 shRNA (short hairpin RNA) was used to silence the expression of PEG 10 gene in HCC QGY-7703 cells, and the colony-forming ability of QGY-7703 cells was detected by Western blotting and colony formation assay. Results: PEG10 mRNA expression level was significantly up-regulated in 67% (20/30) HCC tissues as compared with adjacent non-cancerous tissues. PEG 10 was expressed in 15 types of HCC cell lines. The methylation status of PEG 10 gene's CpG2 island was significantly decreased in 29.4% (5/17) HCC tissue samples, and the overall decreased methylation status of PEG 10 gene's CpG2 island in HCC tissues was verified using bisulfite sequencing. Interestingly, silencing the expression of PEG10 in HCC QGY-7703 cells using shRNA targeting PEG 10 gene markedly inhibited the colony-forming efficiency as compared with the HCC QGY-7703 cells transfected with negative control shRNA (P < 0.05). Conclusion: PEG 10, an imprinted gene, is up-regulated in HCC, and may be closely related with the decreased methylation status of CpG2 island at the promoter of PEG 10 gene. Silencing the expression of PEG10 can inhibit the growth of HCC cells, suggesting that PEG 10 gene may play an important role in the hepatocarcinogenesis, and it may be used as a new marker or a potential therapeutic target for HCC.

AB - Objective: To study the molecular mechanism of dysregulation of PEG 10 (paternally expressed gene 10), an imprinted gene in HCC (hepatocellular carcinoma), and to analyze its effect on the growth of hepatocellular carcinoma cells. Methods: The expression level of PEG10 mRNA was detected by semi-quantitative RT-PCR in 30 paired HCC/adjacent non-cancerous tissues and 15 types of liver cancer cell lines. Methylation status of CpG islands at the promoter of PEG 10 gene in 17 paired HCC/adjacent noncancerous tissue samples in which the expression of PEG 10 gene in cancer tissues was significantly upregulated as compared with non-cancerous tissues was detected using MSP (methylation specific PCR). The PEG10 shRNA (short hairpin RNA) was used to silence the expression of PEG 10 gene in HCC QGY-7703 cells, and the colony-forming ability of QGY-7703 cells was detected by Western blotting and colony formation assay. Results: PEG10 mRNA expression level was significantly up-regulated in 67% (20/30) HCC tissues as compared with adjacent non-cancerous tissues. PEG 10 was expressed in 15 types of HCC cell lines. The methylation status of PEG 10 gene's CpG2 island was significantly decreased in 29.4% (5/17) HCC tissue samples, and the overall decreased methylation status of PEG 10 gene's CpG2 island in HCC tissues was verified using bisulfite sequencing. Interestingly, silencing the expression of PEG10 in HCC QGY-7703 cells using shRNA targeting PEG 10 gene markedly inhibited the colony-forming efficiency as compared with the HCC QGY-7703 cells transfected with negative control shRNA (P < 0.05). Conclusion: PEG 10, an imprinted gene, is up-regulated in HCC, and may be closely related with the decreased methylation status of CpG2 island at the promoter of PEG 10 gene. Silencing the expression of PEG10 can inhibit the growth of HCC cells, suggesting that PEG 10 gene may play an important role in the hepatocarcinogenesis, and it may be used as a new marker or a potential therapeutic target for HCC.

KW - DNA methylation

KW - Liver neoplasms

KW - PEG 10 gene

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Molecular mechanism and function research of highly expressed PEG 10 gene in hepatocellular carcinoma

Abstract

Keywords

ASJC Scopus subject areas

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