Establishment of cell clones with different metastatic potential from the metastatic hepatocellular carcinoma cell line MHCC97

Li, Yan; Tang, Zhao–You; Ye, Sheng‐Long; Liu, Yinkun; Chen, Jie; Xue, Qunji; Gao, Dongmei; Bao, Wei-Hua

doi:10.3748/wjg.7.5.630

Cited by 136 publications

(189 citation statements)

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“…Draw the growth curve by using the average number. Tumor cell doubling time: TD=Tlg2/lg(N/N 0 ) (TD: doubling time; T: time interval, N 0 : initial cell number, N: end-point cell number) [23] .…”

Section: Methodsmentioning

confidence: 99%

Downregulation of Dickkopf-1 is responsible for high proliferation of breast cancer cells via losing control of Wnt/β-catenin signaling

et al. 2010

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Aim: To investigate the role of DKK-1/Wnt/β-catenin signaling in high proliferation of LM-MCF-7 breast cancer cells, a sub-clone of MCF-7 cell line. Methods: Two cell lines (MCF-7 and LM-MCF-7) with different proliferation abilities were used. LM-MCF-7 cells were transiently transfected with the pcDNA3-DKK-1 plasmid encoding the DKK-1 gene (or MCF-7 cells were transfected siRNA targeting DKK-1 mRNA). Flow cytometry analysis and 5-bromo-2′-deoxyuridine (BrdU) incorporation assay were applied to detect the cell proliferation. The expression levels of β-catenin, phosphorylated β-catenin, c-Myc, cyclin D1 and Survivin were examined by Western blot analysis. The regulation of Survivin was investigated by Luciferase reporter gene assay. Results: Western blot and RT-PCR analysis showed that the expression level of DKK-1 was downregulated in LM-MCF-7 relative to MCF-7 cells. Flow cytometry and BrdU incorporation assay showed DKK-1 could suppress growth of breast cancer cells. Overexpression of DKK-1 was able to accelerate phosphorylation-dependent degradation of β-catenin and downregulate the expression of β-catenin, c-Myc, cyclin D1 and Survivin. Luciferase reporter gene assay demonstrated that Survivin could be regulated by β-catenin/ TCF4 pathway. Conclusion: We conclude that the downregulation of DKK-1 is responsible for the high proliferation ability of LM-MCF-7 breast cancer cells via losing control of Wnt/β-catenin signaling pathway, in which c-Myc, cyclinD1 and Survivin serve as essential downstream effectors. Our finding provides a new insight into the mechanism of breast cancer cell proliferation.

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Section: Methodsmentioning

confidence: 99%

Downregulation of Dickkopf-1 is responsible for high proliferation of breast cancer cells via losing control of Wnt/β-catenin signaling

et al. 2010

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“…BEL7402, SMMC7721, and LO2 (normal human liver cells) were purchased from the cell bank of Shanghai Institute of Cell Biology; HepG2 and 293 (Ad5 E1-transformed human embryo kidney cell line) cells were purchased from American Type Culture Collection (Manassas, VA); MHCC97-L and HCCLM3 hepatocellular carcinoma cell lines, which have low and high lung metastatic ability, respectively, were established in the Shanghai Cancer Institute (25). All cells were maintained in DMEM (Life Technologies, Inc., Invitrogen, Carsbad, CA) plus 10% heat-inactivated fetal bovine serum at 37jC in a humidified incubator with 5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

Knockdown of c-Met by adenovirus-delivered small interfering RNA inhibits hepatocellular carcinoma growth in vitro and in vivo

Zhang

Pan

et al. 2005

Molecular Cancer Therapeutics

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c-Met is highly expressed and constitutively activated in various human tumors. We employed adenovirus-mediated RNA interference technique to knock down c-Met expression in hepatocellular carcinoma cells and observed its effects on hepatocellular carcinoma cell growth in vitro and in vivo. Among the five hepatocellular carcinoma and one normal human liver cell lines we analyzed, c-Met was highly expressed and constitutively tyrosine phosphorylated in only MHCC97-L and HCCLM3 hepatocellular carcinoma cells. Knockdown of c-Met could inhibit MHCC97-L cells proliferation by arresting cells at G 0 -G 1 phase. Soft agar colony formation assay indicated that the colony forming ability of MHCC97-L cells decreased by f70% after adenovirus AdH1-small interfering RNA (siRNA)/met infection. In vivo experiments showed that adenovirus AdH1-siRNA/met inhibited the tumorigenicity of MHCC97-L cells and significantly suppressed tumor growth when injected directly into tumors. These results suggest that knockdown of c-Met by adenovirus-delivered siRNA may be a potential therapeutic strategy for treatment of hepatocellular carcinoma in which c-Met is overexpressed. [Mol Cancer Ther 2005;4(10):1577 -84]

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“…20,21 HCC clones derived from the same parent cell line exhibited higher serum AFP levels in nude mice bearing tumor implants with high metastatic potential than in those with low metastatic tumor implants. 22 These findings indicate the potential role of AFP in progression and metastasis of HCC.Regulation of AFP gene expression is a complex process mediated by a number of transcriptional activators and repressors binding to a complex of promoter and enhancer(s) within the AFP gene. 23,24 Clinically, AFP elevation in sera or AFP mRNA expression in HCC occurs more often in HCC patients of younger age 9 and positive for serum HBsAg.…”

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confidence: 99%

High α‐fetoprotein level correlates with high stage, early recurrence and poor prognosis of hepatocellular carcinoma: Significance of hepatitis virus infection, age, p53 and β‐catenin mutations

Shu

Chen²,

Lai

et al. 2004

Intl Journal of Cancer

280

219

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Key words: ␣-fetoprotein; hepatocellular carcinoma; p53; ␤-catenin; tumor stage; prognosis ␣-Fetoprotein (AFP), a member of the albuminoid multigene family located at chromosome 4q11-q13, 1 is abundantly expressed in the fetal yolk sac and liver, 2,3 but not in normal adult tissues. Chromosome 4q is one of the most frequent chromosomal region exhibiting allelic losses in hepatocellular carcinoma (HCC), 4 -7 whereas AFP expression resurges during liver regeneration 8 and in HCC. 2,8 -10 The AFP elevation in HCC has been shown to correlate with poor tumor differentiation, 9,10 tumor burden, 11 early recurrence after tumor resection 12,13 and unfavorable prognosis. 11 Serum AFP elevation concurrent with aberrant growth is usually regarded as coincidental, and its role in HCC progression receives little attention. However, cumulative evidence has shown that AFP plays an important role in the regulation of tumor growth and cell differentiation 14 -17 and can stimulate proliferation of human hepatoma cells, probably through the AFP receptors. 17-19 AFP-producing gastric cancer is more aggressive with higher malignant potential, high frequency of liver metastasis and a poor prognosis than AFP-negative gastric cancers. 20,21 HCC clones derived from the same parent cell line exhibited higher serum AFP levels in nude mice bearing tumor implants with high metastatic potential than in those with low metastatic tumor implants. 22 These findings indicate the potential role of AFP in progression and metastasis of HCC.Regulation of AFP gene expression is a complex process mediated by a number of transcriptional activators and repressors binding to a complex of promoter and enhancer(s) within the AFP gene. 23,24 Clinically, AFP elevation in sera or AFP mRNA expression in HCC occurs more often in HCC patients of younger age 9 and positive for serum HBsAg. 10,11 But the molecular mechanism is not fully understood. The tumor suppressor p53 acts through its binding within the AFP repressor region, displacing bound HNF-3 and altering the chromatin structure at the core promoter, to repress AFP gene expression. 25,26 Recently, it is shown that mutant ␤-catenin can induce p53 expression via the induction of p14(ARF), 27 which in turn leads to suppression of AFP expression through site-specific DNA binding within the AFP repressor domain, and the repression is abolished by mutation within the DNA binding domain of p53 protein. 25 The p53 and ␤-catenin genes are the 2 most commonly mutated genes in HCC, 28 -33 but their potential interplay in AFP elevation remains to be elucidated.In this study, we aimed to examine the AFP levels in HCC with special emphases on their relations to the tumor progression, the related factors including mutations of p53 and ␤-catenin and the usefulness of AFP mRNA detection in the liver for the prediction of early tumor recurrence. MATERIAL AND METHODS PatientsFrom 1987 to 1997, 909 surgically resected primary HCCs were pathologically assessed at the National Taiwan University Hospital. Among them, 781 unif...

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Establishment of cell clones with different metastatic potential from the metastatic hepatocellular carcinoma cell line MHCC97

Abstract: Two clones of the same genetic background but with different biological behaviors were established, which could be valuable models for investigation on HCC metastasis.

Cited by 136 publications

References 0 publications

Downregulation of Dickkopf-1 is responsible for high proliferation of breast cancer cells via losing control of Wnt/β-catenin signaling

Downregulation of Dickkopf-1 is responsible for high proliferation of breast cancer cells via losing control of Wnt/β-catenin signaling

Knockdown of c-Met by adenovirus-delivered small interfering RNA inhibits hepatocellular carcinoma growth in vitro and in vivo

High α‐fetoprotein level correlates with high stage, early recurrence and poor prognosis of hepatocellular carcinoma: Significance of hepatitis virus infection, age, p53 and β‐catenin mutations

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