Proteome analysis of hepatocellular carcinoma cell strains, MHCC97‐H and MHCC97‐L, with different metastasis potentials

Ding, Shi‐Jian; Li, Yan; Shao, Xin; Zhou, Hu; Zeng, Rong; Tang, Zhao–You; Xia, Qi-Chang

doi:10.1002/pmic.200300653

Cited by 147 publications

(102 citation statements)

References 42 publications

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“…Finally, calreticulin downregulation has been recently reported to be associated with tumour metastasis (Ding et al 2004). Interestingly, a role for calreticulin has also been demonstrated in regulating p53 function by affecting its rate of degradation and nuclear localization (Mesaeli & Phillipson 2004).…”

Section: Discussionmentioning

confidence: 99%

A differential proteomic approach to identify proteins associated with thyroid cell transformation

Paron

D’Ambrosio²,

Scaloni³

et al. 2005

Journal of Molecular Endocrinology

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Tumour suppressor p53 is a transcription factor essential for DNA damage checkpoints during cellular response to stress. Mutations in the p53 gene are the most common genetic alterations found in human tumours; most pathogenetic modifications are missense mutations that abolish the p53 DNA-binding function. In the same cell type, distinct p53 missense mutations may determine different phenotypes. The PC Cl3 cell line retains several markers of thyroid differentiation in vitro. Introduction of the V143A mutant p53 allele, which abolishes the p53 DNA-binding function, leads to loss of differentiation markers as well as TSH dependency for growth. Conversely, PC Cl3 cells transfected with the S392A mutant p53 allele, presenting the mutation located outside the DNA-binding domain, show only loss of TSH dependency for growth. To identify molecular differences existing between PC Cl3 cell lines transformed by the V143A and the S392A mutant alleles, a differential proteomic approach was used. Two-dimensional gel electrophoresis analyses indicated that expression of a significant portion of protein species was modified by both p53 mutants. In fact, compared with wild-type PC Cl3 cells, modification of expression in V143A mutant cells occurred in 23·6% of the entire protein species. Conversely, modification of S392A mutant cells affected 14·0% of total proteins. Among these components, 8·3% were common to both mutants. Several of these proteins were identified by mass spectrometry procedures; some proteins, such as HSP90 and T-complex proteins, are already known to be related to p53 function.

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Section: Discussionmentioning

confidence: 99%

A differential proteomic approach to identify proteins associated with thyroid cell transformation

Paron

D’Ambrosio²,

Scaloni³

et al. 2005

Journal of Molecular Endocrinology

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“…Furthermore, increased levels of cofilin expression is detected in clinical tumour samples of oral squamous-cell carcinoma 76 , renal cell carcinoma 77 and ovarian cancer 78 using proteomic and cDNA microarray approaches. Expression of the wild-type or the non-phosphorylatable cofilin mutant S3A increases melanoma cell invasion through a reconstituted basement 79 , and in ovarian surface epithelium (OSE) cells derived from women with a family history of ovarian and/or breast cancer and mutations in the BRCA1 tumoursuppressor gene 80 . The regulated overexpression of cofilin inhibits the invasiveness of human lung cancer H1299 cells by disrupting the actin cytoskeleton at the leading edge of the cell 53 .…”

Section: The Cofilin Pathway In Tumour Invasionmentioning

confidence: 99%

“…However, several studies have found that cofilin is downregulated in cancer and that overexpression is antagonistic to invasion. The downregulation of cofilin is observed in MHCC97-H hepatocellular carcinoma (HCC) cells with high meta-static potential 79 , and in ovarian surface epithelium (OSE) cells derived from women with a family history of ovarian and/or breast cancer and mutations in the BRCA1 tumoursuppressor gene 80 . The regulated overexpression of cofilin inhibits the invasiveness of human lung cancer H1299 cells by disrupting the actin cytoskeleton at the leading edge of the cell 53 .…”

Section: The Cofilin Pathway In Tumour Invasionmentioning

confidence: 99%

The cofilin pathway in breast cancer invasion and metastasis

Wang¹,

2007

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Recent evidence indicates that metastatic capacity is an inherent feature of breast tumours and not a rare, late acquired event. This has led to new models of metastasis. The interpretation of expression-profiling data in the context of these new models has identified the cofilin pathway as a major determinant of metastasis. Recent studies indicate that the overall activity of the cofilin pathway, and not that of any single gene within the pathway, determines the invasive and metastatic phenotype of tumour cells. These results predict that inhibitors directed at the output of the cofilin pathway will have therapeutic benefit in combating metastasis.Tumour cell motility is the hallmark of invasion and an essential step in metastasis 1,2 . The identification of molecular pathways that contribute to tumour cell motility and invasion is essential for understanding how motility is initiated in tumour cells and how the tumour microenvironment contributes to cell migration. The identification of the molecular pathways of tumour cell invasion will provide new diagnostic approaches and targets for the treatment of metastatic cancer. Recent studies using new technologies, including highdensity microarray-based expression profiling, intravital imaging and the collection of invasive tumour cells from live tumours, have started to extend the traditional model of metastasis and supply new diagnostic and therapeutic markers of metastatic disease.According to the traditional model of metastasis, metastases result from a process similar to Darwinian evolution whereby natural selection works on individual tumour cells to select © 2007 Nature Publishing Group Correspondence to: J.C. Condeeli@aecom.yu.edu. Competing interests statementThe authors declare no competing financial interests. for stable genetic changes. The cells so selected are very rare, and the metastatic cells that arise from this progressive selection of stable genetic mutations within the primary tumour cause metastasis late in tumour progression 3 . However, studies of mammary tumours in mice [4][5][6][7] , expression profiling of both whole human breast tumours 8,9 and the invasive subpopulation of tumour cells isolated from rat and mouse mammary tumours [10][11][12] suggest that the metastatic ability of breast tumours is encoded throughout the bulk of the primary tumour, involves transient changes in gene expression and is acquired at much earlier stages of tumour progression than postulated by the traditional model. These results suggest that a Darwinian-like evolution is accompanied by, and may contribute to, microenvironmentinduced transient changes in gene expression that support the invasive and metastatic phenotype. These results have led to new models where the microenvironment initiates the expression of genes that induce cell motility, invasion and metastasis 11,13 . In the 'tumour microenvironment invasion model' it is proposed that oncogenic mutations in tumour cells lead to microenvironments that are potentially encoded throughout the b...

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“…Calumenin transcription was down-regulated in metastatic cells compared to primary tumor cells (43). Calumenin was also down-regulated in hepatocellular carcinoma cells with high metastatic potentials compared to similar cells with low metastatic potentials (44). Mass spectrometry analysis revealed that calumenin could be phosphorylated at Ser-44 and Thr-65 (45,46).…”

Section: +mentioning

confidence: 92%