Suppression of tumorigenicity in human ovarian carcinoma cell line SKOV-3 by microcell-mediated transfer of chromosome 11

Cao, Qiag; Abeysinghe, Harindra R; Chow, Ohn A.; Xu, Jinghua; Kaung, Hui Lee; Fong, Chin To; Keng, Peter C.; Insel, Richard A.; Lee, Wyan Ching Mimi; Barrett, J. Carl; Wang, Nancy

doi:10.1016/s0165-4608(01)00442-3

Cited by 25 publications

(21 citation statements)

References 12 publications

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“…This observation, together with complementation studies involving the transfer of chromosome 17 which resulted in reduced tumourigenicity of an EOC cell line (3), suggest that this chromosome harbours tumour suppressor genes (TSGs). Chromosome 17 contains a number of very well characterized TSGs.…”

Section: Introductionmentioning

confidence: 95%

Chromosome 17q25 genes, RHBDF2 and CYGB, in ovarian cancer

et al. 2012

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Abstract. It has been proposed that the frequent loss of heterozygosity (LOH) of an entire chromosome 17 contig in epithelial ovarian cancers (EOC) is the consequence of the inactivation of multiple tumour suppressor genes on this chromosome. We report the characterization of a 453 Kb 17q25 locus shown previously to exhibit a high frequency of LOH in EOC samples. LOH analysis further defined the minimal region of deletion to a 65 Kb interval flanked by D17S2239 and D17S2244, which contains RHBDF2, CYGB and PRCD as tumour suppressor gene candidates. Tissue specific expression excluded PRCD as a candidate. RHBDF2 was expressed at low levels in the majority of benign and low malignant potential (LMP) tumours, and in a subset of malignant ovarian tumour samples, as compared with primary cultures of normal ovarian surface epithelial cell (NOSE) samples. CYGB was expressed at low levels in the majority of LMP and malignant samples compared with benign and NOSE samples. In contrast to CYGB expression, RHBDF2 was expressed at low or undetectable levels in EOC cell lines exhibiting tumourigenic characteristics and up-regulated in a genetically modified EOC cell line rendered non-tumourigenic. DNA sequence analysis identified variants but no apparent deleterious mutations in either gene. Methylation-specific PCR analysis suggested that promoter methylation of CYGB but not RHBDF2 occurred in 6 of 31 malignant samples. The results combined suggest that RHBDF2 and CYGB may play distinctive roles in ovarian cancer and could be added to the growing roster of chromosome 17 genes implicated in this disease.

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Section: Introductionmentioning

confidence: 95%

Chromosome 17q25 genes, RHBDF2 and CYGB, in ovarian cancer

et al. 2012

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“…5). This interval is believed to contain tumor suppressor genes involved in human ovarian tumors [Viel et al, 1992;Cao et al, 2001]. In our samples, most of the losses occurred in the telomeric region of 11p.…”

Section: Detection Of Loh In Ovarian Cancermentioning

confidence: 84%

Allelic loss analysis by denaturing high-performance liquid chromatography and electrospray ionization mass spectrometry

et al. 2007

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Analysis of allelic imbalance is of great importance for understanding tumorigenesis and the clinical management of malignant disease. Fluorescent-based capillary electrophoresis (CE) of highly polymorphic short tandem repeats (STRs) has become the main method used to detect the loss/gain of alleles. However, there is continued interest in the development of techniques that require no fluorescence and allow the rapid analysis of individual samples. One promising alternative is ion-pair reversed-phase high-performance liquid chromatography (IP-RP-HPLC), which is widely available because of its use in denaturing HPLC. Its applicability in combination with ultraviolet (UV) absorbance detection to the efficient separation of di- and tetranucleotide repeats on the short arm of chromosome 11 was tested using 25 matched pairs of normal and ovarian cancer tissues. Loss of heterozygosity (LOH) could be readily identified for all 13 loci tested, based on changes in the ratios between either the alleles or homo- and heteroduplex signals. However, discrimination between noninformative homo- or hemizygous and heterozygous samples was difficult or impossible when HPLC failed to resolve the alleles. Hyphenation of HPLC with electrospray ionization (ESI) quadrupole ion trap (IT) mass spectrometry (MS) not only allowed the identification of coeluting alleles, but also the reliable detection of a 40% reduction of one allele. The size range of DNA fragments amenable to mass spectrometric analysis was effectively tripled to >300 bp by the use of a linear IT and a Taq DNA polymerase cocktail lacking detergents that otherwise adversely affect ESI.

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“…Additionally, Thy-1 appears to function as a tumor suppressor in several malignancies, including nasopharyngeal and ovarian cancer (Lung et al 2005 ). Loss of heterozygosity (LOH) at 11q23.3-q24.3, where THY1 is mapped in humans, is associated with poor prognosis for ovarian cancer (Cao et al 2001 ;Williams and Gagnon 1982 ). Forced Thy-1 expression suppresses tumorigenicity in the ovarian cancer cell line SKOV-3 (Cao et al 2001 ;Abeysinghe et al 2003 ).…”

Section: Thy-1 In Non-neuronal Contextsmentioning

confidence: 99%

“…Loss of heterozygosity (LOH) at 11q23.3-q24.3, where THY1 is mapped in humans, is associated with poor prognosis for ovarian cancer (Cao et al 2001 ;Williams and Gagnon 1982 ). Forced Thy-1 expression suppresses tumorigenicity in the ovarian cancer cell line SKOV-3 (Cao et al 2001 ;Abeysinghe et al 2003 ). In neuroblastoma, Thy-1 expression correlates inversely with patient survival (Fiegel et al 2008 ).…”

Section: Thy-1 In Non-neuronal Contextsmentioning

confidence: 99%

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Thy-1 Modulates Neurological Cell–Cell and Cell–Matrix Interactions Through Multiple Molecular Interactions

Leyton

Hagood

2013

Advances in Neurobiology

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Thy-1, or CD90, is a glycosylphosphatidylinositol-linked cell surface glycoprotein expressed on multiple cell types, including neurons, thymocytes, fi broblasts, endothelial cells, mesangial cells, and some hematopoietic and stromal stem cells. Thy-1 is developmentally regulated and evolutionarily conserved. Its cellular effects vary between and in some cases within cell types, tissues, and species, indicating that its biological role is context dependent. However, it most often seems to affect cell-cell or cell-matrix interactions and cellular adhesion and migration. In the nervous system, Thy-1 mediates bidirectional cell-cell communication, which modulates cell-matrix adhesion. Neurons express high levels of Thy-1, which interacts with α v β 3 integrin present in astrocytes and stimulates increased astrocyte adhesion to the underlying surface ( trans signaling) and in neurites, the same ligand-receptor association triggers neurite retraction and inhibition of axonal growth ( cis signaling). Although Thy-1 lacks a cytoplasmic domain, it affects multiple intracellular signaling cascades through interaction with a number of molecules within lipid raft microdomains. Improved understanding of how this enigmatic adhesion molecule modulates signaling and cell phenotype may yield novel insights into neurodevelopment and nerve recovery after injury.

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Suppression of tumorigenicity in human ovarian carcinoma cell line SKOV-3 by microcell-mediated transfer of chromosome 11

Cited by 25 publications

References 12 publications

Chromosome 17q25 genes, RHBDF2 and CYGB, in ovarian cancer

Chromosome 17q25 genes, RHBDF2 and CYGB, in ovarian cancer

Allelic loss analysis by denaturing high-performance liquid chromatography and electrospray ionization mass spectrometry

Thy-1 Modulates Neurological Cell–Cell and Cell–Matrix Interactions Through Multiple Molecular Interactions

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