Caveolin-1 Is Down-Regulated in Human Ovarian Carcinoma and Acts as a Candidate Tumor Suppressor Gene

Wiechen, Kai; Diatchenko, Luda; Agoulnik, Alexander I.; Scharff, K. Michael; Schober, Hagen; Arlt, Katharina; Zhumabayeva, Bakhyt; Siebert, Paul D.; Dietel, Manfred; Schäfer, Reinhold; Sers, Christine

doi:10.1016/s0002-9440(10)63010-6

Cited by 252 publications

(228 citation statements)

References 32 publications

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“…We observed decreased expression of caveolin-1 in OVCA cell lines. This observation confirms data published by others (Racine et al, 1999;Bender et al, 2000;Wiechen et al, 2001) that reported loss of caveolin-1 expression in serous ovarian tumors and that forced expression of the gene in a OCa cell line Progesterone-regulated, anti-tumor genes for ovarian cancer V Syed et al (OVCAR-3) resulted in decreases in cell growth and soft agar colony formation (Wiechen et al, 2001). In concordance, we found ectopic expression of caveolin-1 in OVCA cell lines significantly reduced cell growth, soft agar colony formation, and cell motility, but increased caspase-3 activity.…”

Section: Discussionsupporting

confidence: 92%

Identification of ATF-3, caveolin-1, DLC-1, and NM23-H2 as putative antitumorigenic, progesterone-regulated genes for ovarian cancer cells by gene profiling

et al. 2005

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Section: Discussionsupporting

confidence: 92%

Identification of ATF-3, caveolin-1, DLC-1, and NM23-H2 as putative antitumorigenic, progesterone-regulated genes for ovarian cancer cells by gene profiling

et al. 2005

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“…The serine protease inhibitor maspin suppresses breast cancer progression in vivo and in vitro, 38 -40 yet in estrogen receptor-positive breast cancer, high levels of maspin correlate with shorter survival time. 41 Caveolin-1 acts as a growth suppressor in breast and ovarian cancers, 7,42 but induces proliferation in NSCLCs 10 and in prostate cancer cells. 36 It is remarkable that in lung tumors, the growth-promoting effect of caveolin-1 is restricted to NSCLCs, whereas in small cell lung carcinomas (SCLCs), the protein is down-regulated and has retained its tumor-suppressing properties.…”

Section: Discussionmentioning

confidence: 99%

“…Its re-expression in cell lines derived from these tumors can be achieved via treatment with 5-aza-2Јdeoxycytidine and leads to the inhibition of cell growth and survival. [7][8][9][10] The H-REV107-like genes comprise a novel class II tumor suppressor family. 11,12 Two members of this family, murine H-rev107-1 and human HRASLS, were demonstrated to be suppressed in tumors and tumor cell lines due to promoter methylation, and their re-expression was observed after treatment with 5Ј-aza-deoxycytidine.…”

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confidence: 99%

H-REV107-1 Stimulates Growth in Non-Small Cell Lung Carcinomas via the Activation of Mitogenic Signaling

Nazarenko

Kristiansen

Fonfara

et al. 2006

The American Journal of Pathology

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H-REV107-1 , a known member of the class II tumor suppressor gene family , is involved in the regulation of differentiation and survival. We analyzed H-REV107-1 in non-small cell lung carcinomas , in normal lung , and in immortalized and tumor-derived cell lines. Sixty-eight percent of lung tumors revealed positive H-REV107-1-specific staining. Furthermore , survival analysis demonstrated a significant association of cytoplasmic H-REV107-1 with decreased patient survival. This suggested that H-REV107-1 , known as a tumor suppressor , plays a different role in non-small cell lung carcinomas. Knock-down of H-REV107-1 expression in lung carcinoma cells inhibited anchorage-dependent and anchorage-independent growth whereas overexpression of H-REV107-1 induced tumor cell proliferation. Consistent with results of the survival analysis , cytoplasmic localization of the protein was essential for this growth-inducing function. Analysis of signaling pathways potentially involved in this process demonstrated that overexpression of H-REV107-1 stimulated RAS-GTPase activity , ERK1 ,2 phosphorylation, and caveolin-1 expression in the cell lines analyzed. These results indicate that H-REV107-1 is deficient in its function as a tumor suppressor in nonsmall cell lung carcinomas and is required for proliferation and anchorage-independent growth in cells expressing high levels of the protein, thus contributing to tumor progression in a subset of non-small cell lung carcinomas.

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“…The presence of CpG-rich regions does not immediately implicate them as regulated by methylation in general or specifically in breast epithelial cells since more than 50% of all human genes may have associated CpG clusters (Murphy and Jirtle, 2001). Only three of these genes have been shown to be hypermethylated in human cancer, CAV1, THBS1, and TNFRSF10B (Li et al, 1999;Cui et al, 2001;Wiechen et al, 2001;Oue et al, 2003;van Noesel et al, 2003). Of these, THBS1 and CAV1 methylation have been linked specifically to breast cancer (Engelman et al, 1999;Li et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Analysis of methylation-sensitive transcriptome identifies GADD45a as a frequently methylated gene in breast cancer

et al. 2005

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Treatment of the breast cancer cell line, MDAMB468 with the DNA methylation inhibitor, 5-azacytidine (5-AzaC) results in growth arrest, whereas the growth of the normal breast epithelial line DU99 (telomerase immortalized) is relatively unaffected. Comparing gene expression profiles of these two lines after 5-AzaC treatment, we identified 36 genes that had relatively low basal levels in MDAMB468 cells compared to the DU99 line and were induced in the cancer cell line but not in the normal breast epithelial line. Of these genes, 33 have associated CpG islands greater than 300 bp in length but only three have been previously described as targets for aberrant methylation in human cancer. Northern blotting for five of these genes (a-Catenin, DTR, FYN, GADD45a, and Zyxin) verified the array results. Further analysis of one of these genes, GADD45a, showed that 5-AzaC induced expression in five additional breast cancer cell lines with little or no induction in three additional lines derived from normal breast epithelial cells. The CpG island associated with GADD45a was analysed by bisulfite sequencing, sampling over 100 CpG dinucleotides. We found that four CpG's, located approximately 700 bp upstream of the transcriptional start site are methylated in the majority of breast cancer cell lines and primary tumors but not in DNA from normal breast epithelia or matched lymphocytes from cancer patients. Therefore, this simple method of dynamic transcriptional profiling yielded a series of novel methylation-sensitive genes in breast cancer including the BRCA1 and p53 responsive gene, GADD45a.

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Caveolin-1 Is Down-Regulated in Human Ovarian Carcinoma and Acts as a Candidate Tumor Suppressor Gene

Cited by 252 publications

References 32 publications

Identification of ATF-3, caveolin-1, DLC-1, and NM23-H2 as putative antitumorigenic, progesterone-regulated genes for ovarian cancer cells by gene profiling

Identification of ATF-3, caveolin-1, DLC-1, and NM23-H2 as putative antitumorigenic, progesterone-regulated genes for ovarian cancer cells by gene profiling

H-REV107-1 Stimulates Growth in Non-Small Cell Lung Carcinomas via the Activation of Mitogenic Signaling

Analysis of methylation-sensitive transcriptome identifies GADD45a as a frequently methylated gene in breast cancer

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