Corpus ID: 18223202

Signaling in Ovarian Cancer β Factor-That Contribute to the Inhibition of Transforming Growth Expression Profiling Identifies Altered Expression of Genes

  title={Signaling in Ovarian Cancer $\beta$ Factor-That Contribute to the Inhibition of Transforming Growth Expression Profiling Identifies Altered Expression of Genes},
  author={Jan Sunde and H. Donninger and Kongming Wu and Michael E. Johnson and R. Pestell and G. Rose and S. Mok and J. Brady and T. Bonome and M. Birrer},
Ovarian cancer is resistant to the antiproliferative effects of transforming growth factor-B (TGF-B); however, the mechanism of this resistance remains unclear. We used oligonucleotide arrays to profile 37 undissected, 68 microdissected advanced-stage, and 14 microdissected early-stage papillary serous cancers to identify signaling pathways involved in ovarian cancer. A total of seven genes involved in TGF-B signaling were identified that had altered expression >1.5-fold (P < 0.001) in the… Expand

Figures and Tables from this paper

Epithelial-mesenchymal transition in ovarian cancer.
Understanding of the molecular changes associated with ovarian cancer metastasis could lead to the identification of targets for novel therapeutic interventions and Alterations in these cellular pathways candidate them as useful target for ovarian cancer treatment. Expand
Overexpression of SnoN/SkiL, amplified at the 3q26.2 locus, in ovarian cancers: A role in ovarian pathogenesis
Results implicate SnoN levels in multiple roles during ovarian carcinogenesis: promoting cellular proliferation in ovarian cancer cells and as a positive mediator of cell cycle arrest and senescence in non‐transformed ovarian epithelial cells. Expand
A link between mir-100 and FRAP1/mTOR in clear cell ovarian cancer.
Strong candidate miRNAs and their target genes that may contribute to the pathogenesis of clear cell ovarian cancer are revealed, thereby highlighting alternative therapeutic strategies for the treatment of this deadly cancer. Expand
Inhibition of DACH1 activity by short hairpin RNA represses cell proliferation and tumor invasion in pancreatic cancer.
This study suggested that DACH1 expression regulates the pancreatic cancer cell apoptosis through interacting with Bcl-2 signaling axis, whereas it controls cell migration and invasion via epithelial-mesenchymal transition (EMT) process. Expand
Ovarian cancer: insights into genetics and pathogeny.
Ov ovarian carcinogenesis remains a research challenge, due to still numerous unknown factors involved in the malignant transformation sequences, originating from the genetic-molecular alterations and reflected by cellular and tissue expression patterns. Expand
DACH1 Expresison in Osteosarcoma and Its Relationship with Proliferation and Angiogenesis
The aim of this study was to investigate the expression of DACH1 in osteosarcoma as well as its relationship with cell proliferation and angiogenesis in the tumor. DACH1 expression was detected byExpand
Redundant roles of PRDM family members in zebrafish craniofacial development
The data reveal that prDM3, 5, and 16 are involved in the zebrafish craniofacial development and that prdm1a may interact with prdm3,5, and16 in the formation of the cranio-facial skeleton in zebra fish. Expand


Loss of c-myc repression coincides with ovarian cancer resistance to transforming growth factor beta growth arrest independent of transforming growth factor beta/Smad signaling.
Surprising, TGF-beta-induced Ski degradation was not observed in HOSE or CSOC, suggesting that Ski may not function as a T GF-beta/Smad corepressor in ovarian epithelial cells, and suggested that an alternate signaling pathway other than TGF, beta, or Smad may transmit TGF's cell cycle arrest in the ovarian epithelium. Expand
Ovarian carcinoma cell cultures are resistant to TGF-beta1-mediated growth inhibition despite expression of functional receptors.
The results indicate that TGF-beta1 resistance and higher levels of MMP-2 production may be inherent properties of the ovarian cancer phenotype, and the mechanism of growth resistance is downstream of TbetaR-I phosphorylation. Expand
TGFβ-Induced Smad Signaling Remains Intact in Primary Human Ovarian Cancer Cells.
Although OC1, CaOV3, and SkOV3 are not growth inhibited by TGFβ1, they can transmit the TGFα1 signal to turn on a transfected TGF β/Smad reporter gene, p3TP, and all cells up-regulate the endogenous T GFβ target genes Smad7 and PAI-1. Expand
Inhibition of the antiproliferative effect of TGFβ by EGF in primary human ovarian cancer cells
EGF decreases TGFβ-induced mRNA expression of the cell cycle regulator, p15INK4B, contributing to decreased sensitivity of OC cells to the antiproliferative effect of TGF β. Expand
Analysis of specific gene mutations in the transforming growth factor-beta signal transduction pathway in human ovarian cancer.
The findings suggest that mutations in the TGF-beta RI and in its signal transduction pathway are likely responsible for human ovarian carcinogenesis. Expand
Whole genome expression profiling of advance stage papillary serous ovarian cancer reveals activated pathways
The data generated in this study represent a comprehensive list of genes aberrantly expressed in serous papillary ovarian adenocarcinoma and may be useful for the identification of potentially new and novel markers and therapeutic targets for ovarian cancer. Expand
TGF-beta signaling is disrupted in endometrioid-type endometrial carcinomas.
It is suggested that disturbances of the TGF beta RII and SMAD4 expression as well as localization of SMADs may be important to the infiltration of the myometrial wall by the type I endometrial carcinomas. Expand
Bone morphogenic proteins are overexpressed in malignant melanoma and promote cell invasion and migration.
A strong reduction of migratory and invasive properties was observed in these cells, suggesting that BMP4 promotes melanoma cell invasion and migration and therefore has an important role in the progression of malignant melanoma. Expand
Genetic alterations of the transforming growth factor beta receptor genes in pancreatic and biliary adenocarcinomas.
The results indicate that the TGF-beta type I and type II receptor genes are selective targets of genetic inactivation in pancreatic and biliary cancers. Expand
Transforming growth factor-beta receptor type I gene is frequently mutated in ovarian carcinomas.
It is shown that 33% of primary OCs harbor somatic changes in exons 2, 3, 4, and 6 of the TGF-beta receptor I (TbetaR-I) gene, suggesting that resistance to T GF-beta-mediated growth inhibition may frequently involve alterations of the R-I gene. Expand