Transformation of Human Breast Epithelial Cells by c‐Ha‐<i>ras</i> Oncogene

Basolo, Fulvio; Elliott, James; Tait, Larry; Chen, Xiao Qin; Maloney, Terry; Russo, Irma H.; Pauley, Robert J.; Momiki, Shigeru; Caamaño, Jorge; Klein‐Szanto, Andres J.; Koszalka, Maria; Russo, José

doi:10.1002/mc.2940040106

Cited by 146 publications

(119 citation statements)

References 50 publications

Supporting

Mentioning

111

Contrasting

Order By: Relevance

“…The MCF10AT cell line has been derived from the spontaneously immortalized human normal breast epithelial cell line MCF10A cells by stable transfection with mutant T24-H-ras . These are pre-malignant but nontumorigenic cells (Basolo et al, 1991;Miller et al, 1993). In our preliminary experiments, we found that the endogenous APC protein level in MCF10A cells was much lower than in MCF10AT cells (data not shown).…”

Section: Silencing Of Apc Increases Lp-ber In the Pre-malignant Breasmentioning

confidence: 81%

Cigarette smoke condensate-induced level of adenomatous polyposis coli blocks long-patch base excision repair in breast epithelial cells

et al. 2006

View full text Add to dashboard Cite

Our previous studies have shown that treatment with cigarette smoke condensate (CSC) transforms normal breast epithelial cell line, MCF-10A. In the present study, the mechanism of CSC-induced transformation of breast epithelial cells was examined. We first determined whether benzo[a]pyrene (B[a]P)-and CSC-induced levels of APC are capable of inhibiting long-patch base excision repair (LP-BER) since our earlier studies had shown that an interaction of APC with DNA polymerase b (pol-b) blocks strand-displacement synthesis. With the use of a novel in vivo LP-BER assay, it was demonstrated that increased and decreased APC levels in different breast cancer cell lines were associated with a decrease or increase in LP-BER activity, respectively. The effect of APC on LP-BER in malignant and pre-malignant breast epithelial cell lines was produced by either overexpression or knockdown of APC. Furthermore, it was shown that the decreased LP-BER in B[a]P-or CSC-treated premalignant breast epithelial cells is associated with an increased level of APC and decreased cell growth. Our results suggest that the decreased growth allows cells to repair the damaged DNA before mitosis, and failure to repair damaged DNA has the potential to transform premalignant breast epithelial cells.

show abstract

Section: Silencing Of Apc Increases Lp-ber In the Pre-malignant Breasmentioning

confidence: 81%

Cigarette smoke condensate-induced level of adenomatous polyposis coli blocks long-patch base excision repair in breast epithelial cells

et al. 2006

View full text Add to dashboard Cite

show abstract

“…7 Transformation of MCF-10A cells with an activated H-Ras oncogene resulted in premalignant MCF-10AT/MCF-10ANeoT cells (termed NeoT in the figures) 16 that never form tumors, but do form preneoplastic lesions in immunodeficient mice. 8,17 Subsequent serial xenografting in mice created MCF-10CA1a cells (termed CA1a in the figures).…”

Section: Resultsmentioning

confidence: 99%

Translational control of TWIST1 expression in MCF-10A cell lines recapitulating breast cancer progression

Vislovukh

Meng

et al. 2012

Oncogene

View full text Add to dashboard Cite

TWIST1 is a highly conserved basic helix-loop-helix transcription factor that promotes epithelial --mesenchymal transition (EMT). Its misregulation has been observed in various types of tumors. Using the MCF-10A-series of cell lines that recapitulate the early stages of breast cancer formation and EMT, we found TWIST1 to be upregulated during EMT and downregulated early in carcinogenesis. The TWIST1 3 0 UTR contains putative regulatory elements, including miRNA target sites and two cytoplasmic polyadenylation elements (CPE). We found that miR-580, CPEB1, and CPEB2 act as negative regulators of TWIST1 expression in a sequence-specific and additive/cooperative manner.

show abstract

“…The MCF10A cell line was one of a pair of lines that spontaneously immortalized during the long-term culture of human breast epithelium [67]. MCF10A does not exhibit tumorigenicity in immunocompromised mice, but a tumorigenic derivative, MCF10AT, was obtained by transfection of MCF10A with the HRAS T24-oncogene [68], and more aggressive sublines of MCF10AT were produced by cycling through murine hosts [69]. One of these, MCF10CA1a, is also metastatic, and thus the series includes related cell lines with benign, premalignant and metastatic phenotypes [70].…”

Section: Proteomic Profiling Of Models Of Metastasismentioning

confidence: 99%

Breast tumor metastasis: analysis via proteomic profiling

Goodison¹,

Urquidi²

2008

Expert Review of Proteomics

View full text Add to dashboard Cite

The ability to predict the metastatic behavior of a patient's cancer, as well as to detect and eradicate such recurrences, remain major clinical challenges in oncology. While many potential molecular biomarkers have been identified and tested previously, none have greatly improved the accuracy of specimen evaluation over routine histopathological criteria and, to date, they predict individual outcomes poorly. The ongoing development of high-throughput proteomic profiling technologies is opening new avenues for the investigation of cancer and, through application in tissue-based studies and animal models, will facilitate the identification of molecular signatures that are associated with breast tumor cell phenotype. The appropriate use of these approaches has the potential to provide efficient biomarkers, and to improve our knowledge of tumor biology. This, in turn, will enable the development of targeted therapeutics aimed at ameliorating the lethal dissemination of breast cancer. In this review, we focus on the accumulating proteomic signatures of breast tumor progression, particularly those that correlate with the occurrence of distant metastases, and discuss some of the expected future developments in the field.

show abstract

Transformation of Human Breast Epithelial Cells by c‐Ha‐ras Oncogene

Cited by 146 publications

References 50 publications

Cigarette smoke condensate-induced level of adenomatous polyposis coli blocks long-patch base excision repair in breast epithelial cells

Cigarette smoke condensate-induced level of adenomatous polyposis coli blocks long-patch base excision repair in breast epithelial cells

Translational control of TWIST1 expression in MCF-10A cell lines recapitulating breast cancer progression

Breast tumor metastasis: analysis via proteomic profiling

Contact Info

Product

Resources

About