Human Colorectal Cell Lines as a Source for Carcinoembryonic Antigen (Cea)

Leibovitz, Albert; McCombs, William B.

doi:10.1016/b978-0-12-043050-5.50047-0

Cited by 38 publications

(41 citation statements)

References 8 publications

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“…The drug-resistant sublines were grown in the following concentration of MDR-1 substrate: S48-3s ADR10 (10 g/ml adriamycin), S48-3s ACT 0.2 (200 ng/ml actinomycin-D), MCF-7 TX400 (400 ng/ml paclitaxel), MCF-7 AD Int 500 (500 ng/ml adriamycin), ZR-75B TX320 (320 ng/ml paclitaxel), ZR-75B AD600 (600 ng/ml adriamycin), MDA-MB-231 VB100 (100 ng/ml vinblastine), EW36 VCR120 (120 ng/ml vincristine), and 8226 DOX40 (400 nM doxorubicin). The colon cancer cell line, S48-3s, and its drug resistant sublines, S48-3s ADR 10 and S48-3s ACT 0.2 (12,17), were grown in a 1:1 mixture of Iscove's modified Eagle's medium/Ham's F-12 medium supplemented with 10% fetal bovine serum, 2 mM glutamine, 100 units/ml penicillin, and 100 mg/ml streptomycin. All other cell lines were grown in Iscove's modified Eagle's medium supplemented as described above.…”

Section: Methodsmentioning

confidence: 99%

Characterization of Gene Rearrangements Leading to Activation of MDR-1

Huff

Lee

Robey

et al. 2006

Journal of Biological Chemistry

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Expression of the MDR-1/P-glycoprotein gene confers drug resistance both in vitro and in vivo. We previously reported that gene rearrangements resulting in a hybrid MDR-1 transcript represent a common mechanism for acquired activation of MDR-1/P-glycoprotein. We have identified hybrid MDR-1 transcripts in nine MDR-1-overexpressing cell lines and two patients with relapsed ALL. We characterize these rearrangements as follows. 1) Non-MDR-1 sequences in the hybrid MDR-1 transcripts are expressed in unselected cell lines, showing that these sequences are constitutively expressed. 2) The rearrangements occur randomly and involve partner genes (sequences) on chromosome 7 and on chromosomes other than 7. Breakpoints have been characterized in six cell lines. In one, the rearrangement occurred within intron 2 of MDR-1; in the other five, the rearrangement occurred 24 to >96 kb 5 of the normal start of transcription of MDR-1. In one cell line, homologous recombination involving an Alu repeat was observed. However, in the remaining five cell lines, nonhomologous recombination was observed. 3) The rearrangements arise during drug selection. The acquired rearrangements are not detected in parental cells. 4) Five of the six active promoters that captured MDR-1 controlled MDR-1 from a distance of 29 to more than 110 kb 5 to MDR-1. Transcription was initiated in an antegrade or retrograde direction. We conclude that drug selection with natural products targeting DNA or microtubules leads to DNA damage, nonhomologous recombination, and acquired drug resistance, wherein MDR-1 expression is driven by a random but constitutively active promoter.

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Section: Methodsmentioning

confidence: 99%

Characterization of Gene Rearrangements Leading to Activation of MDR-1

Huff

Lee

Robey

et al. 2006

Journal of Biological Chemistry

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“…The SW480 cell line is a colorectal cancer cell line (9) in which the status of APC has previously been reported (2). The FAP colon adenoma (BH, FF, and AA), the sporadic colon adenoma ( (10)(11)(12)(13)(14).…”

Section: Methodsmentioning

confidence: 99%

The APC gene product in normal and tumor cells.

Smith

Johnson

Bryan

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

376

218

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The APC gene has been found to be mutated during the development of sporadic colorectal tumors as well as in the germ line of familial adenomatous polyposis patients. To facilitate the characterization of both normal and mutant APC protein, a series of monoclonal and polyclonal antibodies specific for the APC protein was produced. When lymphoblastoid cell lines derived from seven familial adenomatous polyposis patients with known mutations were analyzed by Western blot, an -300-kDa protein corresponding to the predicted size of full-length APC was detected in all 7 cell lines. In addition, truncated APC proteins corresponding to the product of the known mutated alleles could be detected in 4 of the 7 lines. Similar analysis of 23 colon carcinoma and 9 adenoma cell lines revealed truncated proteins in 24 (75%) of the cell lines. Moreover, 26 (81%) of the colon tumor lines were totally devoid of the normal, full-length protein. In contrast, Western blot analysis of 40 ceDl lines derived from sporadic tumors of other organs detected only full-length APC. Immunohistochemical analysis of APC in normal colonic mucosa revealed cytoplasmic staining with more intense staining in the basolateral margins of the epithelial cell. This staining was markedly increased in the upper portions of the crypts, suggesting an increased level of expression with maturation. These studies provide some initial clues to the function of the cytoplasmic protein APC and demonstrate the feasibility of identifying APC mutations by direct analysis of the APC protein.

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“…To study the effect of 1a,25(OH) 2 D 3 on Id expression and on the angiogenic phenotype, we have used a subline of the human SW480 cell line derived from a Dukes' stage B colon carcinoma (Leibovitz et al, 1976) that expresses 1a,25(OH) 2 D 3 receptor (VDR; SW480-ADH). 1a,25(OH) 2 D 3 treatment induces proliferation arrest and epithelial differentiation in these cells mainly through induction of E-cadherin expression in adherent junctions and inhibition of TCF-4/b-catenin complexes (Palmer et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

1α,25-Dihydroxyvitamin D3 regulates the expression of Id1 and Id2 genes and the angiogenic phenotype of human colon carcinoma cells

et al. 2005

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1a,25-Dihydroxyvitamin D 3 (1a,25(OH) 2 D 3 ) has antitumor activity in addition to its classical action on calcium metabolism and bone tissue biology. It is thought to regulate the expression of multiple target genes and thus modulate processes critical for tumor growth and metastases. Here we show that 1a,25(OH) 2 D 3 differentially regulates the expression of Id1 and Id2 genes, members of a family of transcriptional regulators of cell proliferation and differentiation. 1a,25(OH) 2 D 3 induced epithelial differentiation in SW480-ADH human colon carcinoma cell line by promoting expression of the proteins implicated in adherent junction formation, including E-cadherin, and by inhibiting b-catenin transcriptional activity. 1a,25(OH) 2 D 3 activated the human Id1 gene promoter and rapidly induced Id1 RNA and protein. Ectopic overexpression of Id1 was not sufficient to induce E-cadherin, which was critical for the morphological changes induced by 1a,25(OH) 2 D 3 in SW480-ADH cells. Conversely, Id2 transcription rate, RNA and protein levels were decreased by 1a,25(OH) 2 D 3 . Id2 downregulation by 1a,25(OH) 2 D 3 mediated the antiproliferative effect of 1a,25(OH) 2 D 3 on SW480-ADH cells. In addition, we showed that 1a,25(OH) 2 D 3 changed the levels of the inducer of angiogenesis, vascular endothelial growth factor and the potent antiangiogenic factor thrombospondin-1, leading to a balanced change in the angiogenic potential of SW480-ADH human colon carcinoma cells.

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Human Colorectal Cell Lines as a Source for Carcinoembryonic Antigen (Cea)

Cited by 38 publications

References 8 publications

Characterization of Gene Rearrangements Leading to Activation of MDR-1

Characterization of Gene Rearrangements Leading to Activation of MDR-1

The APC gene product in normal and tumor cells.

1α,25-Dihydroxyvitamin D3 regulates the expression of Id1 and Id2 genes and the angiogenic phenotype of human colon carcinoma cells

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