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. 2003 Jun;129(6):349-54.
doi: 10.1007/s00432-003-0440-z. Epub 2003 May 21.

Analysis of DLC-1 expression in human breast cancer

Marlies Plaumann  1 , Susanne Seitz, Renate Frege, Lope Estevez-Schwarz, Siegfried Scherneck
Affiliations

Analysis of DLC-1 expression in human breast cancer

Marlies Plaumann et al. J Cancer Res Clin Oncol. 2003 Jun.

Abstract

The chromosome region 8p12-p22 shows frequent allelic loss in many neoplasms, including breast cancer (BC). The DLC-1 gene, located on 8p21-p22, might be a candidate tumor suppressor gene in this region. To evaluate the involvement of DLC-1 in breast carcinogenesis we studied DLC-1 mRNA expression in a panel of 14 primary human BC and the corresponding normal breast cells as well as 8 BC cell lines. Low levels or absence of DLC-1 mRNA were observed in 57% of primary BC and 62.5% of BC cell lines, respectively. We could not find any correlation between DLC-1 mRNA expression and deletions at the DLC-1 locus. Transfection of the gene into DLC-1 deficient T-47D cells raised the DLC-1 mRNA level and resulted in inhibition of cell growth and reduced colony-forming capacity. Our results indicate a role of DLC-1 in BC carcinogenesis.

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Figures

Fig. 1.
Fig. 1.
A Representative electropherogram of DLC-1 mRNA expression in breast cancer and normal breast tissues ( upper lane) with expression profile of β-actin mRNA as a semiquantitative analysis standard ( lower lane); N non-tumor tissue, T tumor tissue, M molecular weight markers. B Level of DLC-1 mRNA in beast cancer cell lines and nontumorigenic cell line MCF-10A ( upper lane) with β-actin mRNA as a control ( lower lane); M molecular weight markers
Fig. 2.
Fig. 2.
A Effect of DLC-1 expression on proliferation rate of transfected T-47D cells. The cells were cultured for the indicated numbers of days and cell proliferation was then assessed by WST-1 assay. The average absorbance values obtained from wells without cells served as a blank and were subtracted from all other results. Data points represent the mean of a determination of six wells from a representative experiment that was repeated at least four times. B Colony formation assay of pcDNA3.1-DLC-1 expression vector and pcDNA3.1 expression vector tranfected T-47D cells. The results represent the mean of colony numbers from a representative experiment that was repeated at least twice
Fig. 3.
Fig. 3.
A Summary of expression level and LOH at DLC-1 in various carcinomatous breast tissues. Expression is indicated by the ratio of DLC-1 to β-actin as a semiquantitative analysis control. LOH was determined by LOH analysis and PCR amplification. +indicates the occurrence of LOH, where − indicates the absence of LOH. Markers and their allel status in each of the samples are shown, with dark circles and open circles indicating loss of heterozygosity and retention of heterozygosity, respectively. Homozygosity is shown as hatched circles. B Summary of expression level and deletion at DLC-1 in various breast cancer cell lines. Deletion was determined by HOMOD analysis. Consecutive markers indicating an LOH are underlined. + indicates the occurrence of deletion, where − indicates the absence of deletion. Markers and their allel status in each of the cell line are shown, with dark circles and open circles indicating loss of one allele and retention of both alleles, respectively
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