Characterization of a cell line (SW756) derived from a human squamous carcinoma of the uterine cervix

Freedman, Ralph S.; Bowen, James M.; Leibovitz, Albert; Pathak, Sen; Siciliano, Michael J.; Gallager, H. Stephen; Giovanella, Beppino C.

doi:10.1007/bf02796428

Cited by 31 publications

(21 citation statements)

References 21 publications

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“…Cell lines Cells of the cervical carcinoma lines HeLa, C4-1 (Auersperg and Hawryluk, 1962) and SW756 (Freedman et al, 1982) were grown in monolayer cultures in Eagle's minimum essential medium containing 10% fetal calf serum. Construction of cDNA libraries and screening Cytoplasmic RNA was prepared from tissue culture cells as described (Freese et al, 1983).…”

Section: Methodsmentioning

confidence: 99%

Different human cervical carcinoma cell lines show similar transcription patterns of human papillomavirus type 18 early genes.

Schneider-Gädicke¹,

Schwarz²

1986

The EMBO Journal

415

306

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Neuenheimer Feld 280, 6900 Heidelberg, FRG Communicated by H.zur Hausen Transcription of human papillomavirus type 18 (HPV18) DNA in the human cervical carcinoma cell lines HeLa, C41 and SW756 was studied by nucleotide sequence analysis of HPV18-positive cDNA clones isolated from a HeLa, C41 and SW756 cDNA library, respectively, and the cDNA sequences were used to predict the potential encoded proteins. The cDNA clones from all three cell lines were found to be derived from virus-cell fusion transcripts in which 3'-terminal host cell sequences (different for each cell line) were spliced to 5'-tenminal exon sequences from the HPV18 E6-E7-E1 region.Three different types of cDNA clones can be distinguished according to the splicing patterns observed in the 5' tenminal HPV18 sequences. They carry as potential protein-coding regions the HPV18 specific open reading frames E6 and E6* (generated by splicing and identical with E6 up to the E6* splice junction), E7 and El (only in HeLa). Translation of specific cellular genes from the chimeric viral-cellular transcripts seems to be unlikely. The mapping of the 5'-ends of the virus-cell fusion transcripts indicates that transcription is initiated at a viral promoter. The similar patterns of HPV18 transcription in the three different cervical carcinoma cell lines suggest a functional role of HPV18 early genes for the malignant phenotype of these cells.

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Section: Methodsmentioning

confidence: 99%

Different human cervical carcinoma cell lines show similar transcription patterns of human papillomavirus type 18 early genes.

Schneider-Gädicke¹,

Schwarz²

1986

The EMBO Journal

415

306

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“…Derivation of the HPV-immortalized and ras-transformed cell lines (Woodworth et al, 1988;DiPaolo et al, 1989) and cervical carcinoma-derived cell lines C-4I, C-4II, CaSki, C-33A, HeLa, HT-3, SiHa (all from the American Type Culture Collection), QGH and QGU (Shirasawa et al, 1987) and SW756 (Freedman et al, 1982) have been described previously. Normal ectocervical cells and the cell line CX16-2 were grown in serum-free MCDB153-LB medium (Pirisi et al, 1987).…”

Section: Cell Culturementioning

confidence: 99%

Altered expression of Erg and Ets-2 transcription factors is associated with genetic changes at 21q22.2-22.3 in immortal and cervical carcinoma cell lines

1997

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Human Papillomavirus (HPV) type 16 is the most frequently detected HPV in cervical cancer. Although epidemiologic and experimental evidence indicates a prominent role for HPV infection in the development of this disease, other factors are also involved. Altered expression of the ets family transcription factors erg and ets-2 was found associated with the development of cervical carcinoma. Overexpression also occurred in a HPV-16-immortalized cervical cell line, CX16-2, which has HPV integrated at a translocation breakpoint t(19;21) involving 21q22.2-22.3, where these genes have been mapped. Six of 10 cervical carcinoma cell lines overexpressed ets-2 RNA suggesting an association of overexpression with cervical cell neoplasia. A clonally related pair of cervical carcinoma cell lines, C-4I and C-4II, showed di erential expression of erg and ets-2. C-4I overexpressed ets-2 RNA compared to normal cervical cells and C-4II. C-4II expressed a 5.3 kb erg transcript not seen in C-4I, ectocervical cells or other cervical carcinoma cell lines examined. Pulsed ®eld gel electrophoresis was used to analyse changes in DNA fragments related to structural changes and to construct a physical map encompassing erg and ets-2. Alterations in erg and ets-2 RNA expression in each of three di erent cell lines examined were associated with translocations. Association between altered expression of erg and ets-2 and altered regional structural suggests that these genes are important targets in cervical carcinogenesis.

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“…The cell lines used were C4-1 and C4-2 (26), which were derived from the same biopsy specimen of a squamous cell carcinoma and are therefore of identical clonal origin (27), HeLa, which was derived from an adenocarcinoma of the cervix (28,29), and SW 756, more recently established from a squamous cell carcinoma (30). We found that depending on the origin of the cell line and the chromosomal integration site of the viral DNA, dexamethasone treatment modified the transcription rate of HPV genes differently.…”

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confidence: 99%

Influence of chromosomal integration on glucocorticoid-regulated transcription of growth-stimulating papillomavirus genes E6 and E7 in cervical carcinoma cells.

Doeberitz

Bauknecht

Bartsch

et al. 1991

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

118

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In most cervical carcinoma cells the E6 and E7 genes of specific human papillomaviruses are transcribed from viral sequences integrated into host cell chromosomes. Glucocorticoids activate the promoter elements of various human papillomaviruses in transient-expression assays. We have analyzed the effect of dexamethasone on the transcription rate of human papillomavirus 18 E6 and E7 genes integrated at different chromosomal sites in four cervical cancer cell lines. Dexamethasone led to an increase in the transcription rate of the integrated E6-E7 sequences in C4-1 and C4-2 cells but led to a decrease in SW 756 cells and did not affect the transcription rate in HeLa cells. However, when the viral promoter elements derived from HeLa or SW 756 cells, in which dexamethasone does not activate transcription of the integrated E6-E7 sequences, were tested in transient-expression assays within the same cell lines, dexamethasone consistently activated the viral promoter. It thus appears that dominant regulatory mechanisms presumably depending on the chromosomal integration site are able to override the response of the viral promoter to steroid hormones. The growth rate of all dexamethasonetreated cell lines correlated consistently with the expression of the papillomavirus E6 and E7 genes, supporting their role in the maintenance of the proliferative phenotype of cervical carcinoma cells. Since human papillomaviruses are integrated into the host cell genome at variable, presumably randomly selected chromosomal loci, regulatory mechanisms that influence viral gene expression, and hence cell growth, may differ among cancers of independent clonal origin.

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Characterization of a cell line (SW756) derived from a human squamous carcinoma of the uterine cervix

Cited by 31 publications

References 21 publications

Different human cervical carcinoma cell lines show similar transcription patterns of human papillomavirus type 18 early genes.

Different human cervical carcinoma cell lines show similar transcription patterns of human papillomavirus type 18 early genes.

Altered expression of Erg and Ets-2 transcription factors is associated with genetic changes at 21q22.2-22.3 in immortal and cervical carcinoma cell lines

Influence of chromosomal integration on glucocorticoid-regulated transcription of growth-stimulating papillomavirus genes E6 and E7 in cervical carcinoma cells.

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