Karyotypic analysis of two related cervical carcinoma cell lines that contain human papillomavirus type 18 DNA and express divergent differentiation

Differential Activation of Smads in HeLa and SiHa Cells That Differ in Their Response to Transforming Growth Factor-β

“…In agreement with our results, TGF-␤ has been shown to induce the expression of the plasminogen activator inhibitor gene in SiHa and HeLa cells (17). However, in another study, SiHa cells were reported to be resistant to TGF-␤ because of a mutation in Smad 4 (19 (30,31).…”

Amplification of chromosome 5p correlates with increased expression of Skp2 in HPV-immortalized keratinocytes

“…More recent CGH studies have revealed a high level copy increase of 5p to be a recurrent event during progression of advanced stage CaCx (Heselmeyer et al, 1997;Kirchhoff et al, 1999;Ried et al, 1999;Matthews et al, 2000). Similar markers have been observed in HPV-transformed cell lines (Miller et al, 1971;Durst et al, 1987;Popescu et al, 1987;James et al, 1989;Smith et al, 1989;Macville et al, 1999). Gain of 5p, however, is not observed in low-grade lesions or HR HPV containing keratinocyte cell lines at early passage in vitro (Cottage et al, 2001).…”

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

“…In cell lines of independent clonal origin, transcription of integrated HPV 18 E6-E7 genes was differently influenced by dexamethasone. In C4-1 and C4-2 cells, which were both derived from the same original tumor cell clone (27) and contain only one copy of the HPV 18 genome integrated on chromosome 8 (2), glucocorticoid treatment led to enhanced transcription of integrated viral genes leading to increases in E6-E7 mRNA that were associated with accelerated cell growth. HeLa cells contain 10-50 copies of the viral sequences, integrated preferentially on chromosome 8 at a different site than in C4-1 cells (2, 42) and additionally on chromosomes 5, 9, and 22 (43).…”

“…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.…”