Nucleotide sequences and further characterization of human papillomavirus DNA present in the CaSki, SiHa and HeLa cervical carcinoma cell lines.

Meissner, John D.

doi:10.1099/0022-1317-80-7-1725

Cited by 181 publications

(168 citation statements)

References 52 publications

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“…1 ± 3,38 ± 40 HPV 16 and 18 genotypes account for greater than 65% of all HPV DNA-positive invasive cervical carcinomas in multi-institutional studies 1,41 and are found in the majority of human cervical carcinoma-derived cell lines. 42 In this context, the intervention of HPV infection in the carcinogenesis is mainly supported by E6 and E7 oncoproteins which abrogate p53 and pRb functions; the genes of those two factors retain usually a wild-type form. 43 The recent demonstration, that p53 and pRb disruptions are 44 In order to explore new drugs to treat uterine cervix cancer, we decided to study the responses of three different human cervical carcinoma cell lines under staurosporine exposure.…”

Section: Discussionmentioning

confidence: 99%

Staurosporine-induced apoptosis of HPV positive and negative human cervical cancer cells from different points in the cell cycle

et al. 2001

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In the present study, we compare the sensitivity of CaSki and HeLa cells (HPV positive, wild-type p53) and C33A cells (HPV negative, mutated p53) to a protein kinase inhibitor, the staurosporine (ST). We show that ST can reversibly arrest the three cervical-derived cell lines, either in G1 or in G2/M. Beyond certain ST concentrations or/and over 24 h exposure, the cells underwent apoptosis. This process took place in G1 and G2/M for C33A and CaSki plus HeLa cell lines, respectively. By using an in vitro cell-free system, we demonstrated that cytoplasmic extracts from apoptotic cells were sufficient to induce hallmarks of programmed cell death on isolated nuclei. Moreover, we found that only G2/M cytoplasmic extracts from viable CaSki and HeLa cells supplemented with ST, triggered apoptosis while exclusively G1 cytoplasmic fractions from C33A cells were efficient. Our study describes a possible involvement of the HPV infection or/and p53 status in this different ST-induced apoptosis susceptibility. Cell Death and Differentiation (2001) 8, 234 ± 244.

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Section: Discussionmentioning

confidence: 99%

Staurosporine-induced apoptosis of HPV positive and negative human cervical cancer cells from different points in the cell cycle

et al. 2001

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“…Cervical cancer cell lines CaSki, SiHa (HPV-16-positive), HeLa (HPV-18-positive) and C-33A (HPV-negative) and their growth conditions have been described (Meissner, 1999). Three clonal populations of the HPV-16 cervical cell line W12, 20863 (episomal HPV-16), 20861 and 201402 (integrated HPV-16) were obtained from the laboratories of Dr Margaret Stanley and Dr Paul Lambert (Medical Research Council, UK and University of Wisconsin, WA, USA, respectively).…”

Section: Cell Linesmentioning

confidence: 99%

Human papillomavirus type 16 reduces the expression of microRNA-218 in cervical carcinoma cells

et al. 2007

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Human papillomaviruses (HPVs) are involved in the pathogenesis of cancer of the cervix (CaCx). MicroRNA (miRNA) expression analysis using Ambion (Austin, TX, USA) arrays showed that three miRNAs were overexpressed and 24 underexpressed in cervical cell lines containing integrated HPV-16 DNA compared to the normal cervix. Furthermore, nine miRNAs were overexpressed and one underexpressed in integrated HPV-16 cell lines compared to the HPV-negative CaCx cell line C-33A. Based on microarray and/or quantitative realtime PCR and northern blot analyses, microRNA-218 (miR-218) was specifically underexpressed in HPVpositive cell lines, cervical lesions and cancer tissues containing HPV-16 DNA compared to both C-33A and the normal cervix. Expression of the E6 oncogene of highrisk HPV-16, but not that of low-risk HPV-6, reduced miR-218 expression, and conversely, RNA interference of E6/E7 oncogenes in an HPV-16-positive cell line increased miR-218 expression. We also demonstrate that the epithelial cell-specific marker LAMB3 is a target of miR-218. We also show that LAMB3 expression is increased in the presence of the HPV-16 E6 oncogene and this effect is mediated through miR-218. These findings may contribute to a better understanding of the molecular mechanisms involved in cervical carcinogenesis.

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“…Studies of control and eps8 small interfering RNA (siRNA) -expressing cells derived from HeLa (HPV18 DNA-positive; ref. 30) and SiHa (HPV16 DNA-positive; ref. 30) cervical caner cells indicated that Eps8 played a critical role in cell proliferation in culture and tumor formation in mice.…”

Section: Introductionmentioning

confidence: 99%

“…30) and SiHa (HPV16 DNA-positive; ref. 30) cervical caner cells indicated that Eps8 played a critical role in cell proliferation in culture and tumor formation in mice. By virtue of (a) down-regulation of cyclins D1, D3, and E, (b) elevation of p53 and p21 Waf1/Cip1 , and (c) decrease of hyperphosphorylated Rb, diminished Eps8 could effectively arrest cell cycle at G 1 phase.…”

Section: Introductionmentioning

confidence: 99%

Eps8 decreases chemosensitivity and affects survival of cervical cancer patients

Chen

Shen

Chen

et al. 2008

Molecular Cancer Therapeutics

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The oncoprotein Eps8 facilitates proliferation in fibroblasts and colon cancer cells. However, its role in human cervical cancer is unclear. By immunohistochemical staining and Western blotting, aberrant Eps8 expression was observed in cervical carcinoma compared with normal cervical epithelial cells. Clinicopathologic analysis of 45 patients indicated that Eps8 expression was associated with parametrium invasion and lymph node metastasis, two major poor prognostic factors for early-stage cervical cancer. Kaplan-Meier analysis of cervical cancer specimens also indicated an inverse relationship between the level of Eps8 and the patients' survival rate. Using small interfering RNA of eps8, we observed reduced proliferation and tumorigenesis in Eps8-attenuated HeLa and SiHa cells cultured in dishes or inoculated in mice. Furthermore, diminished Eps8 impeded G 1 -phase progression in HeLa and SiHa cells that might be attributable to reduced expression of cyclins D1, D3, and E, elevated accumulation of p53 and its downstream target p21 Waf1/Cip1 , and suppressed hyperphosphorylation of retinoblastoma. Alteration of these cell cycle -related proteins could be reversed by ectopic Eps8, implicating that the effect of Eps8 on the mentioned cell cycle modulators was specific. Notably, the augmented expression of p53 by diminished Eps8 was at least due to its decreased turnover rate. Concurrent with p53 up-regulation and the decrement of Src and AKT activity, Eps8-attenuated HeLa and SiHa cells exhibited increased chemosensitivity to cisplatin and paclitaxel. Together, our findings implicate the involvement of Eps8 in chemoresistance and show its importance in prognosis of cervical cancer patients. [Mol Cancer Ther 2008;7(6):1376 -85]

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Nucleotide sequences and further characterization of human papillomavirus DNA present in the CaSki, SiHa and HeLa cervical carcinoma cell lines.

Cited by 181 publications

References 52 publications

Staurosporine-induced apoptosis of HPV positive and negative human cervical cancer cells from different points in the cell cycle

Staurosporine-induced apoptosis of HPV positive and negative human cervical cancer cells from different points in the cell cycle

Human papillomavirus type 16 reduces the expression of microRNA-218 in cervical carcinoma cells

Eps8 decreases chemosensitivity and affects survival of cervical cancer patients

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