Vlasta Sovová

Czech Academy of Sciences, Institute of Molecular Genetics

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EŠ

Eva Šloncová

Czech Academy of Sciences

Zdena Tuháčková

Czech Academy of Sciences

Dana Kučerová

Czech Academy of Sciences, Institute of Molecular Genetics

Martina Vojtěchová

Czech Academy of Sciences, Institute of Molecular Genetics

H Cerná

University of Chemistry and Technology, Prague

JŠ

Jitka Štokrová

Czech Academy of Sciences

Jan Hlaváček

Czech Academy of Sciences, Institute of Organic Chemistry and Biochemistry

I Hlozánek

Institute of Clinical and Experimental Medicine

T G Todorov

bioMérieux (United States)

P Frič

Charles University

Cooperative Institutions

Czech Academy of Sciences, Institute of Molecular Genetics

Czech Academy of Sciences

Charles University

Czech Academy of Sciences, Institute of Organic Chemistry and Biochemistry

Institute of Molecular Genetics

Czech Academy of Sciences, Institute of Experimental Medicine

Bulgarian Academy of Sciences

Institute of Haematology and Blood Transfusion

Czech Academy of Sciences, Institute of Physiology

Institute of Molecular Biology

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c‐myc Gene activation as a permanent trait of RSV‐infected quail cells

International Journal of Cancer (1993)

Vlasta Sovová Helena Fidlerová I Hlozánek Robert R. Friis

A high level of c-myc gene expression was found to be a constant feature of v-src transformation. The c-myc gene product was analyzed in quail embryo cells transformed by different mutants of Rous sarcoma virus (RSV) that were temperature-sensitive with respect to various parameters of v-src function. The high-level expression of c-myc proved not to be temperature-sensitive: at both permissive (35 degrees C) and non-permissive (41 degrees C) temperatures, the same high levels of c-myc gene product were found for all RSV mutants tested. This result, in agreement with earlier evidence for a v-src-induced proliferative stimulus which was unaffected by ts mutants at the non-permissive temperature, shows that certain v-src functions have not yet been fully characterized.

Rous sarcoma virus

Permissive

10.1002/ijc.2910530621

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Citations (10)

Response of HT29 cells to butyrate depends on time of exposure and glucose deprivation

International Journal of Molecular Medicine (2002)

Dana Kučerová Jitka Štokrová Jan Korb Eva Šloncová Zdena Tuháčková

The high level of alkaline phosphatase activity in HT29 cells induced after 2 or 5 days of butyrate treatment was decreased during their prolonged exposure (about 30 days) to this agent together with a decrease of sensitivity to apoptosis. However, an enormous additive effect on alkaline phosphatase activity was found after butyrate treatment of glucose-starved cells. In concert with this finding, the substructural analysis revealed a dense brush border, tendency to polarization and morphologically normal mitochondria. It can be concluded that prolonged butyrate treatment of HT29 cells attenuated their response to this agent. On the other hand, glucose deprivation, as another inductor of differentiation, was found to increase the sensitivity of HT29 cells to butyrate.

10.3892/ijmm.10.6.779

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Citations (8)

Angiotensin II receptors on colorectal carcinoma cells.

International Journal of Molecular Medicine (1998)

Dana Kučerová Blanka Železná Eva Šloncová Vlasta Sovová

The presence of angiotensin II receptors was found on cells of three colorectal carcinoma cell lines. The binding assays with 125I-labelled angiotensin II and ligands specific for angiotensin AT1 or AT2 receptors showed that angiotensin receptors on colorectal cancer cells are mostly of the AT2 type. The binding capacity of tumor cells was not significantly changed by butyrate-induced differentiation.

10.3892/ijmm.2.5.593

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Citations (13)

Initiation factor eIF2B not p70 S6 kinase is involved in the activation of the PI‐3K signalling pathway induced by the v‐src oncogene

FEBS Letters (2003)

Martina Vojtěchová Eva Šloncová Dana Kučerová J. Jiřička Vlasta Sovová

Our data show that in hamster fibroblasts transformed by Rous sarcoma virus (RSV), the phosphoinositide 3′‐kinase (PI‐3K)/Akt/glycogen synthase kinase 3 antiapoptotic pathway is upregulated and involved in increased protein synthesis through activation of initiation factor eIF2B. Upon inhibition of PI‐3K by wortmannin, phosphorylation of 70‐kDa ribosomal protein S6 kinase (p70 S6k) and its physiological substrate, ribosomal protein S6, decreased in the non‐transformed cells but not in RSV‐transformed cells. Thus PI‐3K, which is thought to be involved in regulation of p70 S6k, signals to p70 S6k in normal fibroblasts, but it does not appear to be an upstream effector of p70 S6k in fibroblasts transformed by v‐ src oncogene, suggesting that changes in the PI‐3K signalling pathway upstream of p70 S6k are induced by RSV transformation.

Ribosomal s6 kinase

Wortmannin

10.1016/s0014-5793(03)00415-0

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Expression and interaction of different catenins in colorectal carcinoma cells

International Journal of Molecular Medicine (2001)

Dana Kučerová Eva Šloncová Zdena Tuháčková Martina Vojtěchová Vlasta Sovová

Aberrant signalling activities of beta-catenin, originally identified as a component of cell-adhesion complexes, are now considered to be an important factor in colorectal carcinogenesis. However, recently it was shown that also gamma- as well as p120 catenins have a dual role either in cell adhesion or in affecting some gene activation. Therefore, the levels and interactions of these three catenins in human colorectal carcinoma cell lines were analysed. A great heterogeneity in the expression of all catenins tested was found in colorectal carcinoma cell lines HT29 and LS174T. Detailed analysis of beta-catenin interactions was done. GST-APC fragment-fused proteins were used to absorb beta-catenin and its complexes from cell lysates. Similarly, the E-cadherin binding capacity of the residual pool of beta-catenin was analysed using the GST-ECT construct. It was found that the level of beta-catenin does not necessarily depend either on the APC or beta-catenin gene mutations and that co-precipitation of beta-, gamma-, and p120 catenins is not limited to cells that express E-cadherin.

10.3892/ijmm.8.6.695

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Citations (4)

Comparison of methods used for detection of mycoplasma contamination in cell cultures, sera, and live-virus vaccines.

PubMed (1993)

T. Benisheva Vlasta Sovová I Ivanov G Opalchenova

Two methods for detection of mycoplasma contamination in cell cultures, sera, and live-virus vaccines were compared: the direct culture test and the DNA staining method employing bisBenzimide (Hoechst No. 33258). Contamination by different species of mycoplasma was found in 39% samples tested. It is recommended to use both techniques for a reliable detection of mycoplasma contamination.

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Changes in c-src activity in a human colon cancer cell line during differentiation

Oncology Reports (1997)

Vlasta Sovová Dana Kučerová Marketa Liskova Eva Šloncová Zdena Tuháčková

Sodium butyrate

10.3892/or.4.2.451

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Citations (2)

Rous sarcomas induced by heterotransplantation of virogenic rat tumour cells in mice

International Journal of Cancer (1972)

J Bubeník Magdalena Barešová Burkhard Micheel Vlasta Sovová Rashika El Ridi

Abstract The virogenic sarcoma RSL was induced in inbred Lewis rats by the Schmidt‐Ruppin variant of Rous virus (SR‐RSV). Heterotransplantation of RSL cells to newborn C57BL/10Sn mice gave rise to mouse sarcomas in approximately 10% of the recipients. The properties of one of these mouse sarcomas, designated as RSM, were compared with those of the original rat tumour line RSL. It was found that (1) RSL cells did not contain detectable amounts of infectious chicken, rat or mouse sarcoma virus. However, in contact with permissive chicken fibroblasts the RSL cells produced malignant conversion of avian cells accompanied by the formation of infectious RSV. RSL cells carried a tumour‐associated transplantation antigen (TATA) of Rous sarcomas, a group‐specific (gs) antigen of avian leukoviruses and a membrane antigen (MA), characteristic of Rous sarcomas, detectable by indirect immunofluorescence and cross‐reacting with MA of mouse Rous sarcomas. The MA characteristic of tumours induced by mouse leukoviruses was not detected in the membrane of RSL cells. (2) RSM cells did not contain detectable amounts of oncogenic avian, mouse or rat viruses in an infectious form. Neither contact of these cells with permissive chicken c/o fibroblasts nor heterotransplantation of RSM tumours to chickens led to malignant conversion of avian cells. Gs antigen of avian leukoviruses was not detectable in RSM cells. However, TATA and MA characteristic of Rous sarcomas were present. Neither MA nor TATA induced by mouse leukoviruses was detected in RSM cells. The results obtained indicate that the non‐infectious RSV genome present in rat virogenic cells is able to induce tumours in a further mammalian species.

Rous sarcoma virus

10.1002/ijc.2910100311

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Citations (11)

The v-Src and c-Src tyrosine kinases immunoprecipitated from Rous sarcoma virus-transformed cells display different specificities to three commonly used peptide substrates

Martina Vojtěchová Zdena Tuháčková Jan Hlaváček Jiřı́ Velek Vlasta Sovová

Rous sarcoma virus

Immunoprecipitation

10.1135/css200306119

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Citations (0)

Presence of group-specific antigen of avian sarcoma leukosis complex in subcellular fractions of tumours induced by Schmidt-Ruppin strain of Rous sarcoma virus.