The mts1 gene and control of tumor metastasis

Grigorian, Mariam; Tulchinsky, E.; Zain, Sayeeda; Ebralidze, Alexander K.; Крамеров, Д. А.; Kriajevska, Marina; Georgiev, G.P.; Lukanidin, E. M.

doi:10.1016/0378-1119(93)90070-j

Cited by 86 publications

(56 citation statements)

References 20 publications

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“…Thus, in both inducible and constitutive systems, the expression of the antisense S100A4 RNA resulted in the inhibition of the metastatic capability of A11 cells. Grigorian et al (1993) also observed a reduction in metastasis by transfecting CSML100 cells with an antisense S100A4 construct. Therefore, S100A4 probably plays a critical role in the acquisition of the metastatic phenotype of LLC cells and some other tumor cells as well.…”

Section: Discussionmentioning

confidence: 78%

“…Enforced expression of the S100A4 protein in tumor cells results in enhancement of motility (Takenaga et al, 1994a;Ford and Zain, 1995). S100A4 is also expressed in normal cells and tissues which exhibit highly motile ability (JacksonGrusby et al, 1987;Ebralidze et al, 1989;Ford and Zain, 1995;Grigorian et al, 1993;Takenaga et al, 1994b). Furthermore, the expression of S100A4 was induced during the di erentiation of promyelocytic leukemia HL60 cells, coinciding with the expression of motile phenotype (Takenaga et al, 1994c).…”

Section: Discussionmentioning

confidence: 99%

“…These results strongly implicate S100A4 in cytoskeletal dynamics and/or cell motility. Supporting this, embryonic trophoblast cells, lymphoid cells and macrophages, all of which are highly motile, are found to express a relatively high amount of S100A4 (Jackson-Grusby et al, 1987;Ford and Zain, 1995;Ebralidze et al, 1989;Grigorian et al, 1993;Takenaga et al, 1994b,c). Furthermore, we and others have recently demonstrated the enhanced cell motility in S100A4 cDNA-transfected tumor cells (Takenaga et al, 1994a;Ford et al, 1995).…”

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confidence: 88%

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Expression of antisense RNA to S100A4 gene encoding an S100-related calcium-binding protein suppresses metastatic potential of high-metastatic Lewis lung carcinoma cells

1997

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S100A4 (also known as pEL98/mts1/p9Ka/18A2/42A/ calvasculin/FSP1/CAPL), a member of S100-related calcium-binding proteins, has been implicated to play a role in metastasis. In the present study, we examined the e ect of antisense S100A4 RNA on metastatic potential of Lewis lung carcinoma (LLC) cells. High-metastatic A11 cells were transfected with the expression vector containing S100A4 cDNA in an inverted (antisense) orientation under the transcriptional control of the mouse metallothionein promoter. Treatment of a stably transfected clone (AS10 cells) with Zn 2+ resulted in the suppression of the experimental metastatic ability, which was accompanied with the expression of antisense S100A4 RNA and the suppression of the S100A4 expression at both the mRNA and the protein levels. To further con®rm the e ect of antisense S100A4 RNA, we established several clones after retroviral transduction with an antisense S100A4 construct. Notably, reduced metastatic potential was also evident in these clones. In the antisense S100A4 RNA-expressing cells, cell motility and in vitro invasiveness were found to be suppressed.

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Section: Discussionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 88%

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Expression of antisense RNA to S100A4 gene encoding an S100-related calcium-binding protein suppresses metastatic potential of high-metastatic Lewis lung carcinoma cells

1997

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“…We and others have shown that the increased expression of S100A4 in tumour cells by introduction of the S100A4 gene resulted in an enhancement of cell motility and invasive and metastatic potential of tumour cells (Davies et al, 1993;Parker et al, 1994;Takenaga et al, 1994a). On the other hand, reduction of the expression of S100A4 by means of antisense S100A4 RNA or anti-S100A4 ribozyme in high-metastatic tumour cells resulted in the suppression of their invasive and metastatic capabilities (Grigorian et al, 1993;MaeLandsmo et al, 1996;Takenaga et al, 1997a). Although the precise functions of the S100A4 protein are not fully understood, recent studies implicate that the protein interacts with cytoskeletal proteins such as non-muscle tropomyosins (Takenaga et al, 1994c(Takenaga et al, , 1994d and myosin (Kriajevska et al, 1994; in a Ca 2+ -dependent manner and thereby modulates cell motility (Takenaga et al, 1994a(Takenaga et al, , 1994d.…”

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confidence: 95%

Suppression of metastasis-associated S100A4 gene expression by gamma-interferon in human colon adenocarcinoma cells

Takenaga

1999

Br J Cancer

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Summary S100A4 belongs to the S100 subfamily of calcium-binding proteins and has been suggested to be directly involved in invasion and metastasis of rodent and human tumour cells. The present study demonstrates that interferon gamma (IFN-γ), but not IFN-α and IFN-β, downregulates the S100A4 mRNA level in colon adenocarcinoma WiDr cells in time-and dose-dependent manners. The effect was not associated with any cytotoxicity and was specific for the S100A4 mRNA, since the levels of the S100A6 and GAPDH mRNAs were not significantly affected by the treatment. IFN-γ also strongly suppressed the S100A4 mRNA expression in HT-29 cells, but weakly in Colo201 cells. Flow cytometric analysis revealed that the level of the IFN-γ receptor expression in Colo201 cells was lower than that in WiDr and HT-29 cells, suggesting that the suppression of the S100A4 expression by IFN-γ depends on the amount of cell surface IFN-γ receptor protein. IFN-γ had no effect on the transcription rate of the S100A4 gene but reduced the stability of the S100A4 mRNA. WiDr cells treated with IFN-γ showed reduced motile ability, further supporting the assumption that the S100A4 gene product is involved in controlling cell motility.

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“…There is also the possibility of bias in relying on one single animal system for the detection of genes and/or fragments of DNA that can cause metastatsis. However, previous studies using the equivalent all mammary system have identified two genes, p9Ka (S1OOA4) (Davies et al, 1993) and osteopontin (Oates et al, 1996), that have been shown subsequently to induce metastasis in other rodent systems (Ambartsumian et al, 1996;Davies et al, 1996) or in which reduction of their expression using antisense technology blocks the development of the metastatic state in other rodent systems (Behrend et al, 1994;Gardner et al, 1994;Grigorian et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Generation of metastatic variants by transfection of a rat non-metastatic epithelial cell line with genomic DNA from rat prostatic carcinoma cells

Beesley²,

Smith³

et al. 1998

Br J Cancer

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Summary Prostate cancer is the second leading cause of male death from malignant disease in Europe and in the USA. Failure to prevent or eliminate metastatic dissemination is a fundamental problem underlying the current inadequate treatment of prostate cancer, and novel therapeutic strategies are required if this disease is to be successfully managed. No independent markers are yet available to predict the behaviour of any individual prostate cancer, particularly its potential to metastasize, and there is now an urgent prerequisite to identify and characterize genes specifically involved in determining the metastatic phenotype of prostate cancer cells before any biologically appropriate treatment modality can be devised. To identify DNA sequences that trophically promote the metastatic phenotype, we have established a new transfection assay with which to monitor activity of prostate cancer genomic DNA. Rat prostatic G and AT6.1 cell lines derived from the same original Dunning R3327 rat prostatic carcinoma exhibit, respectively, low-and high-metastatic phenotypes when grown in syngeneic Copenhagen rats. Rat mammary epithelial cell line 'Rama 37' derived originally from Wistar-Furth rats yields benign non-metastasizing adenomas when inoculated subcutaneously into syngeneic animals. In this report, the Rama 37 cell line is successfully used as the recipient cell-line for transfected DNA fragments extracted from rat prostatic carcinoma G and AT6.1 cells. New metastatic variants of Rama 37 cells have been generated. Enzymatically fragmented genomic DNA from rat metastatic prostate carcinoma cell lines was co-transfected together with plasmid pSV2neo into parental Rama 37 cells, followed by culture in the presence of Geneticin-G418 to select for the transfected cells. To enable subsequent identification of metastasis-promoting DNA sequences, the fragmented genomic DNA sequences were covalently attached to specifically engineered linker DNA molecules to flank the genomic DNA before transfection. Thereafter, the resulting transfectants were pooled and inoculated into mammary fat pads of female Wistar-Furth rats. Metastases produced by the transfectant cells in vivo were reestablished from secondary tumours and probed for the presence of the specific synthetic oligonucleotide sequences that flanked, and hence identified, the presence of the transfected DNA. These new metastatic cells are shown to provide a sensitive assay system with which to detect DNA sequences responsible for conveying the metastatic phenotype of prostate cancer when inoculated into syngeneic rats.Keywords: DNA transfection; Dunning prostatic carcinoma cells; Rama 37 cell-line; metastatic phenotype Adenocarcinoma of the prostate is now the most common human non-cutaneous malignant neoplasm to affect men. In the USA and Europe, it is the second leading cause of male deaths from malignant disease after lung cancer (Foster, 1990;Boring et al, 1994). Despite the increasing incidence of this disease, current knowledge of molecular mechanisms underlying pr...

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The mts1 gene and control of tumor metastasis

Cited by 86 publications

References 20 publications

Expression of antisense RNA to S100A4 gene encoding an S100-related calcium-binding protein suppresses metastatic potential of high-metastatic Lewis lung carcinoma cells

Expression of antisense RNA to S100A4 gene encoding an S100-related calcium-binding protein suppresses metastatic potential of high-metastatic Lewis lung carcinoma cells

Suppression of metastasis-associated S100A4 gene expression by gamma-interferon in human colon adenocarcinoma cells

Generation of metastatic variants by transfection of a rat non-metastatic epithelial cell line with genomic DNA from rat prostatic carcinoma cells

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