2006
DOI: 10.1002/ijc.22106
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The expression of metastasis suppressor MIM/MTSS1 is regulated by DNA methylation

Abstract: MIM/MTSS1 was initially described as a gene missing in invasive bladder cancer cell lines. Functional analysis revealed that MIM is an actin binding protein involved in the regulation of actin cytoskeleton dynamics. MIM was shown to be sonic hedgehog (Shh) signaling dependent and synergizes with the effects of Gli transcription factors. Overexpression of MIM in cell lines leads to the inhibition of cell proliferation. In this study, we showed that the inhibition of cell growth by MIM is anchorage independent. … Show more

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Cited by 46 publications
(47 citation statements)
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“…MTSS1 was first described as a potential metastasis suppressor in bladder cancer (Lee et al, 2002), and its regulatory mechanism is still unknown. MTSS1 expression was considered to be methylation-dependent owing the presence of a CpG island in its 5 0 -flanking region (Utikal et al, 2006). In contrast, we found that DNMT3B suppressed the expression of MTSS1, which is independent of significant changes in promoter methylation status.…”
Section: Discussionmentioning
confidence: 53%
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“…MTSS1 was first described as a potential metastasis suppressor in bladder cancer (Lee et al, 2002), and its regulatory mechanism is still unknown. MTSS1 expression was considered to be methylation-dependent owing the presence of a CpG island in its 5 0 -flanking region (Utikal et al, 2006). In contrast, we found that DNMT3B suppressed the expression of MTSS1, which is independent of significant changes in promoter methylation status.…”
Section: Discussionmentioning
confidence: 53%
“…These data suggest that DNMT3B represses MTSS1 expression via a DNA methylation-independent mechanism. One study found that 5-Aza-dC upregulated MTSS1 expression in bladder cancer cells (Utikal et al, 2006), but a different group did not see the same effect of 5-Aza-dC on MTSS1 expression in T24, J82, SW170 or VMCub3 bladder cancer cells (Nixdorf et al, 2004). Thus, MTSS1 expression is not completely independent of promoter methylation, even in the same type of cancer.…”
Section: Discussionmentioning
confidence: 99%
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“…The mechanism for the down-regulation of MTSS1 may involve DNA methylation (13,14). Although the relevance of such down-regulation to tumor progression, in particular, metastasis, has not yet been confirmed, several lines of evidence have indicated a role of MTSS1 in cell morphogenesis.…”
mentioning
confidence: 99%
“…Using two sets of clinical samples, a strong correlation between the expression level of miR-548j and lymph node metastasis and survival has been observed in BC patients (52). (58,59) resulting in activation of RhoA and stress fiber formation (60). Ectopic expression of miR-182 enhances BC cell mobility and invasion and increases pulmonary colonization of BC cells (60).…”
Section: Mirs Targeting Metastasis-suppressing Genesmentioning
confidence: 99%