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  • Wang, JunUniversity of Houston, United States (author)

miR-206 inhibits cell migration through direct targeting of the actin-binding protein coronin 1C in triple-negative breast cancer

  • Article/chapterEnglish2014

Publisher, publication year, extent ...

  • 2014-07-12
  • Wiley,2014
  • printrdacarrier

Numbers

  • LIBRIS-ID:oai:DiVA.org:kth-165342
  • https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-165342URI
  • https://doi.org/10.1016/j.molonc.2014.07.006DOI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:130285595URI

Supplementary language notes

  • Language:English
  • Summary in:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • QC 20150427
  • Patients with triple-negative breast cancer (TNBC) have an overall poor prognosis, which is primarily due to a high metastatic capacity of these tumors. Novel therapeutic approaches to target the signaling pathways that promote metastasis are desirable, in order to improve the outcome for these patients. A loss of function of a microRNA, miR-206, is related to increased metastasis potential in breast cancers but the mechanism is not known. In this study, we show that miR-206 was decreased in TNBC clinical tumor samples and cell lines whereas one of its predicted targets, actin-binding protein CORO1C, was increased. Expression of miR-206 significantly reduced proliferation and migration while repressing CORO1C mRNA and protein levels. We demonstrate that miR-206 interacts with the 3'-untranslated region (3'-UTR) of CORO1C and regulates this gene post-transcriptionally. This post-transcriptional regulation was dependent on two miR-206-binding sites within the 3'-UTR of CORO1C and was relieved by mutations of corresponding sites. Further, silencing of CORO1C reduced tumor cell migration and affected the actin skeleton and cell morphology, similar to miR-206 expression, but did not reduce proliferation. In accordance with this, overexpression of CORO1C rescued the inhibitory effect of miR-206 on cell migration. Our findings suggest that miR-206 represses tumor cell migration through direct targeting of CORO1C in TNBC cells which modulates the actin filaments. This pathway is a novel mechanism that offers a mechanistic basis through which the metastatic potential of TNBC tumors could be targeted.

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Added entries (persons, corporate bodies, meetings, titles ...)

  • Tsouko, EfrosiniUniversity of Houston, United States (author)
  • Jonsson, PhilipUniversity of Houston, United States (author)
  • Bergh, JonasKarolinska Institutet (author)
  • Hartman, JohanKarolinska Institutet (author)
  • Aydogdu, EylemUniversity of Houston, United States (author)
  • Williams, Cecilia,1969-University of Houston, United States(Swepub:kth)u1ygqmuy (author)
  • Karolinska InstitutetUniversity of Houston, United States (creator_code:org_t)

Related titles

  • In:Molecular oncology: Wiley8:8, s. 1690-7021878-02611574-7891

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