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. 2018 Aug 7;8:11805. doi: 10.1038/s41598-018-29546-9

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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miR-191 acts as the downstream effecter of MED1 mediated cellular functions. (A–C) Functional implications of MED1 or miR-191 overexpression in breast cancer. MCF7 cells were transfected with MED1 or miR-191 or PC (control vector) and MTT assay was performed (48 hrs post transfection) to measure effect on cell survival. The results show that both MED1 and miR-191 promote cell survival (A). (B,C) Wound healing assay was performed to observe the effect of miR-191 and MED1 on cell migration. MCF7 cells were transfected with MED1 or miR-191 or control vector and gap or wound closure was observed (B) using Nikon microscope, 10X magnification and % gap closure was quantified using arbitrary scale (C). Graph shows that more healing (gap closure) was observed in response to both miR-191 and MED1 overexpression, hence both MED1 and miR-191 impart enhanced cell migratory capacity to the cells. (D–F) MED1 mediated cellular effects are miR-191 dependent. MCF7 cells were transiently transfected with MED1/PC (vector control) along with inhibition of miR-191(anti-miR-191)/Ctrl and effect on cell survival was looked for using MTT assay (D). Increase in cell survival due to MED1 overexpression was significantly reduced when miR-191 was inhibited along with MED1 overexpression (E). Wound healing assay was performed to confirm the effect of MED1 and miR-191 on cell migration. Levels of MED1 were transiently overexpressed along with/without miR-191 inhibition (using anti-miR-191/ctrl) and gap closure was observed after 24 hrs. Comparatively, lesser gap was filled when MED1 overexpression was coupled with miR-191 inhibition (F) when quantified using arbitrary scale thereby, confirming that miR-191 is a downstream effecter for MED1 mediated cellular migration. (G) qRT-PCR data showing transcript levels of JUN, FOS, EGFR, VEGF, MMP1 and ERBB4 on miR-191 or MED1 overexpression/inhibition. GAPDH has been used for normalization of qRT-PCR data. (H) qRT-PCR data showing transcript levels of JUN, FOS, EGFR, VEGF, MMP1 and ERBB4 on MED1 overexpression or miR-191 inhibition. (I) qRT-PCR data showing transcript levels of established miR-191-target genes (SATB1, CDK6 and BDNF) in response to both miR-191 or MED1 overexpression/inhibition. GAPDH has been used for normalization of qRT-PCR data. (J) qRT-PCR data showing transcript levels of established miR-191-target genes (SATB1, CDK6 and BDNF) on MED1 overexpression or miR-191 inhibition. (**P<0.05, (**P<0.05, * P<0.1). Error bars denote + SD.