The relationship between miR-26a expression and clinicopathological parameters in breast cancer.

<p>The relationship between miR-26a expression and clinicopathological parameters in breast cancer.</p

The expression of miR-26a was reduced in breast cancer cell lines and clinical specimens.

<p>A. Expression of miR-26a in the 2 immortalized normal mammary epithelium cell lines and 4 breast cancer cell lines. B. Average expression level of miR-26a in human breast cancer tissues and normal breast tissues. MiRNA abundance was normalized to 5s rRNA. *P<0.05 compared with control.</p

MCL-1 is the target of miR-26a.

<p>A. Putative miR-26a binding sites in the 3′UTR region of MCL-1 and interspecies conservation of seed matching sequences (gray box). B. Expression of MCL-1 in the 2 immortalized normal mammary epithelium cell lines and 4 breast cancer cell lines. C. Western blot assay for MCL-1 expression after MDA-MB-231 and MCF-7 cells were transfected with miR-26a for 48 hours. *P<0.05 compared with control.</p

Knockdown of MCL-1 suppresses cell proliferation, clonogenicity and induces cell apoptosis.

<p>A. Does effect and time effect of transfection of MCL-1-siRNA on the proliferation of MDA-MB-231 and MCF-7 cells. B. The functional role of MCL-1 in breast cancer cell growth was analyzed by colony formation of MDA-MB-231 and MCF-7 cells. The evaluation of colony numbers was shown in the panel. C. Influence of MCL-1 on apoptosis in breast cancer cells was monitored by flow cytometry. The percentage of Annexin V-FITC positive cells to the total cells was shown in the bar graphs. *P<0.05 compared with control.</p

Overexpression of miR-26a lead to reduced cell viability and decreased clonogenicity.

<p>A. Dose effect. Cells were transfected with miR-26a at the indicated concentrations for 48 hours. B. Time effect. Cells were transfected with 50 µM of miR-26a for indicated periods. C. Morphologic changes of MDA-MB-231 and MCF-7 cells in response to miR-26a inhibition. D. Influence of miR-26a on colony formation of MDA-MB-231 and MCF-7 cells. Representative dishes are presented (left). The number of colony was counted for each well of six-well plates and the evaluation of colony numbers was shown in the y-axis of the right panel. *P<0.05 compared with control.</p

Figure S1 from miR-200b and miR-200c as Prognostic Factors and Mediators of Gastric Cancer Cell Progression

Figure S1 - PDF file 1773K, miR-200a expression levels is unchanged in human gastric cancer.(A) The expression levels of miR-200a was detected in 36 gastric cancer patients by qRT-PCR. Data are shown as fold change of gastric cancer relative to adjacent normal tissues. (B) Relative expression of miR-200a in 7 cell lines derived from gastric cancer and one nonmalignant gastric cell line (GES-1) was determined by qRT-PCR. Data are presented as mean � SD from at least three separate experiments</p

Table S1 from miR-200b and miR-200c as Prognostic Factors and Mediators of Gastric Cancer Cell Progression

Table S1 - PDF file 47K, miR-200b and miR-200c is downregulated in primary gastric cancer</p

Effect of miR-26a on apoptosis in breast cancer cells.

<p>FACS analysis of MDA-MB-231 and MCF-7 cells transfected with miR-26a for 48 hours. The percentage of Annexin V-FITC positive cells to the total cells was shown in the bar graphs. *P<0.05 compared with control.</p

MiR-26a sensitized breast cancer cells to paclitaxel.

<p>A. Viability of MDA-MB-231, MCF-7, MDA-MB-435, MDA-MB-468 cells was determined by MTT assay 72 hours after treatment. The percentage of the cell viability as compared with itself without paclitaxel treatment was presented. The concentrations of miR-26a and paclitaxel were 50 µM and 0.12 nM, respectively. B. Western blot assay for MCL-1 expression 48 hours after treatment in MDA-MB-231 cells. *P<0.05.</p

Ectopic restoration of miR-26a inhibited cell migration.

<p>In the wound healing assay, uniform scratches were made in MDA-MB-231 and MCF-7 cells, then serial photographs were obtained at indicated time posttransfection.</p