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. 2017 Sep 8;292(43):17939–17949. doi: 10.1074/jbc.M116.773978

Figure 5.

Figure 5.

miR-215–PCAT-1 axis modulates CRKL expression and CRKL-regulated cell growth. A, dysegulated genes in SMMC7721 cells after delivery of miR-215 or siPCAT-1 using gene-profiling arrays (left). Cluster analysis of mRNAs expression profiles of the miR-215 group or the siPCAT-1 group versus the NC RNA group. Overexpression is coded in red, whereas decreased expression is indicated in green (right). B, candidate gene expression was validated using qRT-PCR. All data of gene expression were normalized to β-actin mRNA expression levels. C, protein expression of CRKL. D, inhibition of CRKL expression suppresses SMMC7721 cell proliferation. Left panel, different doses of NC RNA or CRKL siRNAs were transfected into SMMC7721 cells. Cell number was counted at 48 h after transfection. 30 nm NC RNA or CRKL siRNA was transfected into SMMC7721 cells. Cell number was counted at 24, 48, or 72 h after transfection. E, colony formation assays. 30 nm NC RNA or CRKL siRNA was transfected into SMMC7721 cells. After 10 days, colony number in each well was counted. F, overexpression of CRKL prevents anti-tumorigenic properties of miR-215 in HCC. *, p < 0.05; **, p < 0.01.