Skip to main content

Advertisement

Fig. 6 | Molecular Cancer

Fig. 6

From: LINC01133 as ceRNA inhibits gastric cancer progression by sponging miR-106a-3p to regulate APC expression and the Wnt/β-catenin pathway

Fig. 6

LINC01133 attenuates the EMT and metastatic abilities of GC cells through APC/Wnt signaling pathway. a Identification of 93 commonly changed targeted mRNAs of miR-106a-3p from the four publicly profile datasets (TargetScan, microT-CDS, TargetMiner, and mirDIP). Different color areas represented different datasets. The cross areas meant the commonly changed mRNAs of miR-106a-3p. b GO analysis and significant enriched GO terms of 93 commonly changed targeted mRNAs in gastric cancer on their biological process (BP). The statistically significant results were defined with -log10 (P value) > 1.30 as the cut-off criterion. c, d Dual luciferase assay demonstrating the effect on TOP/FOP reporter activity in HEK-293FT cells, AGS cells transfected with shLINC01133 vector or SGC-7901 cells with LINC01133 overexpression. Results were normalized to a Renilla transfection control. e Dual luciferase assay showing the effect on TOP/FOP reporter activity in AGS cells following reduced expression of LINC01133 and/or inhibition of miR-106a-3p. f Immunoblot assay of E-cadherin, vimentin, N-cadherin, APC, and total and nuclear β-catenin proteins in AGS cells transfected with shLINC01133–2 and/or miR-106a-3p inhibitor. Numbers showed quantification of relative protein amount. GAPDH was used as an internal control. Lamin B1 was used as an endogenous control for the cell nuclear fraction. g Schematic diagram of the regulatory mechanism of LINC01133/miR-106a-3p/APC axis in the inhibition of GC proliferation and metastasis. Error bars: mean ± SD, n = 3. *P < 0.05 versus corresponding control

Back to article page