Fig 2: Reducing cell-cell adhesion facilitates MDA-MB231 cells' aggregation. (a1–a3) Pattern evolution of the coculture system with E-cad and N-cad inhibited and (b1–b3) pattern evolution of the control group (with no inhibition), where the scale bar is 500 μm.

Fig 3: Silencing of CDH2, LEP, POSTN, TIMP1 and VEGFC enhanced the chemosensitivity of the colon cancer cells. After different concentrations (0.5, 1, 2 and 4 µg/ml) of 5-FU treatment, cell viability and the IC50 values of 5-FU were monitored using a Cell Counting Kit-8 assay in the HCT116 and LoVo cells following silencing of (A) CDH2, (B) LEP, (C) POSTN, (D) TIMP1 and (E) VEGFC. The data was analyzed using an unpaired Student's t-test and expressed as the mean ± SD. Each assay was performed independently 3 times. *P<0.05; **P<0.01; ***P<0.001. OD, optical density; si, small interfering; 5-FU, 5-fluorouracil.

Fig 4: NR2F1-AS1 promotes the poor prognosis and malignant phenotype of GC cells by activating EMT. (A) The data of TCGA GC were divided into two groups: low-expression group and high-expression group of NR2F1-A1. The whole genome expression of these two groups was enriched by GSEA and the enrichment in the EMT pathway was detected by Xiantao. (B) Xiantao was used to analyze the correlation between the expression of NR2F1-AS1 and EMT markers, and a heat map was drawn. (C) Si-control, si-NR2F1-AS1-1, and si-NR2F1-AS1-2 were transfected into BGC823 and SGC7901 cell lines to detect the expression of NR2F1-AS1 by qRT-PCR. (E) The cell proliferative ability by cell viability assay. (F) The proportion of apoptosis by TUNEL assay. (D) The expression of NR2F1-AS1 was detected by qRT-PCR after NR2F1-AS1-OE and EV were transfected in BGC823 and SGC7901 cell lines. (G) Transfect NR2F1-AS1-OE and EV into BGC823 and SGC7901 to detect the invasiveness of the cells by Transwell assay. (H) The morphology of cell colonies was observed after transfection of NR2F1-AS1-OE and EV in BGC823 and SGC7901. (I) After transfection of NR2F1-AS1-OE and EV in BGC823 and SGC7901, the expression of EMT markers was detected by WB. (J) After transfection of NR2F1-AS1-OE and EV in BGC823 and SGC7901, the expression of CDH2 and VIM was detected by immunofluorescence. *p < 0.05; **p < 0.01; ***p < 0.001.

Fig 5: MiR-509-3 inhibits ovarian cancer cells proliferation and invasion. a Cell cycle analysis of A2780, HEY, and UWB1.289 when transfected with miR-509-3 mimics. miR-509-3 increased the percentage of G0/G1 phase significantly in A2780, HEY, and UWB1.289 cell lines. b MTT and plate clonogenic assay of three ovarian cancer cells. MiR-509-3 decreased relative cell viability at different time points (day 2 to day 5) and cell clonal number in 6-well plates. c Transwell assay was performed to determinate the effects of miR-509-3 overexpression on migration and invasion of A2780, HEY, and UWB1.289 cells. MiR-509-3 decreased the number of migrated cells. d Intraperitoneal tumor formation assay of HEY or UWB 1.289 in nude mice. MiR-509-3 impaired the number of abdominal metastasis (HEY, 15.33 ± 2.40 vs. 7.33 ± 1.20, P < 0.05; UWB1.289 27 ± 4.35 vs. 9 ± 1.55, P < 0.05) and tumor burden (HEY, 0.52 ± 0.07 vs. 0.25 ± 0.04, P < 0.05; UWB1.289 0.39 ± 0.07 vs. 0.15 ± 0.02, P < 0.05) in vivo. The red arrows indicate the tumor metastatic nodules. e Western blot of the EMT and cell cycle associated markers in miR-509-3 overexpressing cells. MiR-509-3 significantly downregulated ZEB1, N-cad, β-Catenin, Vimentin, Snail, and Slug but upregulated E-cad expression. G0/G1 arrest related markers CDK4, CDK6, CCND1, and p21 were also downregulated