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Fig. 2 | Journal of Hematology & Oncology

Fig. 2

From: MiR-509-3 augments the synthetic lethality of PARPi by regulating HR repair in PDX model of HGSOC

Fig. 2

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

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