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Fig. 3 | Molecular Cancer

Fig. 3

From: LncRNA TROJAN promotes proliferation and resistance to CDK4/6 inhibitor via CDK2 transcriptional activation in ER+ breast cancer

Fig. 3

TROJAN promoted cell proliferation through the regulation of G1/S cell cycle entry. a qRT-PCR analysis TROJAN transcription in MCF7 cells expressing control (Ctrl) or TROJAN short-hairpin RNAs (shRNAs). n = 3 independent experiments. Unpaired t test was used. b In vitro growth curves of MCF7 and T47D cells expressing Ctrl or TROJAN shRNAs. n = 3 independent experiments. Two-way ANOVA analysis was used. c qRT-PCR detection of TROJAN transcription in MCF7 cells overexpressing a control vector (Vec) or TROJAN. n = 3 independent experiments. Unpaired t test was used. d In vitro growth curves of MCF7 cells expressing Vec or TROJAN. n = 3 independent experiments. Two-way ANOVA analysis was used. e, f In vivo growth of MCF7 cells (42 days; mean ± standard error of mean; n = 7) expressing Ctrl or TROJAN shRNA. Tumor volume quantification and representative tumor images are shown. Two-way ANOVA analysis was used. g Pathway analysis of 694 down regulated genes after TROJAN knockdown identified by a microarray. Top 10 pathways according to -log10 (P value) are shown. h Flow cytometry analysis showing the constituent ratios of different cell cycle phases in the TROJAN knockdown MCF7 and T47D cell lines. n = 3 independent experiments. i Immunohistochemical detection of Ki67 in a mammary fat pad xenograft model generated by injecting MCF7 cells with TROJAN knockdown. The H-score is shown. Unpaired t test was used. j IC50 values of PD in MCF7, MCF7 with TROJAN knockdown, PD resistance MCF7 (PDR) and PDR with TROJAN knockdown cells. n = 3 independent experiments. One-way ANOVA analysis was used. k In vitro growth assay of MCF7, MCF7 with TROJAN knockdown, PD resistance MCF7 (PDR) and PDR with TROJAN knockdown cells treated with 0.1 μM PD. n = 3 independent experiments. Two-way ANOVA analysis was used. *p < 0.05, **p < 0.01 and ***p < 0.001

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