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Fig. 2 | Molecular Cancer

Fig. 2

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

Fig. 2

Anti-TROJAN ASO therapy sensitized ER+ breast cancer cells to PD. a In vitro free-uptake assay in T47D cells. Cells were treated by 0 or 40 μM of the ASO. The qRT-PCR detection of TROJAN expression. n = 3 independent experiments. Unpaired t test. b Cell viability of T47D treated with different concentration of ASO. n = 3 independent experiments. c Clonogenic survival assays of MCF7 cells treated with ASO in combination with palbociclib (PD), ribociclib (Ribo), abemaciclib (Abema), fulvestrant (Ful), everolimus (Evero) or tamoxifen (Tam). n = 3 independent experiments. d In vitro growth assay of MCF7 and T47D cells treated with ASO in combination with palbociclib (PD), ribociclib (Ribo), abemaciclib (Abema), fulvestrant (Ful), everolimus (Evero) or tamoxifen (Tam). n = 3 independent experiments. Unpaired t test. e In vitro growth assays of MCF7 and T47D cells that were treated with 0.1 μM PD or/and 40 μM anti-TROJAN ASO. n = 3 independent experiments. Two-way ANOVA analysis was used. f One ER+ breast cancer patient-derived organoid treated with 0.1 μM PD or/and 40 μM anti-TROJAN ASO. The viability as measured by OD450 is shown. Scale bar: 100 μm. n = 3 independent experiments. One-way ANOVA analysis was used. g, h In vivo growth of MCF7 cells (mean ± standard error of mean; n = 6) after 17 days of treatment with PD and anti-TROJAN ASO, individually or in combination. Tumor volume quantification g and representative tumor images h are shown. Each row in h represents a treatment. Columns represent repetitions. Two-way ANOVA analysis was used. i, j Clonogenic survival assays in MCF7 cells i and PDR cells j treated with 0.1 μM PD or/and 40 μM anti-TROJAN ASO. The number of colonies is shown. n = 3 independent experiments. One-way ANOVA analysis was used. *p < 0.05, **p < 0.01, ***p < 0.001 and NS: not significant

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