Fig. 1: Profiling of SRPK1 expression in the parental and cisplatin-resistant breast cancer cells. | Communications Biology

Fig. 1: Profiling of SRPK1 expression in the parental and cisplatin-resistant breast cancer cells.

From: SRPK1 acetylation modulates alternative splicing to regulate cisplatin resistance in breast cancer cells

Fig. 1

a MCF7, MCF7R, 231 and 231R cells were treated with DMF or different concentrations of cisplatin for 1 day (1D) or 5 days (5D). The cell survival was then assessed by the MTS viability assay. The reading of cisplatin-treated cells was normalized against that of DMF-treated cells. Data points: mean ± SD; n = 3. b The IC50 of cisplatin for the indicated cell lines was derived from the above MTS viability assay using the Hill equation. Bars: mean ± SD; n = 4; ***p < 0.001 by Student’s t-test. D: days of cisplatin treatment. c The indicated cells were treated with DMF or 10 µM cisplatin for 5 days. Immunoblotting was then performed with the SRPK1 antibody. d The knockdown efficiency of the siRNA SMARTpool targeting SRPK1 (siK1) and overexpression of Myc-tagged SRPK1 (Myc-K1) were verified by immunoblotting. e MCF7R cells were transfected with siK1 and 231R with Myc-K1, and subjected to MTS viability assays. The IC50 of cisplatin was derived using the Hill equation. Bars: mean ± SD; n = 4; *p < 0.05 by Student’s t-test. Cisp: cisplatin. sictrl: negative control siRNA. ctrl: control pCMV-myc vector. The Western blots in (c) and (d) are representative of three and four experiments with similar results, respectively.

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