Fig. 7: Modulating SRG expression impacts AS and aggressiveness of PCa cells. | Nature Communications

Fig. 7: Modulating SRG expression impacts AS and aggressiveness of PCa cells.

From: Intron retention is a hallmark and spliceosome represents a therapeutic vulnerability in aggressive prostate cancer

Fig. 7

a qPCR analysis showing the knockdown efficiency of ESRP1 and/or KHDRBS3. PC3 cells were treated with non-targeting siRNAs (siNC) or with siRNAs targeting ESRP1 and/or KHDRBS3 (20 nM; 72 h). Error bars represent the mean ± SD (n = 3). b Knocking down ESRP1 or/and KHDRBS3 inhibits clonal development in PC3 cells. Shown were representative images of two repeat experiments (left) and quantification data (right). Error bars represent the mean ± SD (n = 3). c–e Knocking down ESRP1 or/and KHDRBS3 inhibits proliferation (c), migration and invasion (d), and sphere formation (e) in PC3 cells. Cell proliferation (viability) was determined by MTT assays (c). Data represent the mean ± SD from a representative experiment with four technical repeats and the experiment was replicated two times with similar results. Migration and invasion were determined by counting cells of five random 10× fields (d) (mean ± SD; n = 5). Spheres were enumerated 9 days after plating (4000 cells/well) (e) (mean ± SD; n = 3). f RNA-seq analysis of PC3 cells depleted of ESRP1 and KHDRBS3, individually or in combination, by specific siRNAs. Shown are the relative fold changes (upper) and absolute number (bottom) of the identified DSEs (differentially spliced evets) in indicated contexts. siES + KH denotes double knockdown by siRNAs against ESRP1 and KHDRBS3. All P-values were calculated using two-tailed unpaired Student’s t-test. Source data are provided as a Source Data File.

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