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. Author manuscript; available in PMC: 2019 Oct 4.
Published in final edited form as: Adv Exp Med Biol. 2019;1164:119–139. doi: 10.1007/978-3-030-22254-3_10

Fig. 5. Proposed mechanism for role of aberrant splicing of PIK3CD in PCa disparities.

Fig. 5

EA cell lines (e.g. VCaP) and patient specimens show “normal”/low expression of SFs, such as SRSF2 (left panel). Normal splicing of PIK3CD pre-mRNA generates the long variant containing exon 20, which encodes the p110δ-L protein that has low oncogenic properties. Aberrant over-expression of SRSF2 in AA cell lines (MDA PCa 2b) and patient samples results in differential alternative splicing of PIK3CD (right panel). This generates p110δ-S protein that has higher oncogenic signaling and is resistant to CAL-101 (idelalisib).