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. Author manuscript; available in PMC: 2021 Jul 13.
Published in final edited form as: Cancer Cell. 2020 Jun 11;38(1):129–143.e7. doi: 10.1016/j.ccell.2020.05.003

Figure 3: PP2A de-phosphorylates PKA substrates and inhibits the growth of SCLC.

Figure 3:

(A) Immunoblot for phosphorylated PKA substrates (pPKA) and PKA-Cα from NJH29 and NCI-H82 cells treated with 10 μM PP2Ai for increasing amounts of time. HSP90 is a loading control. (B) Immunoblot for the indicated proteins from NJH29 cells treated with 100 μM 8-Br-cAMP, 20 μM H89 (PKAi), and/or 10 μM PP2Ai. (C) Immunoblot for the indicated proteins from NJH29 cells treated with 10 μM of SMAP-1154 for various amounts of time. HSP90 is a loading control. (D-E) Growth curve (D) and waterfall plot (E) of NCI-H69 xenografts treated with SMAP DT-061 (labeled SMAP-061), Cisplatin, or SMAP-061 and Cisplatin (n=10-13). (F) Quantification of TUNEL staining of NCI-H69 SCLC tumors from (D).

Data are presented as mean ± SEM. NS, not significant, p<0.05*, p<0.01**, p<0.001.

See also Figure S3.