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. 2021 Dec 6;18(8):1822–1840. doi: 10.1080/15548627.2021.2002108

Figure 8.

Figure 8.

PIK3C3 and ATG12 contribute to tumorigenicity and Dox resistance. (A,B) Xenograft model of chemotherapy in nude mice. Six nude mice in each group were subcutaneously injected with indicated cells for 1 week, mice were treated with Dox combined with or without CQ for two weeks. Mean tumor weights were quantified around another three weeks later (B). ****P < 0.0001. (C) Immunoblots of SH3BGRL, PIK3C3, ATG12, SQSTM1, LC3B, PARP, cleaved (c)-PARP, CASP3 and c-CASP3 in the indicated mice tumor tissues. ACTB was used as a loading control. (D) Statistical analysis of SQSTM1, c-CASP3 and c-PARP expressions in the indicated six group mice tumors. Error bars represent mean ± s.d.*P < 0.05, **P < 0.01, ***P < 0.001. (E) Transcriptional expression analysis of classical genes involved in Dox resistance from RNA-Seq of MCF-7 and MDA-MB-453 cells with SH3BGRL expression alteration. (F) Translational expression analysis of general genes involved in Dox resistance based on polyribosome profiling results of MDA-MB-453 cells.