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. Author manuscript; available in PMC: 2022 May 19.
Published in final edited form as: Oncogene. 2021 Nov 19;40(50):6772–6785. doi: 10.1038/s41388-021-02117-5

Figure 4. PKR promotes tumorigenesis and paclitaxel sensitivity in vivo.

Figure 4

(A-C) Cell proliferation curves in SKOV3 (A), MCF7 (B), and TOV21G (C) cell lines.

(D-I) Cell migration (Transwell assay) in parental and PKR-KO SKOV3, MCF7, and TOV21G cells. Representative fields were shown in E (SKOV3), G (MCF7), and I (TOV21G). Data in panels A-D, F, and H are expressed as mean ± SEM from three independent experiments. **: p<0.01, ***: p<0.001 (unpaired Student’s t-test).

(J, K) Deletion of PKR inhibited tumor growth, but promoted paclitaxel resistance in animals. Cells were injected subcutaneously into female athymic mice on both flanks. Paclitaxel (12 mg/kg) was injected through intraperitoneal every other day for 2 weeks. The initial treatment was done at day 7 post cell injection. Tumors were excised and photographed at the endpoint (J).

(L, M) Enhanced expression of PKR improved paclitaxel sensitivity in vivo. A lower dose of paclitaxel (8 mg/kg) was used in this experiment. The control groups (SKOV3/PBS) in panels J and K are identical to control groups in panels L and M. Data in panels K and M are expressed as mean ± SEM from all tumors of each group. *: p<0.05, **: p<0.01, ***: p<0.001 (unpaired Student’s t-test).

(N) Immunohistochemistry (IHC) staining of cleaved caspase 3 to determine cell death in tumor samples in panel L. Cl-caspase 3-positive cells were quantified from three random fields in each tumor. ***: p<0.001 (unpaired Student’s t-test).