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. 2021 Mar 8;13(3):433. doi: 10.3390/v13030433

Figure 2.

Figure 2

HPV16 E7 upregulates and interacts with PKM2 in cervical cancer cells. (A) HPV16 E7 interacts with PKM2 in SiHa cells. SiHa cell extracts (0.5 mg) were subject to co-immunoprecipitation using an anti-HPV16 E7 antibody. Normal IgG was used as a negative control. The input lane represents 50 μg of cell extracts. (B) GST proteins fused to HPV18 E7 (GST-18E7) and HPV45 E7 (GST-45E7) were incubated with 293T cell extracts overexpressing HA-tagged PKM2 (HA-PKM2). GST was used as a negative control. PKM2 was detected by western blot using an anti-HA antibody. GST fusion proteins were visualized by Coomassie blue staining. Intervening lanes were deleted and indicated by vertical lines. (C) PKM2 levels were higher in HPV+ than in HPV− cervical cancer cells. Cell extracts were subject to western blot. Intervening lanes were deleted and indicated by vertical lines. (D) The levels of PKM2 mRNA was higher in SiHa cells than C33A cells. Total RNA was subject to semi-quantitative RT-PCR. The number of PCR cycle was 25 for PKM2 and 22 for GAPDH. (E) HPV16 E7 increased the level of PKM2. Cells were transfected with an empty (mock) or HPV16 E7-expressing plasmid. Cell extracts were subject to western blot. Actin was used as a loading control.