PIPKIγ Regulates CCL2 Expression in Colorectal Cancer by Activating AKT-STAT3 Signaling

Figure 2

Upregulated PIP5Iγ increased CCL2 expression in CRC cancer cells. (a) Stable shPIP5K1C-expressing SW480 and LOVO cells were grown in normal medium for 48 h, and PIP5K1C mRNA levels were measured by quantitative PCR with reverse transcription (RT-qPCR) (, data are the ) (b) Western blot analysis of the effect of PIPKIγ knockdown in SW480 and LOVO cells. Experiments were repeated twice, and representative results are presented. (c, d) Stable shPIP5K1C-expressing SW480 and LOVO cells were grown in normal medium for 48 h, and GM-CSF, M-CSF, CCL2, CCL5, IL4, IL10, IL13, and TGFB1 mRNA levels were measured by quantitative PCR with reverse transcription (RT-qPCR) (, data are the ). (e) Stable shPIP5K1C-expressing SW480 and LOVO cells were grown in FBS-free medium for 48 h, and ELISAs were performed to determine CCL2, CCL5, and TGFB1 levels in the CM from sh-Ctrl and sh-PIP5K1C SW480 and LOVO cells (, data are the ). (f) Western blot analysis of the effect of PIPKIγ overexpression in HCT116 and SW620 cells. Experiments were repeated twice, and representative results are presented. (g) q-PCR analysis of the mRNA level of CCL2 in PIPKIγ-overexpressing HCT116 and SW620 cells. (h) ELISA was performed to determine the protein level of CCL2 in PIPKIγ-overexpressing HCT116 and SW620 cells cultured in FBS-free medium.

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