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Angiopoietin‐like protein 2 ( ANGPTL 2) plays an important role in inflammatory carcinogenesis and tumor metastasis by activating tumor angiogenesis and tumor cell chemotaxis and invasiveness. However, it is unclear whether  ANGPTL 2 expression has an effect on tumor cell survival. Here, we explored that possibility by determining whether  ANGPTL 2 expression altered survival of human colorectal cancer cell lines treated with antineoplastic drugs. To do so, we generated  SW 480 cells expressing  ANGPTL 2 ( SW 480/ ANGPTL 2) and control ( SW 480/ C trl) cells. Apoptosis induced by antineoplastic drug treatment was significantly decreased in  SW 480/ ANGPTL 2 compared to control cells. Expression of anti‐apoptotic  BCL ‐2 family genes was upregulated in  SW 480/ ANGPTL 2 compared to  SW 480/ C trl cells. To assess signaling downstream of  ANGPTL 2 underlying this effect, we carried out  RNA  sequencing analysis of  SW 480/ ANGPTL 2 and  SW 480/ C trl cells. That analysis, combined with  in vitro  experiments, indicated that  S yk‐ PI 3 K  signaling induced expression of  BCL ‐2 family genes in  SW 480/ ANGPTL 2 cells. Furthermore,  ANGPTL 2 increased its own expression in a feedback loop by activating the spleen tyrosine kinase–nuclear factor of activated T cells ( S yk– NFAT ) pathway. Finally, we observed a correlation between higher  ANGPTL 2 expression in primary unresectable tumors from colorectal cancer patients who underwent chemotherapy with a lower objective response rate. These findings suggest that attenuating  ANGPTL 2 signaling in tumor cells may block tumor cell resistance to antineoplastic therapies.

cancer science

Angiopoietin‐like protein 2 renders colorectal cancer cells resistant to chemotherapy by activating spleen tyrosine kinase–phosphoinositide 3‐kinase‐dependent anti‐apoptotic signaling