HNRNPL affects the proliferation and apoptosis of colorectal cancer cells by regulating PD-L1.

Colorectal cancer (CRC) ranks fourth among all human cancers in the world. HNRNPL plays an oncogenic role in various cancers, but is not discussed yet in CRC. The presents study aims to investigate the role of HNRNPL in CRC development. The mRNA and protein levels of HNRNPL in CRC cells were measured by RT-qPCR and western blot. The cell viability, colony formation, and apoptosis were evaluated after CRC cells were transfected with shRNA-HNRNPL. Also, the invasion and migration of transfected cells were respectively detected by transwell and wound-healing assays. Besides, tumor-bearing mice were established after C57BL/6 mice received injection of CRC cells with or without overexpression plasmid of HNRNPL, accompanied with anti-PD-L1 treatment. Expression of Ki67 in tumor tissue was detected using immunohistochemistry. HNRNPL was up-regulated in CRC cells, and transfection with shRNA-HNRNPL led to the decreases in cell viability, migration, invasion, and the increase in apoptosis of CRC cells. HNRNPL was verified to be a potential binding protein of PD-L1. Overexpression of HNRNPL promoted tumor growth in vivo, which was attenuated by anti-PD-L1 treatment. HNRNPL promotes the tumor growth and development of CRC by regulating PD-L1, which may direct us a new method to treat CRC.