PRR11 Promotes Proliferation and Migration of Colorectal Cancer through Activating the EGFR/ERK/AKT Pathway via Increasing CTHRC1

Objective. Colorectal cancer (CRC) is a common prevalent malignant tumor globally. The prognosis of CRC patients remains poor due to a lack of effective treatment strategy. Proline-rich 11 (PRR11) is an emerging oncogene in cancers, while its effect in CRC remains unclear. Hence, the present study aimed to identify the function of PRR11 on CRC progression and study the detailed mechanism. Methods. Cell proliferation ability was determined by Cell Counting Kit-8 (CCK-8) assay and 5-ethynyl-2'-deoxyuridine (EdU) staining. Transwell invasion assay detected cell invasion ability. Wound healing assay assessed cell migration ability. Xenograft tumor was established to evaluate tumor growth. Quantitative real-time polymerase chain reaction (qRT-PCR), Western blot and immunohistochemistry were performed to determine mRNA or protein levels. Results. PRR11 was elevated in CRC. PRR11 silencing suppressed CRC cell proliferation, invasion, and migration ability. Besides, PRR11 silencing inhibited EGFR/ ERK/ AKT pathway via restraining Collagen triple helix repeat containing-1 (CTHRC1) expression. Furthermore, knockdown of PRR11 suppressed CRC tumor growth in vivo. Conclusion. PRR11 was highly expressed in CRC. PRR11 silencing suppressed proliferation, invasion, migration, and tumor growth of CRC through inhibiting the EGFR/ERK/AKT pathway via restraining CTHRC1 expression. PRR11 may be a valuable therapeutic target for CRC.