RESUMEN
Aim: This study aimed to investigate the role of LINC00513 in colorectal cancer (CRC) progression.Materials & methods: Cell proliferation was evaluated using Cell Counting Kit-8. Cell migration was detected with transwell assay. RNA pull-down was applied for verifying the interactions between LINC00513, IGF2BP1 and connective tissue growth factor (CTGF).Results: LINC00513, IGF2BP1 and CTGF levels were upregulated in CRC. Knockdown of LINC00513 significantly inhibited the malignant behavior of CRC cells. LINC00513 increased CTGF mRNA stability by binding with IGF2BP1. Furthermore, overexpression of IGF2BP1 or CTGF reversed the inhibitory effect of LINC00513 shRNA on CRC progression.Conclusion: LINC00513 promoted CRC cell malignant behaviors through IGF2BP1/CTGF.
Colorectal cancer (CRC) progression seriously threatens the health of people. This study showed that LINC00513 (a long noncoding RNA), insulin-like growth factor-2 mRNA-binding protein 1 (IGF2BP1) and connective tissue growth factor (CTGF) were significantly upregulated in CRC tissues. Furthermore, the knockdown of LINC00513 inhibited CRC malignant progression in vitro. Mechanistically, LINC00513 increased CTGF mRNA stability in CRC cells by binding with IGF2BP1. As expect, the impact of LINC00513 downregulation on CRC cell proliferation and migration was declined by the overexpression of IGF2BP1 or CTGF. Taken together, LINC00513 upregulation promoted CRC malignant progression by regulating the IGF2BP1/CTGF axis. We believe that this study will help overcome CRC.