CTCF-induced upregulation of LINC01207 promotes gastric cancer progression via miR-1301-3p/PODXL axis.

Background: Long non coding RNAs (lncRNAs) have been validated to be involved in the complicated biological processes during tumor progression. LINC01207 has been identified as an oncogene in several cancer types. However, the function of LINC01207 and its underlying molecular mechanism in gastric cancer (GC) are poorly understood.

Methods: The expression level of LINC01207, miR-1301-3p and PODXL mRNA was detected in GC tissues and cells by RT-qPCR. The level of PODXL protein was examined by western blot. Colony formation assay, EdU assay, TUNEL assay, caspase-3 activity test and transwell assays were carried out to analyze the effect of LINC01207 on GC cell proliferation, apoptosis, migration and invasion. The interaction between RNAs was confirmed by luciferase reporter assay, RNA pull-down assay and RIP assay.

Results: LINC01207 was expressed at high level in GC tissues and cells. Silencing of LINC01207 impaired GC cell proliferation, migration and invasion but promoted cell apoptosis. Mechanistically, LINC01207 acted as a ceRNA by sponging miR-1301-3p to upregulate PODXL. Besides, miR-1301-3p silencing or PODXL overexpression could abolish the inhibitory effect of LINC01207 knockdown on GC cell growth and migration. CCCTC-binding factor (CTCF) could transcriptionally activate LINC01207 in GC cells.

Conclusions: CTCF-induced activation of LINC01207 contributes to GC progression through regulating miR-1301-3p/PODXL axis.