LncRNA TUSC7 regulates oxidative stress level by targeting miR-23b in colorectal cancer and thus inhibits cell proliferation, migration and invasion.

Abstract

Currently, multiple studies have shown that long non-coding ribonucleic acid TUSC7 exerts an anti-tumor effect in a variety of cancers. However, the function and underlying regulatory mechanism of lncRNA TUSC7 in CRC remain unclear. The relative fluorescence intensity of MMP9 in the cancer and in peritoneal tissues was measured by immunofluorescence. Peritoneal macrophages in BALB/c mice were sorted out using flow cytometry. The abdominal circumference of mice was measured. Moreover, the correlation between TUSC7 and miR-23b was detected by diluciferase experiment and the expressions of TUSC7 and miR-23b were analyzed using real-time fluorescence quantitative PCR. Last, the effect of TUSC7 on peritoneal macrophages was detected. The relative fluorescence intensity of MMP9 in cancer was significantly stronger than that it in the surrounding tissues. Measurements of abdominal circumference in mice showed that TUSC7 inhibited the metastasis of CRC. The results of dual luciferase assay and RT-qPCR experiment showed that TUSC7 could target and inhibit miR-23b. The expressions of P22, P47, gp91, p-STAT6, p-STAT3, IL-4 and IL-10 were remarkably increased in TUSC7 OE group compared with those in NC group, while the expressions of p-SHP2, MMP2 and MMP9 were evidently reduced in contrast with those in NC group. The viability, proliferation, migration and invasion of CRC cells could be inhibited by TUSC7 OE, which was reversed by TUSC7 KD. LncRNA TUSC7 can regulate the oxidative stress level and promote the M2 polarization of macrophages through targeting miR-23b of peritoneal macrophage in CRC, thus inhibiting cell proliferation, migration and invasion.