关键词:

甲状腺癌, 长链非编码RNA, POTEM-4, miR-363-3p, 增殖, 侵袭

Abstract:

Objective　To investigate the effect of long noncoding RNA (lncRNA) POTEM-4 on the malignant biological behaviors of thyroid cancer cells and its mechanism of action. Methods　The research was from March 2024 to January 2025. The GEO database was used to analyze the expression of POTEM-4 in thyroid cancer tissues. The expression levels of POTEM-4 in thyroid cancer cell lines KTC-1, 8505C, FTC-133, and SW579 were detected by the quantitative real-time polymerase chain reaction (qPCR). POTEM-4 low-expression plasmid and negative control plasmid were transfected into the FTC-133 cells, respectively, and named as an sh-POTEM-4 group and an sh-NC group. The effects of low-expression POTEM-4 on the proliferation and invasion of the FTC-133 cells were detected by the clone formation assay and Transwell assay, respectively. The bioinformatics technology and dual luciferase reporter assay were used to verify the targeting effect of POTEM-4 and miR-363-3p in the FTC-133 cells. The effect of low-expression POTEM-4 on the expression of miR-363-3p was detected by qPCR. The effect of low-expression POTEM-4 on the expression of the NF-κB signaling pathway proteins p65, p50, tumor necrosis factor receptor-associated factor 2 (TRAF2), and tumor necrosis factor receptor-associated factor 6 (TRAF6) was detected by Western blot. The statistical methods used were t test and one-way analysis of variance. Results　POTEM-4 was highly expressed in the thyroid cancer tissues (P<0.01). The expression levels of POTEM-4 in the KTC-1, 8505C, FTC-133, and SW579 cells were significantly higher than that in the thyroid epithelial HTori-3 cells (all P<0.01). POTEM-4 low-expression plasmid could effectively reduce the expression of POTEM-4 in the FTC-133 cells (t=16.320, P<0.01). The numbers of clones formed in the sh-POTEM-4 group and the sh-NC group were 45.52±6.17 and 149.20±12.65, respectively, indicating that the low expression of POTEM-4 inhibited the FTC-133 cells' proliferation ability (t=7.367, P<0.01). The invasion numbers of FTC-133 cells in the sh-POTEM-4 group and the sh-NC group were 38.07±10.84 and 137.30±9.31, respectively, indicating that the low expression of POTEM-4 inhibited the FTC-133 cells' invasion ability (t=6.942, P<0.01). POTEM-4 could target and bind to miR-363-3p (t=7.950, P<0.01). The low expression of POTEM-4 promoted the expression of miR-363-3p in the FTC-133 cells (t=5.840, P<0.01). Compared with those in the sh-NC group, the expression levels of p65, p50, TRAF2, and TRAF6 proteins in the NF-κB signaling pathway in the FTC-133 cells in the sh-POTEM-4 group were lower (all P<0.01). Conclusions　POTEM-4 is highly expressed in thyroid cancer. The downregulation of POTEM-4 inhibits the proliferation and invasion of FTC-133 cells by regulating the miR-363-3p/NF-κB axis.

Key words:

Thyroid cancer, Long noncoding RNA, POTEM-4, MiR-363-3p, Proliferation, Invasion