Objective:To elucidate the effect of long non-coding RNA (lncRNA) H19 on the apoptosis of thyroid cancer cells and its mechanism.Methods:Thyroid cancer FTC133 cells were cultured in vitro, treated and divided into lncRNA H19 small interfering RNA (siRNA) group and negative control group, and Flow cytometry was used to detect cell apoptosis; real-time quantitative polymerase chain reaction (Real-time PCR) and Western blotting were used to detect the mRNA and protein expression levels of apoptosis-related molecules B cell lymphoma/leukemia-2 (bcl-2), bcl-2 associated X protein (bax) and cysteinyl aspartate-specific protease (Caspase)-3; Western blotting was used to detect the relationship between the effect of lncRNA H19 on the apoptosis of thyroid cancer cells and the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt) signaling pathway, mean between two groups were compared using t-test. Results:The apoptosis rate in experimental group was higher than that in control group [(25.06±0.32)% compare (7.85±0.24)%, t=96.207, P<0.01). In experimental group, the bcl-2 mRNA expression was lower than that in control group (0.43±0.05 compare 1.02±0.06, t=3.521, P<0.01), the bax mRNA expression was higher than that in control group (1.64±0.09 compare 1.01±0.07, t=5.261, P<0.01)] and the Caspase-3 mRNA expression was higher than that in control group (1.86±0.12 compare 1.03±0.09, t=7.342, P<0.01). In experimental group, the expression of bax was higher than that in control group (0.924±0.081 compare 0.408±0.124, t=5.147, P<0.01) and Caspase-3 was higher than that in control group (0.826±0.077 compare 0.345±0.113, t=5.109, P<0.01), while the expression of bcl-2 protein was lower than that in control group (0.203±0.067 compare 0.885±0.090, t=7.368, P<0.01). In experimental group, the expression of p-PI3K was lower than that in control group (0.189±0.021 compare 0.798±0.081, t=7.873, P<0.01) and p-Akt was lower than that in control group (0.208±0.038 compare 0.822±0.089, t=7.423, P<0.01) . Conclusion:Knockdown of lncRNA H19 can promote apoptosis of thyroid cancer cells by regulating PI3K/Akt signaling pathway, which plays an important role in the occurrence and development of thyroid cancer.

Objective:To observe the effect of sorafenib on ferroptosis in thyroid cancer TPC-1 cells, and to provide a new strategy for the treatment of thyroid cancer.Methods:Thyroid cancer TPC-1 cells were cultured in vitro, treated and divided into sorafenib group and negative control group, and cell counting kit-8 (CCK-8) assay was used to detect cell viability; Dichlorofluorescein (DCFH-DA) probe was used to detect reactive oxygen species (ROS) production; Western blotting experiment was used to detect the protein expression levels of ACSL4, SLC7A11 and GPX4; Malondialdehyde (MDA) kit was used to detect the content of MDA in thyroid cancer cells. Analysis of variance was used for the mean comparison between multiple groups, and t-test was used for the comparison between the two groups. Results:The cell absorbance value of sorafenib intervention group (1.29±0.17) was significantly lower than that of control group (1.86±0.23, t=2.695, P<0.05); The fluorescence intensity of ROS in TPC-1 cells treated with sorafenib (1.833±0.293) was significantly higher than that in the control group (0.825±0.186, t=2.801, P<0.05); Western blotting experiments showed that the expression level of ACSl4 protein (0.954±0.091) after sorafenib intervention was higher than that in the control group (0.442±0.132, t=5.314, P<0.05), and the protein expression level of SLC7A11 (0.293±0.087) was significantly lower than that in the control group (0.897±0.098, t=7.916, P<0.05), the protein expression level of GPx4 (0.325±0.051) was also lower than that of control cells (0.893±0.069, t=9.325, P<0.05). The results of MDA detection showed that the expression level of MDA in sorafenib intervention group (30.661±3.192) was significantly higher than that in control group (19.285±1.406, t=5.901, P<0.05). Conclusion:Sorafenib can promote the ferroptosis process of thyroid cancer cells and accelerate the death of thyroid cancer cells.

Objective:To observe the effect of microRNA (miRNA, miR)-630 in thyroid cancer (TC) cells on the expression of the epithelial-mesenchymal transition (EMT) marker Slug, and its influence on cell invasion.Methods:A total of 40 cases of papillary TC and their para-cancerous specimens were collected from the Department of General Surgery of Hebei Medical University from January 2018 to December 2019. The real-time quantitative polymerase chain reaction (Real-time PCR) was used to detect the expression level of miR-630 in TC and its adjacent tissues. After transfecting miR-630 mimics into human TC cell line TPC-1, the expression level of Slug gene was detected by Real-time PCR, and the regulatory effect of miR-630 on Slug gene was observed by double luciferase reporter gene assay. The overexpression Slug plasmid and miR-630 mimics were co-transfected into TPC-1 cells. Transwell cell invasion assay was used to observe the effect of miR-630 and Slug expression on the invasion of TC cells.Results:Real-time PCR results showed that the expression level of miR-630 in papillary TC tissues was (1.13±0.07), significantly lower than that in adjacent tissues (5.33±0.08) with the difference being statistically significant ( t=15.472, P<0.05), and miR-630 mimics up-regulated miR-630 in papillary TC cells, and Slug mRNA expression level (0.48±0.09) was also significantly lower than that in control group (1.03±0.07, t=7.132, P<0.05). The luciferase activity of miR-630 mimics and Slug 3′wild-type co-transfection group was significantly lower than that of control group (0.38±0.03, t=13.021, P<0.05). However, in the co-transfected group of miR-630 mimics and Slug 3′mutant, the luciferase activity did not change significantly (1.08±0.02 vs. 1.02±0.03, t=1.122, P>0.05). The number of invasive cells in mir-630 mimics group (241.3±42.4) was significantly less than that in control group (467.5±51.7, t=3.214, P<0.05). Compared with the negative control group (418.3±31.2), the invasion ability of the cells co-transfected with miR-630 mimics and Slug overexpression plasmids (411.6±28.3) was not statistically different ( t=1.131, P>0.05). Conclusion:miR-630 can inhibit the invasion ability of TC cells by targeting Slug.