Objective:To observe the regulatory effect of microRNA (miR)-221 on phosphatase and tensin homologue deleted on chromosome 10 (PTEN) gene in thyroid cancer (TC) cells and its influence on the invasion ability of TC cells.Methods:A total of 30 cases of TC papillary carcinoma tissue specimens were collected from April 2018 to December 2019 in the General Surgery Department of the Second Hospital of Hebei Medical University. The expression of miR-221 and PTEN gene was detected in TC and adjacent tissues by Real-time PCR. After transfecting miR-221 mimic into human TC cell line TPC-1, dual luciferase reporter gene assay was used to observe the regulation of miR-221 on PTEN gene. After TPC-1 cells were transfected with PTEN overexpression plasmids combined with miR-221 mimics, the effects of miR-221 and PTEN expression on the invasion of TC cells were examined by Transwell assay. T test was used for comparison between two groups. Results:Real-time PCR results indicated that miR-221 expression (4.12±0.09) was significantly higher in TC tissues than that in adjacent tissues (1.32±0.06, t=18.320, P<0.01). miR-221 was negatively correlated with PTEN mRNA expression in TC ( r=-0.429, P<0.05). The relative luciferase activity of PTEN in the miR-221 mimic transfection group (0.35±0.04) was significantly lower than that in the control group (1.05±0.03, t=12.120, P<0.05). Moreover, the number of invasive cells in the miR-221 mimic group (352.1±37.2) was significantly higher than that in the control group (189.7±23.1, t=3.135, P<0.01). In addition, after co-transfection with PTEN overexpression plasmids, compared with the negative control group (168.7±17.6), the number of invasive cells in TC (165.0±16.2) had no significant difference ( t=1.060, P>0.05). Conclusion:MiR-221 can promote the invasion ability of TC cells, and its mechanism may be related to the targeted inhibition of PTEN expression.

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.

Purpose: Recent studies have shown that long non-coding RNA (lncRNA) play an important role in cancer metabolism and development. The lncRNA small nucleolar RNA host gene 7 (SNHG7) was reported to be upregulated in colorectal cancer and contribute to its progression. In the current study, we investigated the role of lncRNA-SNHG7 in breast cancer and explored the underlying mechanism. Methods: We monitored the expression of lncRNA-SNHG7 in breast cancer tissues and breast cancer cell lines. We evaluated the effects of lncRNA-SNHG7 on cell proliferation and glycolysis in breast cancer cells by knocking down or overexpressing lncRNA-SNHG7. We searched for the potential microRNA (miRNA) target of lncRNA-SNHG7 and evaluated the effects of the target miRNA on glycolysis. We evaluated the potential regulation of lncRNA-SNHG7 by c-Myc. Results: LncRNA-SNHG7 was up-regulated in both breast cancer tissues and breast cancer cell lines. Knocking down lncRNA-SNHG7 inhibited breast cancer cell proliferation while overexpressing lncRNA-SNHG7 enhanced cell proliferation. Knocking down lncRNA-SNHG7 resulted in decreased expression of lactate dehydrogenase A (LDHA) and decreased glycolysis. LncRNA-SNHG7 targeted miR-34a-5p to regulate LDHA expression and glycolysis. c-Myc bound to promoter of lncRNA-SNHG7 and positively regulated lncRNA-SNHG7 expression. Conclusion: We demonstrated that c-Myc regulated glycolysis through the lncRNA-SNHG7/miR-34a-5p/LDHA axis in breast cancer cells.