RESUMEN
BACKGROUND: Thyroid cancer (TC) is a common malignant tumor in the endocrine system. In recent years, the incidence and recurrence rates of TC have been raising due to increasing work pressure and irregular lifestyles. Thyroid-stimulating hormone (TSH) is a specific parameter for thyroid function screening. This study aims to explore the clinical value of TSH in regulating the progression of TC, so as to find a breakthrough for the early diagnosis and treatment of TC. AIM: To explore the value and safety of TSH in the clinical efficacy of patients with TC. METHODS: 75 patients with TC admitted to the Department of Thyroid and Breast Surgery of our hospital from September 2019 to September 2021 were selected as the observation group, and 50 healthy subjects were selected as the control group during the same period. The control group was treated with conventional thyroid replacement therapy, and the observation group was treated with TSH suppression therapy. The soluble interleukin (IL)-2 receptor (sIL-2R), IL-17, IL-35 levels, free triiodothyronine (FT3), free tetraiodothyronine (FT4), CD3+, CD4+, CD8+, CD44V6, and tumor supplied group of factor (TSGF) levels were observed in the two groups. The occurrence of adverse reactions was compared between the two groups. RESULTS: After treatment with different therapies, the levels of FT3, FT4, CD3+, and CD4+ in the observation group and the control group were higher than those before treatment, while the levels of CD8+, CD44V6, and TSGF were lower than those before treatment, and the differences were statistically significant (P < 0.05). More importantly, the levels of sIL-2R and IL-17 in the observation group were lower than those in the control group after 4 wk of treatment, while the levels of IL-35 were higher than those in the control group, and the differences were statistically significant (P < 0.05). The levels of FT3, FT4, CD3 +, and CD4 + in the observation group were higher than those in the control group, and the levels of CD8+, CD44V6, and TSGF were lower than those in the control group. There was no significant difference in the overall incidence rate of adverse reactions between the two groups (P > 0.05). CONCLUSION: TSH suppression therapy can improve the immune function of patients with TC, lower the CD44V6 and TSGF levels, and improve serum FT3 and FT4 levels. It demonstrated excellent clinical efficacy and a good safety profile.
RESUMEN
Objective: To understand the regulation of long noncoding RNA DLX6-AS1-mediated miR-26a/EZH2 axis in the growth of colorectal cancer (CRC) cells. Methods: The expression of DLX6-AS1, miR-26a, and EZH2 was detected in CRC tissues by quantitative reverse transcription-polymerase chain reaction. The CRC HT-29 cell line was selected for transfection and subjected to observe the growth by MTT and colony formation assays, cell cycle by flow cytometry, and migration and invasion by wound healing and Transwell assays, respectively. Finally, the expression of cycle- and metastasis-related proteins was detected by Western blotting. Results: DLX6-AS1 and EZH2 were increased, with a decreased miR-26a in CRC tissues, showing significant negative correlations between DLX6-AS1 and miR-26a, and between miR-26a and EZH2. CRC patients at advanced stage or with lymphatic metastasis had higher DLX6-AS1 expression. Dual-luciferase reporter gene assay uncovered the targeting correlations between DLX6-AS1 and miR-26a, or miR-26a and EZH2. After transfection of DLX6-AS1 siRNA or EZH2 siRNA, the growth and metastasis of CRC cells were suppressed, arresting the cells in G0/G1 phase, with a magnificent reduction in the ratio of cells in S phase or G2/M phase; meanwhile, Cyclin D1, Vimentin, and MMP9 expressions decreased evidently, whereas E-cadherin expression was upregulated. Changes above were fully reversed after transfection of miR-26a inhibitor, whereas si-EZH2 transfection abolished the positive role of miR-26a inhibitor on growth of CRC cells. Conclusion: Silencing DLX6-AS1 may block the malignant features of CRC cells by inhibiting the expression of EZH2 through upregulation of miR-26a. Thus, it is critical to the development and progression of CRC.
