MicroRNA-150-5p affects cell proliferation, apoptosis, and EMT by regulation of the BRAFV600E mutation in papillary thyroid cancer cells.

Papillary thyroid cancer (PTC) is the most common endocrine malignancy. Studies have confirmed an association between microRNA (miRNA) and the BRAFV600E mutation in various cellular biological processes of PTC. This study aimed to clarify the potential relationship between miR-150-5p and the BRAFV600E mutation in PTC. Human PTC cell lines B-CPAP and TPC-1 were transfected with the miR-150-5p mimic, an inhibitor, and the corresponding controls. Then, cell proliferation, viability, and apoptosis were detected by bromodeoxyuridine, trypan blue exclusion, and flow cytometry assays. The expressions of the main factors of cell cycle, epithelial mesenchymal transition (EMT), and DNA mismatch repair were examined by Western blot analysis and a real-time quantitative polymerase chain reaction. Additionally, pc-BRAFV600E was transfected into B-CPAP and TPC-1 cells to determine the relationship between miR-150-5p and BRAFV600E . In addition, the methyl ethyl ketone (MEK)/extracellular signal-regulated kinase (ERK) signal pathway was examined using Western blot analysis. Overexpression of miR-150-5p promoted cell proliferation and viability, inhibited apoptosis, and upregulated cell cycle factor expressions at 50 passages of B-CPAP and TPC-1 cells after transfection. Overexpression of miR-150-5p led to an obvious decrease in E-cadherin expression, but enhanced N-cadherin, Slug and Vimentin, ZEB1, and Snail expression. Moreover, overexpression of miR-150-5p markedly suppressed POLD3, MSH2, and MSH3 expression. Furthermore, BRAFV600E overexpression increased the expression level of miR-150-5p in TPC cells, and overexpression of telomerase reverse transcriptase further enhanced the promoting effect of BRAFV600E on miR-150-5p expression in B-CPAP and TPC-1 cells. Finally, BRAFV600E overexpression activated the MEK/ERK signal pathway in B-CPAP and TPC-1 cells. These data indicated that miR-150-5p promoted cell proliferation, suppressed apoptosis, and accelerated the EMT process by regulation of the BRAFV600E mutation. Our findings will help elucidate the pathogenesis of PTC and identify biomarkers.

Changes and prognostic value of serum vascular endothelial growth factor in patients with differentiated thyroid cancer.

OBJECTIVE: To evaluate the changes and the prognostic value of serum vascular endothelial growth factor (VEGF) in patients with differentiated thyroid cancer (DTC). SUBJECTS AND METHODS: A total of 79 patients with DTC and 30 healthy individuals were divided into four groups: (1) a healthy control group (n = 30); (2) DTC without recurrence (n = 35; 23 papillary, 12 follicular); (3) DTC with local recurrence (n = 24; 15 papillary, 9 follicular), and (4) DTC with lung metastasis (n = 20; 13 papillary, 7 follicular). Serum VEGF and thyroglobulin levels were measured in all patients. RESULTS: Serum levels of VEGF were significantly higher in the lung metastasis group than in the other three groups (p < 0.05). Serum thyroglobulin concentration positively correlated with VEGF expression (r = 0.8678, p < 0.001) in patients with thyroid cancer recurrence. Multivariate Cox regression analysis showed that clinical staging (OR = 1.851, 95% CI 1.04-3.47; p = 0.038), noncompliance with postoperative thyroxin replacement therapy (OR = 1.935, 95% CI 1.03-3.65; p = 0.042) and postoperative levels of thyroglobulin (OR = 1.892, 95% CI 1.01-3.56, p = 0.032) were independent predictors for thyroid cancer recurrence. Every additional 100 ng/l of serum VEGF levels increased the risk of thyroid cancer recurrence by 20.3%; but this did not reach statistical significance (OR = 1.203, 95% CI 0.95-1.52; p = 0.125). CONCLUSIONS: Serum VEGF increased in patients with recurrent thyroid cancer following surgical therapies. The predictive value of serum VEGF requires further investigation.

[Curative effect of stereotactic 186Re endocavitary irradiation on cystic craniopharyngioma].

OBJECTIVE: To evaluate the treatment results of stereotactic (186)Re intracavitary irradiation in the patients with craniopharyngioma. METHODS: Nineteen patients were treated with stereotactic (186)Re intracavitary irradiation, including 12 males and 7 females (average age, 37.2 years). Among them 12 patients had a solitary cyst, whereas 7 patients with mixed structure (e.g., a large cyst with a small solid portion). The mean volume of the cystic portion of the tumor before irradiation was 8390 mm(3). RESULTS: The patients were followed up for 6 months to 3 years. The retraction of the cyst was complete in 7 patients, cyst volume decreased more than 50% in 5 patients and less than 50% in 7 cases. Among the 8 patients with visual acuity deficit before irradiation, 5 were improved. No hypopituitarism occurred in patients with normal pituitary function before treatment. One of the 4 patients with hypopituitarism was improved, 3 of the 5 patients with diabetes insipidus was improved. CONCLUSION: Stereotactic (186)Re endocavitary irradiation for the treatment of cystic craniopharyngioma is a safe and effective procedure.

lncRNA CCAT1 promotes cell proliferation, migration, and invasion by down-regulation of miR-143 in FTC-133 thyroid carcinoma cell line.

Thyroid cancer is a common malignant tumor. Long non-coding RNA colon cancer-associated transcript 1 (lncRNA CCAT1) is highly expressed in many cancers; however, the molecular mechanism of CCAT1 in thyroid cancer remains unclear. Hence, this study aimed to investigate the effect of CCAT1 on human thyroid cancer cell line FTC-133. FTC-133 cells were transfected with CCAT1 expressing vector, CCAT1 shRNA, miR-143 mimic, and miR-143 inhibitor, respectively. After different treatments, cell viability, proliferation, migration, invasion, and apoptosis were measured. Moreover, the regulatory relationship of CCAT1 and miR-143, as well as miR-143 and VEGF were tested using dual-luciferase reporter assay. The relative expressions of CCAT1, miR-143, and VEGF were tested by qRT-PCR. The expressions of apoptosis-related factors and corresponding proteins in PI3K/AKT and MAPK pathways were analyzed using western blot analysis. The results suggested that CCAT1 was up-regulated in the FTC-133 cells. CCAT1 suppression decreased FTC-133 cell viability, proliferation, migration, invasion, and miR-143 expression, while it increased apoptosis and VEGF expression. CCAT1 might act as a competing endogenous RNA (ceRNA) for miR-143. Moreover, CCAT1 activated PI3K/AKT and MAPK signaling pathways through inhibition of miR-143. This study demonstrated that CCAT1 exhibited pro-proliferative and pro-metastasis functions on FTC-133 cells and activated PI3K/AKT and MAPK signaling pathways via down-regulation of miR-143. These findings will provide a possible target for clinical treatment of thyroid cancer.

lncRNA CCAT1 promotes cell proliferation, migration, and invasion by down-regulation of miR-143 in FTC-133 thyroid carcinoma cell line

Thyroid cancer is a common malignant tumor. Long non-coding RNA colon cancer-associated transcript 1 (lncRNA CCAT1) is highly expressed in many cancers; however, the molecular mechanism of CCAT1 in thyroid cancer remains unclear. Hence, this study aimed to investigate the effect of CCAT1 on human thyroid cancer cell line FTC-133. FTC-133 cells were transfected with CCAT1 expressing vector, CCAT1 shRNA, miR-143 mimic, and miR-143 inhibitor, respectively. After different treatments, cell viability, proliferation, migration, invasion, and apoptosis were measured. Moreover, the regulatory relationship of CCAT1 and miR-143, as well as miR-143 and VEGF were tested using dual-luciferase reporter assay. The relative expressions of CCAT1, miR-143, and VEGF were tested by qRT-PCR. The expressions of apoptosis-related factors and corresponding proteins in PI3K/AKT and MAPK pathways were analyzed using western blot analysis. The results suggested that CCAT1 was up-regulated in the FTC-133 cells. CCAT1 suppression decreased FTC-133 cell viability, proliferation, migration, invasion, and miR-143 expression, while it increased apoptosis and VEGF expression. CCAT1 might act as a competing endogenous RNA (ceRNA) for miR-143. Moreover, CCAT1 activated PI3K/AKT and MAPK signaling pathways through inhibition of miR-143. This study demonstrated that CCAT1 exhibited pro-proliferative and pro-metastasis functions on FTC-133 cells and activated PI3K/AKT and MAPK signaling pathways via down-regulation of miR-143. These findings will provide a possible target for clinical treatment of thyroid cancer.

Risk factors for persistent atrial fibrillation following successful hyperthyroidism treatment with radioiodine therapy.

OBJECTIVE: To investigate the predicting factors for persistent atrial fibrillation (AF) following radioiodine therapy for hyperthyroidism. METHODS: Standard 12-lead ECG and 24-h Holter monitoring were performed in 94 patients (38 males, mean age 46.1±8.2 years) with persistent AF following radioiodine therapy for hyperthyroidism. Left ventricular (LV) function was assessed with two-dimensional echocardiography. RESULTS: Euthyroidism or hypothyroidism was achieved in 81% and 19% of the patients, respectively, after radioiodine therapy. At the end of follow-up (1.6±1.3 years), LV ejection fraction in the 52 patients with LV dysfunction was increased from 39.3±3.3% to 59.0±5.5% (p<0.01). In the 38 patients with pre-treatment paroxysmal AF, no AF was documented during the follow-up. In the 45 patients with pre-treatment persistent AF, AF was found in 27 (60%) during the follow-up. Multivariate logistic regression analysis showed that more than 55 years old in age (RR 2.76, 95% CI: 1.16-8.79, p<0.01), duration of hyperthyroidism (RR 3.08, 95% CI: 1.22-11.41, p<0.01) and duration of pre-treatment atrial fibrillation (RR 2.96, 95% CI: 1.31-7.68, p<0.01) were independent predictors for persistent AF following radioiodine therapy. CONCLUSION: Older age, duration of hyperthyroidism and pre-treatment duration of AF are risk factors for persistent AF following radioiodine therapy.