Objective We aim to evaluate the technique of identifying parathyroid glands with carbon nanoparticle suspension (CNPS) in thyroid surgeries from the perspectives of degrees of declining intact parathyroid hormone (iPTH), operation time, and time of postoperative stay. Methods A total of 156 patients who underwent thyroid surgeries in General Surgical Department of Xiangya Hospital between May 2012 and May 2015 were involved in the study. A total of 78 patients were injected with CNPS during the surgery (CNPS group); the other 78 patients received normal saline (control group). Cases were classified into 3 surgical approaches: conventional partial thyroidectomy, conventional total thyroidectomy, and endoscopic partial thyroidectomy. Degrees of declining iPTH were tested to determine the severity of parathyroid injury. Operation time and postoperative hospital stay time were recorded. A P value of less than .05 was considered statistically significant. Results For levels of declining iPTH, there was no statistically significant (ss) difference in conventional thyroid surgery. In endoscopic partial thyroidectomy, it was 23.37 ± 16.20 versus 11.94 ± 11.23 pg/mL (P = .02, ss). The operation time of conventional total thyroidectomy was 210.10 ± 83.75 versus 164.84 ± 69.22 minutes (P = .03, ss), while it was 193.04 ± 75.53 versus 127.67 ± 60.06 minutes (P = .007, ss) in endoscopic thyroidectomy. Conclusions CNPS is not beneficial for protecting the function of parathyroid gland in thyroid surgery from the perspective of declining iPTH. Applying CNPS in conventional total thyroidectomy and endoscopic partial thyroidectomy will also lead to significantly prolonged operation time.

This study was aimed to identify the prognostic risk markers for thyroid papillary carcinoma (TPC) by bioinformatics. The clinical data of TPC and their microRNAs (miRNAs) and genes expression profile data were downloaded from The Cancer Genome Atlas. Elastic net-Cox's proportional regression hazards model (EN-COX) was used to identify the prognostic associated factors. The receiver operating characteristic (ROC) curve and Kaplan-Meier (KM) curve were used to screen the significant prognostic risk miRNA and genes. Then, the target genes of the obtained miRNAs were predicted followed by function prediction. Finally, the significant risk genes were performed literature mining and function analysis. Total 1046 miRNAs and 20531 genes in 484 cases samples were identified after data preprocessing. From the EN-COX model, 30 prognostic risk factors were obtained. Based on the 30 risk factors, 3 miRNAs and 11 genes were identified from the ROC and KM curves. The target genes of miRNA-342 such as B-cell CLL/lymphoma 2 (BCL2) were mainly enriched in the biological process related to cellular metabolic process and Disease Ontology terms of lymphoma. The target genes of miRNA-93 were mainly enriched in the pathway of G1 phase. Among the 11 prognostic risk genes, v-maf avian musculoaponeurotic fibrosarcoma oncogene homologue F (MAFF), SRY (sex-determining region Y)-box 4 (SOX4), and retinoic acid receptor, alpha (RARA) encoded transcription factors. Besides, RARA was enriched in four pathways. These prognostic markers such as miRNA-93, miRNA-342, RARA, MAFF, SOX4, and BCL2 may be used as targets for TPC chemoprevention.

Background Thyroid cancer is the most prevalent endocrine malignancy. Long non-coding RNA (lncRNA) MIR31HG is abnormally expressed in thyroid cancer tissues. However, the precise, critical role of MIR31HG in thyroid cancer development remains unclear. Methods MIR31HG, microRNA (miR)-761 and mitogen-activated protein kinase 1 (MAPK1) were quantified by quantitative real-time PCR (qRT-PCR) and immunoblotting. Cell viability, proliferation, apoptosis, invasion and migration abilities were evaluated by MTS, 5-Ethynyl-2′-Deoxyuridine (EdU), flow cytometry, transwell and wound-healing assays, respectively. Dual-luciferase reporter assays were used to validate the direct relationship between miR-761 and MIR31HG or MAPK1. Results MIR31HG was overexpressed in human thyroid cancer, and its overexpression predicted poor prognosis. Suppression of MIR31HG impeded cell proliferation, invasion and migration, as well as promoted cell apoptosis in vitro, and diminished the growth of xenograft tumors in vivo. Mechanistically, MIR31HG targeted and regulated miR-761. Moreover, miR-761 was identified as a molecular mediator of MIR30HG function in regulating thyroid cancer cell behaviors. MAPK1 was established as a direct and functional target of miR-761 and MAPK1 knockdown phenocopied miR-761 overexpression in impacting thyroid cancer cell behaviors. Furthermore, MIR31HG modulated MAPK1 expression by competitively binding to miR-761 via the shared binding sequence. Conclusion Our findings demonstrate that MIR31HG targets miR-761 to regulate the functional behaviors of thyroid cancer cells by upregulating MAPK1, highlighting a strong rationale for developing MIR31HG as a novel therapeutic target against thyroid cancer.

Background: Long non-coding RNAs (lncRNAs) possess pivotal roles in human cancers, including thyroid cancer. In this study, we sought to elucidate the precise action of MIR31HG in the functional behaviors of thyroid cancer cells.Methods: MIR31HG, microRNA (miR)-761 and mitogen-activated protein kinase 1 (MAPK1) were quantified by quantitative real-time PCR (qRT-PCR) or immunoblotting analysis. Cell viability, proliferation, apoptosis, invasion, and migration abilities were evaluated by MTS, 5-Ethynyl-2’-Deoxyuridine (EdU), flow cytometry, transwell and wound-healing assays, respectively. Dual-luciferase reporter assays were performed to validate the relationship between miR-761 and MIR31HG or MAPK1. Mouse xenografts were formed to assess the effect of MIR31HG on tumor growth.Results: MIR31HG expression was at high levels in thyroid cancer. Suppression of MIR31HG impeded cell proliferation, invasion, and migration, as well as promoted cell apoptosis in vitro, and diminished the growth of xenograft tumors in vivo. Mechanistically, MIR31HG targeted and regulated miR-761. Moreover, the effects of MIR31HG suppression was partly dependent on increased abundance of miR-761. MAPK1 was established as a direct and functional target of miR-761. Furthermore, MIR31HG involved the modulation of MAPK1 expression through competitively binding to miR-761 by the shared binding sequence.Conclusion: Our findings demonstrate the workings of an undescribed regulatory network, in which MIR31HG targets miR-761 to regulate MAPK1 expression, leading to the alteration of the functional behaviors of thyroid cancer cells.