Clinical implications and immune implications features of TARS1 in breast cancer.

Background: There has been an increase in the number of women suffering from breast cancer in recent years, and discovering new therapeutic targets and efficacy predictive markers is critical for comprehensive breast cancer treatment. Methods: First, we used bioinformatics methods to analyze TARS1(encoding cytoplasmicthreonyl-tRNA synthetase) expression, prognosis, and clinicopathological characteristics in TCGA database breast cancers, and then we collected breast cancer specimens from our center for validation. TARS1 was then subjected to GSEA (Gene Set Enrichment Analysis) enrichment analysis, GO/KEGG pathway enrichment analysis, and breast cancer immune infiltration characterization. As a last step, we examined TARS1's effects on breast cancer cell behavior with cellular assays. Results: The overexpression of TARS1 has been found in several malignant tumors, including breast cancer, and has been linked to poor prognoses. Breast cancers with large primary tumors and negative hormone receptors are more likely to overexpress TARS1. Overexpression of TARS1 promotes the infiltration of T cells, such as Tregs and Th2s, while inhibiting the infiltration of NK cells and CD8+ T cells, which are anticancer cells in breast cancer. TARS1 was also found to be co-expressed with the majority of immune checkpoint-related genes, and breast cancer with TARS1 overexpression responded better to immunotherapy. By knocking down TARS1, breast cancer cells were prevented from proliferating and invading, as well as exhibiting other malignant biological properties. Conclusion: According to our study, TARS1 may be an oncogene in breast cancer and may be a biomarker of efficacy or a target of immunotherapy in breast cancer.

miR-671-5p repressed progression of papillary thyroid carcinoma via TRIM14.

The pivotal role of dysregulated miRNAs in development of papillary thyroid carcinoma has been emphasized in recent research. miR-671-5p was previously documented to function as a tumor suppressor. However, the role and mechanism of miR-671-5p in progression of papillary thyroid carcinoma remain to be further studied. Data from functional assays indicated that forced expression of miR-671-5p decreased cell viability, repressed cell proliferation, migration, and invasion in papillary thyroid carcinoma cells. In vivo study showed that miR-671-5p overexpression inhibited tumor growth, downregulated Ki67, and decreased tumor volume and weight. Tripartite motif containing 14 (TRIM14) was verified as downstream target of miR-671-5p. The expression of TRIM14 was suppressed by miR-671-5p in papillary thyroid carcinoma. Overexpression of TRIM14 increased cell viability, and promoted the proliferation, migration, and invasion of papillary thyroid carcinoma. Moreover, TRIM14 counteracted the suppressive effect of miR-671-5p overexpression on papillary thyroid carcinoma cell growth. In conclusion, miR-671-5p repressed progression of papillary thyroid carcinoma through downregulation of TRIM14, providing a promising target for therapy of papillary thyroid carcinoma.

Adenomatous hyperplastic intratracheal ectopic thyroid tissue: a case report.

Intratracheal ectopic thyroid (ITET) is a rare disease, with limited cases reported in the literature. ITET is an unusual congenital abnormality and can be easily mistaken for a respiratory illness. We present a case of a 61-year-old man with a history of slight discontinuous hemoptysis for 2 years. A tracheal mass, which appeared to be connected to the left thyroid gland, was found by chest computed tomography scan. Ultrasound revealed one suspiciously malignant, solid and hypoechoic nodule in the left thyroid gland. After the thyroid origin of the mass was confirmed by bronchoscopic biopsy, the patient underwent segmental resection and anastomosis of the trachea, together with left thyroidectomy. Histopathology of the tracheal tumor showed adenomatous hyperplastic ITET, and the orthotopic left thyroid gland showed nodular goiter with atypical adenomatous hyperplasia. Clinical suspicion is warranted in patients presenting with a tracheal tumor seemingly connected to the thyroid gland, particularly in patients who have imaging features suggestive of a malignant tumor in the orthotopic thyroid but without confirmative histopathology of malignancy before surgery.

Upregulation of miR-496 Rescues Propofol-induced Neurotoxicity by Targeting Rho Associated Coiled-coil Containing Protein Kinase 2 (ROCK2) in Prefrontal Cortical Neurons.

OBJECTIVE: Early exposure to general anesthesia in children might be a potentially highrisk factor for learning and behavioral disorders. The mechanism of neurotoxicity induced by general anesthesia was not defined. miR-496 could regulate cerebral injury, while the roles of miR- 496 in neurotoxicity were not elucidated. Therefore, we aimed to investigate the effects of miR- 496 in neurotoxicity induced by propofol. METHODS: Primary Prefrontal Cortical (PFC) neurons were isolated from neonatal rats and treated with propofol to induce neurotoxicity. Cell viability was detected by (3-(4,5-Dimethylthiazol- 2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and cell apoptosis was assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The target relationship of miR-496 and Rho Associated Coiled-Coil Containing Protein Kinase 2 (ROCK2) was explored using luciferase assays. RESULTS: Propofol decreased cell viability, promoted cell apoptosis, and decreased the expression of miR-496 in PFC neurons in a dose-dependent manner. Overexpression of miR-496 attenuated neurotoxicity induced by propofol in PFC neurons. ROCK2 was a target of miR-496, and miR-496 oppositely modulated the expression of ROCK2. Besides, propofol increased the expression of ROCK2 through inhibiting miR-496 in PFC neurons. Overexpression of miR-496 attenuated propofol- induced neurotoxicity by targeting ROCK2 in PFC neurons. CONCLUSION: miR-496 was decreased in PFC neurons treated with propofol, and overexpression of miR-496 attenuated propofol-induced neurotoxicity by targeting ROCK2. miR-496 and ROCK2 may be promising targets for protecting propofol-induced neurotoxicity.

Long-term monitoring and modeling of polychlorinated dibenzo-p-dioxins and dibenzofurans from municipal solid waste incinerators and surrounding area in northern Taiwan.

Municipal solid waste incinerators (MSWIs) have long been the major contributors of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) to ambient air in Taiwan. After stringent MSWI emission standards were introduced in 2001, the long-term continuous monitoring of flue gas and ambient air quality became necessary to ensure the effectiveness of the related control strategies. Three MSWIs and the surrounding ambient air were investigated in the current study for PCDD/F characteristics during 2006 to 2011. The average concentrations in the flue gas ranged from 0.008 ~ 0.0488 ng I-TEQ/Nm(3), which is much less than the emission standard in Taiwan (0.1 ng I-TEQ/Nm(3)) (I-TEQ is the abbreviation of International Toxic Equivalent). This led to extremely low levels in the ambient air, 0.0255 pg I-TEQ/Nm(3), much less than the levels seen in most urban areas around the world. Additionally, the results obtained using the Industrial Source Complex Short-Term Dispersion Model (ISCST3) indicate that the PCDD/F contributions from the three MSWIs to the ambient air were only in the range from 0.164 ~ 0.723 %. Principal component analysis (PCA) showed that the PCDD/Fs in the air samples had very similar characteristics to those from mobile sources. The results thus show that stringent regulations have been an effective control strategy, especially for urban areas, such as Taipei City.