RESUMO
The present study aimed to explore the clinical value of color Doppler ultrasound combined with serum tumor markers, including calcitonin (CT) and carcinoembryonic antigen (CEA), for the diagnosis of medullary thyroid carcinoma (MTC). A total of 39 patients with MTC (MTC group), 50 patients with papillary thyroid carcinoma (PTC) (PTC group) and 30 patients with thyroid adenoma (benign control group) were enrolled in the present study. The patients were hospitalized at the Affiliated Hospital of Qingdao University from January 2012 to December 2018 and were diagnosed through surgical procedures and pathology laboratory results. The ultrasound results, as well as serum CT and CEA results, were collected and analyzed. A significant difference was observed between the MTC and PTC groups in regards to morphology, margin, aspect ratio, calcification, internal blood flow and lymph node metastasis (all P<0.01). There was also a significant difference between the MTC and benign control group in regards to internal echo, calcification, internal blood flow and lymph node metastasis (all P<0.01). In addition, the levels of serum CT and CEA in the MTC group were significantly higher than those in the PTC and the benign control groups (both P<0.01). For patients with MTC, the levels of serum CT and CEA were significantly associated with maximum tumor diameter, lymph node metastasis and the patient state after treatment (all P<0.01). Furthermore, the sensitivities of ultrasound, serum CT and CEA for the diagnosis of MTC were 76.92, 74.36 and 68.23%, respectively. The value for the combination of the three markers (94.87%) was significantly higher compared with the sensitivity value of each separate marker (all P<0.05). In conclusion, color Doppler ultrasound combined with detecting the levels of serum tumor markers (CT and CEA) significantly improved the diagnostic efficiency for MTC, which could be useful for the clinical diagnosis and treatment of MTC.
RESUMO
BACKGROUND: Myocardial infarction occurs due to insufficient (ischemia) blood supply to heart for long time; plasmacytoma variant translocation 1 (PVT1) is a long non-coding RNAs (lncRNAs) involved in the pathogenesis of various diseases, including heart disease; However, few studies have explored its role. The present study evaluated the effects of lncRNA PVT1 on hypoxic rat H9c2 cells. METHODS: Hypoxic injury was examined by measuring cell viability and apoptosis by using cell counting kit-8 activity and flow cytometry assays. Gene expressions after hypoxia were estimated by quantitative real time polymerase chain reaction and the signaling pathway were explored by Western blot analysis. RNA immunoprecipitation and luciferase reporter assays were applied to examine the interactions among genes. Data were analyzed using t-test with one-way or two-way analysis of variance. RESULTS: The lncRNA PVT1 is up-regulated in hypoxia-stressed H9c2 cells and knockdown of PVT1 mitigates hypoxia-induced injury in H9c2 cells. PVT1 acts as a sponge for miR-135a-5p and knockdown of PVT1 attenuated the increased hypoxia-induced injury by up-regulating miR-135a-5p. Forkhead box O1 (FOXO1) was identified as a target of miR-135a-5p, and the expression was negatively regulated by miR-135a-5p. The exploration of the underlying mechanism demonstrated that knockdown of FOXO1 reversed PVT1/miR-135a-5p mediated hypoxia-induced injury in H9c2 cells. CONCLUSIONS: PVT1 plays a crucial role in hypoxia-injured H9c2 cells through sponging miR-135a-5p and then positively regulating FOXO1.
