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The description rate for nodules >5 mm in diameter in the radiographic interpretation reports was 30.8% (52/169 patients), of whom 17.3% (9/52 patients) were referred to the endocrinology department for further careful examination. Incidental findings in the thyroid gland were relatively common on CT images of the oral and maxillofacial region. Oral radiologists tend to focus specifically on the oral and maxillofacial region during diagnosis on oral and maxillofacial CT images, but should pay the same careful attention to observe adjacent regions, such as the thyroid gland. Copyright © 2020, Spandidos Publications.The PI3K/Akt pathway is an attractive therapeutic target in the treatment of pancreatic cancer, as it was demonstrated to be aberrantly regulated in pancreatic cancer cells. The present study aimed to investigate the therapeutic potential of the novel Akt inhibitor MK-2206 in human pancreatic cancer cell lines. Pancreatic cancer cell survival following MK-2206 treatment was assessed using the Cell Counting Kit-8 (CCK-8) assay, colony formation and determination of the apoptotic rate by flow cytometry following annexin-V-fluorescein isothiocyanate/propidium iodide staining. The effects of MK-2206 alone or in combination with gemcitabine on pancreatic cell proliferation were assessed using the CCK-8 assay. Western blotting was used to examine the effects of the two drugs on Akt protein expression. The results demonstrated that MK-2206 inhibited the proliferation and induced apoptosis of the Mia PaCa-2 and Panc-1 pancreatic cancer cell lines. In addition, CCK-8 cytotoxicity test showed that combined administration of MK-2206 with gemcitabine enhanced the cytotoxic efficacy of gemcitabine. Furthermore, a low dose of MK-2206 (1 µM) combined with gemcitabine was enough to inhibit Akt phosphorylation. Taken together, these results provided some insight into the underlying mechanism of the anticancer effects of MK-2206 on pancreatic cancer cells. Copyright © 2020, Spandidos Publications.The long non-coding (lnc)RNA cancer susceptibility 11 (CASC11) promotes gastric cancer, however its role in other diseases is unknown. The present study demonstrated upregulation of lncRNA CASC11 and microRNA (miR)-21 in hepatocellular carcinoma (HCC). Furthermore, the expression of CASC11 was positively correlated with that of miR-21 in HCC tumors. Moreover, overexpression of lncRNA CASC11 led to upregulation of miR-21 in HCC cells, whereas overexpression of miR-21 had no effect on CASC11 levels. The levels of lncRNA CASC11 and miR-21 were found to be upregulated in the plasma of patients with HCC during chemotherapy. In vitro cell experiments demonstrated upregulation of lncRNA CASC11 in HCC cells treated with carboplatin. Additionally, overexpression of lncRNA CASC11 promoted, whereas its knockdown inhibited the viability of HCC cells following carboplatin treatment. Finally, overexpression of miR-21 ameliorated the effects of lncRNA CASC11 knockdown on cell viability. Thus, these findings suggest that upregulation of lncRNA CASC11 is involved in the development of chemoresistance to carboplatin in patients with HCC, via the upregulation of miR-21. Copyright © 2020, Spandidos Publications.Differentiated thyroid cancer (DTC) is the most common thyroid cancer with a relatively high survival rate. The association between certain risk factors of distant metastasis (DM) remains uncertain. In order to assess the prognosis of patients with DTC better, the present study aimed to investigate the synergistic effects between histologic subtype, tumor size, lymph node metastasis (LNM) status and extrathyroidal extension (ETE) on the incidence of DM in DTC. Data of 96,788 patients with DTC were obtained from the Surveillance, Epidemiology and End Results database. The association between clinicopathological factors and DM was evaluated by univariate and multivariate analyses. The synergistic effects of relevant factors were determined by measuring the relative excess risk due to interaction (RERI), attributable proportion due to interaction (AP) and synergy index (SI). The results demonstrated that tumor size, LNM status, histologic subtype and ETE were independent risk factors for DM [odds ratio (OR)=2.433; P less then 0.001; OR=3.998; P less then 0.001; OR=6.266; P less then 0.001; and OR=3.873; P less then 0.001, respectively]. In addition, a significant additive synergistic effect on DM was identified between ETE and histologic subtype, ETE and LNM status, as well as between ETE and tumor size (RERI=34.097; AP=0.706; SI=3.585; RERI=6.425; AP=0.410; SI=1.781; and RERI=76.973; AP=0.864; SI=7.930, respectively). Therefore, the results of this study revealed that ETE with follicular thyroid histology, N1 stage or large tumor size may have a synergistic effect on the risk of DM in patients with DTC. These results suggested that individualized treatment may benefit patients with DTC, and when ETE coexists with one of the identified risk factors, radical treatments may be required. Copyright © 2020, Spandidos Publications.Melanoma is the most aggressive and lethal type of skin cancer. The aim of the present study was to illustrate the molecular mechanism of makorin ring finger protein 2 (MKRN2) control of melanoma cell proliferation. The expression level of MKRN2 was detected in human malignant melanoma cell lines by immunoblotting and reverse transcription-quantitative PCR. Short hairpin RNAs for MKRN2 were designed and transfected into melanoma cells, and the proliferation of these cells was detected by MTT and colony formation assays. selleck chemical The interaction of MKRN2 with P53 was detected by co-immunoprecipitation and glutathione S-transferase pulldown assays. The ubiquitination of P53 by MKRN2 was detected by in vitro ubiquitination assays. A P53-knockout cell line was generated using the CRISPR-Cas9 method. MKRN2 exhibited higher expression levels in melanoma cells, and downregulation of MKRN2 inhibited melanoma cell growth in a P53-dependent manner. MKRN2 regulated melanoma cell proliferation by interacting and ubiquitylating P53, which suggests that MKRN2 may be a potential therapeutic target for melanoma. Copyright © 2020, Spandidos Publications.
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