Nicolaisenfagan2687

Hsa_circ_0016760 was aberrantly upregulated in NSCLC, which was associated with poor prognosis of patients (P less then 0.05). Hsa_circ_0016760 silencing suppressed NSCLC cell proliferation, migration and invasion in vitro (P less then 0.01). Hsa_circ_0016760 facilitated FGF5 expression via sponging miR‑145‑5p. The miR‑145‑5p upregulation or FGF5 downregulation reversed the promoting effect of hsa_circ_0016760 on NSCLC cell proliferation, migration and invasion in vitro (P less then 0.01). In addition, hsa_circ_0016760 silencing inhibited tumor growth in vivo (P less then 0.01), and decreased Ki67 expression in xenograft tumors. In conclusion, hsa_circ_0016760 exacerbated the malignant development of NSCLC by sponging miR‑145‑5p/FGF5.MicroRNA (miRNA/mir)‑490‑3p has been defined as a tumor suppressor in different types of cancer, including breast cancer. However, miR‑490‑3p has been shown to function as a tumor suppressor and promoter in a context‑dependent manner in hepatocellular and lung cancer. Contrary to previous studies, the present study revealed that miR‑490‑3p expression was significantly higher in invasive ductal carcinoma (IDC) tissue specimens, the most common form of breast cancer, compared to tumor‑adjacent normal tissue specimens (n=20). Its expression was also higher in the more metastatic breast cancer cell line, MDA‑MB‑231, compared to the non‑metastatic breast cancer cell line, MCF7, and the moderately metastatic breast cancer cell line, MDA‑MB‑468. The expression of miR‑490‑3p was induced following transforming growth factor (TGF)‑β‑induced epithelial‑to‑mesenchymal transition (EMT) in MCF10A cells. Gain‑and loss‑of‑function assays revealed that the expression of miR‑490‑3p regulated the proliferation, colony formation, EMT, migration and invasion in vitro, but not the apoptosis of MDA‑MB‑468 and MDA‑MB‑231 cells. The knockdown of miR‑490‑3p expression in MDA‑MB‑231 cells inhibited experimental metastasis in a tumor xenograft assay. As in lung cancer, miR‑490‑3p was found to target and downregulate the expression of the tumor suppressor RNA binding protein poly r(C) binding protein 1 (PCBP1). PCBP1 protein and miR‑490‑3p expression inversely correlated in patients with ductal carcinoma in situ (DCIS; n=10; no nodal involvement) and IDC (n=10; different stages of metastatic progression) with a significantly higher miR‑490‑3p expression in patients with IDC compared to those with DCIS. The expression of miR‑490‑3p was negatively associated with both overall and disease‑free survival in the patients with breast cancer included in the present study. On the whole, the results confirm a pro‑metastatic role of miR‑490‑3p in IDC, establishing it as a biomarker for disease progression in these patients.In recent years, a number of tyrosine kinase inhibitors (TKIs) have been approved for the treatment of non‑small cell lung cancer. These novel treatments exhibit improved efficacy and toxicity when compared to conventional chemotherapy agents. TKIs are administered orally, which has the advantages of improved flexibility and convenience for the patients. CCT241533 However, challenges have arisen in the use of these novel agents. Prescribing drugs for patients with hepatic or renal function impairment poses a challenge for clinicians due to the large pharmacokinetic variability in each individual patient. Moreover, several TKIs have been shown to cause laboratory test abnormalities normally associated with hepatic or renal injury. The aim of the present review was to discuss the effects of hepatic and renal function impairment on the pharmacokinetic variability of 17 TKIs and their potential hepatotoxicity and nephrotoxicity, and to recommend dose adjustment for patients with hepatic or renal impairment.Adipocytes are the main stromal cells in the mammary microenvironment, and crosstalk between adipocytes and breast cancer cells may play a critical and important role in cancer maintenance and progression. Tumor‑induced differentiation to beige/brown adipose tissue is an important contribution to the hypermetabolic state of breast cancer. However, the effect of epithelial cell‑beige adipocyte communication on tumor progression remains unclear. To contribute to the understanding of this phenomenon, we characterized components present in conditioned media (CM) from beige adipocytes (BAs) or white adipocytes (WAs), and evaluated the effects of BA‑ and WA‑CM on both adhesion and migration of tumor (LM3, 4T1 and MC4‑L1) and non‑tumor (NMuMG) mouse mammary epithelial cell lines. Additionally, we analyzed the expression of ObR, CD44, vimentin, MMP‑9, MCT1 and LDH in tumor and non‑tumor mouse mammary epithelial cell lines incubated with BA‑CM, WA‑CM or Ctrol‑CM (control conditioned media). 3T3‑L1 preadipocytes differentiated into beige adipocytes upon PPARγ activation (rosiglitazone) displaying characteristics that morphologically resembled brown/beige adipocytes. Levels of UCP1, CIDEA, GLUT4, leptin, MCT4 and FABP4 were increased, while adiponectin, caveolin 1 and perilipin 1 levels were decreased in BAs with respect to WAs. Tumor cell lines revealed lower cell adhesion and increased cell migration after incubation with BA‑ and WA‑CM vs. Ctrol‑CM. ObR and MMP‑9 in MC4‑L1 cells were significantly increased after incubation with BA‑CM vs. WA‑ and Ctrol‑CM. In addition, MC4‑L1 and LM3 cells significantly increased their migration in the presence of BAs, suggesting that new signals originating from the crosstalk between BAs and tumor cells, could be responsible for this change. Our results indicate that beige adipocytes are able to regulate the behavior of both tumor and non‑tumor mouse mammary epithelial cells, favoring tumor progression.The Ras/Raf/MEK/MAPK signaling cascade is frequently activated in human cancer and serves a crucial role in the oncogenesis of pediatric low‑grade gliomas (PLGGs). Therefore, drugs targeting kinases among the mitogen‑activated protein kinase (MAPK) effectors of receptor tyrosine kinase signaling may represent promising candidates for the treatment of PLGGs. The aim of the present study was to elucidate the anticancer effects of the MEK inhibitor Selumetinib on two low‑grade glioma cell lines and the possible underlying effects on intracellular signal transduction. The two cancer cell lines displayed different levels of sensitivity to Selumetinib, as Res186 cells were resistant (IC50>1 µM), whereas Res259 cells were sensitive (IC50≤1 µM) to MEK inhibition. Despite the different levels of sensitivity, Selumetinib mediated the phosphorylation of AKT and MEK in both cell lines and suppressed the phosphorylated MAPK cascades. In addition, Selumetinib induced cell cycle arrest at the G0/G1 phase by downregulating the expression levels of cyclin D1 and p21 and upregulating those of p27 compared with those in the control cells. A Res259 cell line with acquired resistance to Selumetinib (Res259/R) was next established and biologically and molecularly characterized, and it was demonstrated that addition of a selective cAMP‑dependent protein kinase A inhibitor to Selumetinib overcame drug resistance in Res 259/R cells. In conclusion, the results of the present study provided three low‑grade glioma cell line models characterized by sensitivity, intrinsic and acquired resistance to Selumetinib, which may be usuful tools to study new mechanisms of chemoresistance to MEK inhibitors and to explore alternative therapeutic strategies in low‑grade gliomas for personalization of treatment.Osteosarcoma (OS) is one of the most aggressive malignancies, accompanied by an elevated incidence and a decreased rate of healing. Recently, several long non‑coding RNAs (lncRNAs) have been reported to be involved in OS progression. Although tumor suppressor candidate 7 (TUSC7) was reported as a novel lncRNA, little is known about its biological functions in OS. The present study was designed to explore whether TUSC7 was involved in the pathological development of OS using various methods, including hematoxylin and eosin staining, Cell Counting Kit‑8 assay, colony formation assay and Transwell assay. The present study revealed that TUSC7 expression was downregulated in OS tissues and cell lines compared with in normal tissues and cell lines. Functionally, the current results revealed that overexpression of TUSC7 inhibited OS cell proliferation, migration and invasion, while promoting apoptosis in vitro and in vivo. Next, the subcellular distribution of TUSC7 was examined by nuclear/cytoplasmic RNA fractionation and reverse transcription‑quantitative PCR. Mechanistic studies revealed that TUSC7 exerted its role by sponging microRNA (miR)‑181a in OS cell lines. Ras association domain family member 6 (RASSF6) was confirmed as a target gene of miR‑181a, and the expression levels of RASSF6 were negatively regulated by miR‑181a. Additionally, the results of rescue experiments suggested that overexpression of miR‑181a neutralized the inhibitory effects of TUSC7 overexpression on OS cells. Overall, the present study demonstrated that the tumor suppressor role of TUSC7 in OS progression was mediated through the miR‑181a/RASSF6 axis, which may represent a new therapeutic target for OS.Subsequently to the publication of the above paper, the authors have drawn to our attention that, owing to errors made in the compilation of the images in Fig. 6, the images shown in Fig. 6A‑C in the article were selected incorrectly (essentially, the images shown in Fig. 6A and B were alterative presentations of the same data shown in Fig. 6C). The authors were able to re‑examine the original data files and retrieve the correct data panels. The revised version of Fig. 6, featuring the corrected data panels for Fig. 6A‑C, is shown opposite. Note that the revisions made to this figure do not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this Corrigendum, and apologize to the readership for any inconvenience caused. [the original article was published in Oncology Reports 36 2017-2024, 2016; DOI 10.3892/or.2016.4995].Long non‑coding RNAs (lncRNAs) are markedly involved in cancer progression. Thus, identification of these lncRNAs can aid in the treatment of cancer. The present study focused on investigating the overall biological function, mechanism of action and clinical importance of lncRNA AC245100.4 in prostate cancer (PCa). The present study identified that AC245100.4 expression was significantly upregulated in PCa tissues and cell lines. Knockdown of AC245100.4 impaired tumor growth in an animal model. Biological function analysis indicated that AC245100.4 overexpression notably promoted cell proliferation and migration, while knockdown of AC245100.4 suppressed cell proliferation and migration. Mechanism studies focused on the competing endogenous RNA (ceRNA) network of AC245100.4. Bioinformatics predictions indicated that both AC245100.4 and retinoblastoma binding protein 5 (RBBP5) had microRNA (miR) response elements for miR‑145‑5p. This was further verified using a dual luciferase and RNA immunoprecipitation assays.