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Radiomic Phenotypes Separate Atypical Teratoid/Rhabdoid Tumors via Medulloblastoma.
ROC curve analysis proved the good performance of the model. EGFR targets The Kaplan-Meier survival curve showed that the mortality in high-risk group was significantly higher. The survival analysis results of each lncRNA were also consistent with the prediction in Cox regression. Conclusions Our results suggested that the 11-lncRNA risk scoring model may provide a new insight for predicting prognosis of LUSC patients.Objective Non-small cell lung cancer (NSCLC) accounts for the majority of lung cancer, with an unfavorable prognosis of 5-year survival rates. It is of great clinical significance to further search for more efficacious and novel targets for diagnosis and therapeutic strategies. This study aimed at clarifying the role of long non-coding RNA (lncRNA) NORAD in proliferation, invasion and migration and tumor growth of NSCLC. Materials and methods In this study, mRNA levels of lncRNA NORAD were examined by RT-PCR. CCK-8 assay was applied to test cell viability. Furthermore, wound healing assay and transwell assay were performed to detect the migration and invasion of A549 cells, respectively. Immunohistochemistry was applied to assess the levels of CXC chemokine receptor (CXCR) 4 and CXC chemokine ligand (CXCL) 12. Mice models of NSCLC in vivo were exploited to further examine the potential role of NORAD in tumor growth. Key proteins related to Ras homolog gene family member A (RhoA) GTPase/Rho-associated kinase (RhoA/ROCK) pathway were determined by Western blot. Results NORAD has elevated the levels in NSCLC tissues and cells. NORAD interference dramatically inhibited tumor growth and suppressed A549 cell proliferation, migration and invasion by downregulating CXCR4 and CXCL12 expression. RhoA/ROCK signaling pathway was activated in NSCLC. Conclusions This study revealed that the downregulation of lncRNA NORAD could slow down the progression of NSCLC by regulating CXCR4 and RhoA/ROCK signaling pathway.Objective CSE1L (human chromosomal segregation 1-like) is reported to be able to affect cell apoptosis, invasiveness, and migration. The purpose of this study was to uncover the regulatory effects of CSE1L on cell phenotypes of oral cancer and the underlying mechanism. Materials and methods CSE1L levels in oral cancer cells were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot. CSE1L overexpression and knockdown models were constructed in CAL-27 and HN6 cells, respectively. Changes in proliferative and migratory abilities in oral cancer cells affected by CSE1L and microphthalmia-associated transcription factor (MITF) were assessed by cell counting kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU) and wound healing assay. Meanwhile, potential influences of CSE1L and MITF on relative levels of E-cadherin and Vimentin in oral cancer cells were detected. Finally, regulatory effects of CSE1L and MITF on the Akt/mTOR pathway were evaluated by detecting expression levels of p-Akt, Akt, p-mTOR, and mTOR. Results CSE1L was upregulated in oral cancer cells. Knockdown of CSE1L in HN6 cells attenuated proliferative and migratory abilities, as well as downregulated Vimentin and upregulated E-cadherin. Overexpression of CSE1L in CAL-27 cells yielded the opposite results. MIFT level was positively regulated by CSE1L. Overexpression of MITF partially reversed regulatory effects of CSE1L on proliferative ability of oral cancer cells. Moreover, silence of CSE1L suppressed the Akt/mTOR pathway, which was reversed by overexpression of MITF. Conclusions CSE1L promotes the proliferative and migratory abilities in oral cancer cells by positively regulating MITF, thus activating the Akt/mTOR pathway.Objective This study was designed to investigate the expression characteristics of CSN6 in oral squamous cell carcinoma (OSCC), and to further explore the mechanism of how it promotes the malignant progression of this cancer. Patients and methods The expressions of CSN6 and TIMP-2 in tumor tissue samples and adjacent normal ones collected from 36 OSCC patients were detected via quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), and the interplay between their expression levels and the clinical indicators or prognosis of OSCC patients was analyzed as well. Meanwhile, the expressions of CSN6 and TIMP-2 in OSCC cell lines were further verified via qRT-PCR. In addition, CSN6 overexpression and knockdown models were constructed using lentivirus in OSCC cell lines, CAL-27, and Tca8113. At the same time, transwell and cell wound healing assays were conducted to uncover the impact of CSN6 on the function of OSCC cells. Finally, the potential mechanism was explored using Luciferase reporter gene and recovery t CSN6 was remarkably upregulated both in OSCC tissues and cell lines, which is remarkably relevant to the incidence of lymph node or distant metastasis and poor prognosis of OSCC patients. Additionally, we verified that CSN6 may promote OSCC malignant progression by regulating TIMP-2.Objective Identification of novel and reliable biomarkers is crucial for the early detection and prognosis prediction of esophageal squamous cell carcinoma (ESCC). In this study, we aimed to explore the potential clinical significance of serum exosomal miR-182 in ESCC. Patients and methods A total of 125 patients with ESCC and 60 healthy volunteers were enrolled in this study. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to detect the serum exosomal miR-182 level. Then, the associations between serum exosomal miR-182 levels and clinicopathological features, as well as clinical outcome were further investigated. Results Serum exosomal miR-182 levels were significantly higher in pre-operative ESCC patients than in normal controls and post-operative ESCC patients. In addition, the receiver operating characteristic (ROC) curve analysis showed that the serum exosomal miR-182 could well differentiate ESCC patients from the healthy controls. Moreover, high serum exosomal miR-182 expression was strongly associated with worse clinical parameters including differentiation, lymph node metastasis, and TNM stage. ESCC patients in the high serum exosomal miR-182 group had significantly shorter overall survival and relapse free survival than those in the low serum exosomal miR-182 group. Furthermore, serum exosomal miR-182 was an independent prognostic indicator for ESCC. Conclusions Collectively, serum exosomal miR-182 might serve as a promising biomarker for predicting the unfavorable prognosis of ESCC.
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