Tongue squamous cell carcinoma (TSCC) is the most common type of oral cancer and is an aggressive head and neck malignancy. Increasing studies have demonstrated that long noncoding RNAs (lncRNAs) play important roles in diverse biological cell processes, such as cell development, fate decisions, cell differentiation, cell migration, and invasion. In our study, we showed that long noncoding RNA colorectal neoplasia differentially expressed (CRNDE) expression was upregulated in TSCC cell lines and tissues. Overexpression of CRNDE increased the TSCC cell proliferation, cell cycle, and cell invasion. Moreover, ectopic expression of CRNDE inhibited the miR‐384 expression in the SCC1 cell and increased the Kirsten Ras (KRAS), cell division cycle 42, and insulin receptor substrate 1 expression, which were the direct target genes of miR‐384. We demonstrated that the miR‐384 expression was downregulated in the TSCC samples compared with the paired adjacent nontumor samples. The expression of CRNDE was negatively correlated with the expression of miR‐384 in the TSCC samples. Overexpression of miR‐384 suppressed TSCC cell proliferation, cell cycle, and invasion. Furthermore, we demonstrated that CRNDE promoted TSCC cell proliferation and invasion through inhibiting miR‐384 expression. These results suggested that CRNDE acts as an oncogene in the development of TSCC, which partially occurs through inhibiting miR‐384 expression.
In this study, we aimed to develop and validate nomograms for predicting long-term overall survival (OS) and cancer-specific survival (CSS) in major salivary gland cancer (MSGC) patients. These nomograms were developed using a retrospective cohort (N=4218) from the Surveillance, Epidemiology, and End Results (SEER) database, and externally validated using an independent data cohort (N=244). We used univariate, and multivariate analyses, and cumulative incidence function to select the independent prognostic factors of OS and CSS. Index of concordance (c-index) and calibration plots were used to estimate the nomograms’ predictive accuracy. The median follow-up period was 34 months (1–119 months). Of 4218 MSGC patients, 1320 (31.3%) died by the end of the follow-up; of these 1320 patients, 883 (20.9%) died of MSGC. The OS nomogram, which had a c-index of 0.817, was based on nine variables: age, sex, tumor site, tumor grade, surgery performed, radiation therapy and TNM classifications. The CSS nomogram, which had a c-index of 0.829, was based on the same nine variables plus race. External validation c-indexes were 0.829 and 0.807 for OS and CSS, respectively. Based on SEER database, we have developed nomograms predicting five- and eight-years OS and CSS for MSGC patients with perfect accuracy. These nomograms will help clinicians customize treatment and monitoring strategies in MSGC patients.
Background: Salivary adenoid cystic carcinoma (SACC) is one of the most common malignant cancers of the salivary gland, and 32.4-72.0% of SACC cases exhibit neural invasion (NI), however, the molecular mechanism underlying the high invasion potential of SACC remains unclear. Methods: The present study investigated the role of epidermal growth factor receptor (EGFR) in the AKT inhibition- or mitogen-activated protein kinase kinase (MEK)-induced NI and epithelial-mesenchymal transition (EMT) in SACC cells using EGFR, PI3K and MEK inhibitors. SACC 83 cell viability was assessed using an MTT assay, and a wound healing assay was performed to evaluate cell migration. Immunohistochemical staining with streptavidin peroxidase was used to detect the positive expression rate of EMT, AKT, phosphorylated (p)-AKT, ERK and p-ERK proteins. The impact of EGFR, PI3K and MEK inhibitors on tumor growth and NI was examined in a xenograft model in nude mice. Results: EGF and EGFR are effective in increasing cell viability, migration and invasion. SACC metastasis is affected by the PI3K/AKT and MEK/ERK pathways, both of which are initiated by EGF/EGFR. The EMT and NI are regulated by the EGF/EGFR, PI3K/AKT and MEK/ERK pathways. The present findings demonstrate the importance of suppressed EGFR/AKT/MEK signaling in NI in SACC by neural-tumor co-culture in vitro. Furthermore, our preclinical experiment provides solid evidence that injection of EGFR, PI3K and MEK inhibitors obviously suppressed the tumor growth and NI of SACC cells in nude mice. Conclusion: It was identified that inhibitors of EGFR, PI3K/AKT or MEK/ERK suppressed the proliferation, migration and NI of SACC-83 cells via downregulation of the PI3K/AKT or MEK/ERK pathways. It was also demonstrated that inhibition of EGFR abolishes EMT in SACC by inhibiting the signaling of PI3K/AKT and MEK/ERK. The present results suggest the potential effectiveness of targeting multiple oncogenes associated with downstream pathways of EGF/EGFR, as well as potential therapeutic targets to limit NI in SACC by PI3K/AKT or MEK/ERK inhibition.
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