Our findings reveal that ASA inhibits the proliferation and promotes apoptosis in the human colon cancer cell line SW480. Down-regulation of Bcl2 expression might represent a potential mechanism by which ASA induces apoptosis in this COX-2 negative colon cancer cell line. Our results also suggest that ASA decreases the invasive potential of these colon cancer cells. Decreased CEA content and CD44v6 expression and elevated nm23 expression may contribute to the effect of ASA on invasive potential of SW480 colon cancer cells.

Multidrug resistance (MDR) is a major clinical obstacle in the successful treatment of patients with metastatic nasopharyngeal carcinoma (NPC). Results from previous studies suggest that microRNAs (miRNA) may be involved in promoting MDR in multiple cancer types. However, the role of miR‑125b in modulating the MDR of NPC is elusive. In the present study, miR‑125b expression in cisplatin (DDP) ‑resistant CNE2 cells (CNE2/DDP) was compared with parental counterparts, using reverse transcription‑quantitative polymerase chain reaction. A >3‑fold reduction in miR‑125b expression levels was observed in CNE2/DDP cells compared with parental CNE2 cells. Ectopic expression of miR‑125b by transfecting CNE2/DDP cells with miR-125b mimics, increased DDP‑induced cytotoxicity, apoptosis and chemosensitivity. By contrast, suppression of miR-125b by transfecting CNE2 cells with miR‑125b inhibitors, reduced DDP‑induced cytotoxicity and apoptosis, and facilitated cisplatin resistance. The results suggest that miR‑125b may regulate the sensitivity of NPC cells to DDP by modulating the expression levels of antiapoptotic factor B-cell CLL/lymphoma 2. Collectively, the results of the present study highlight miR‑125b as a potential therapeutic target for reversing MDR in NPC.

Background. Long noncoding RNAs (lncRNAs) play important roles in the tumorigenesis and progression of various cancer types; however, their roles in the development of invasive pituitary adenomas (PAs) remain to be investigated. Methods. lncRNA microarray analysis was performed for three invasive and three noninvasive PAs. Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed, and coexpression networks between lncRNA and mRNA were constructed. Furthermore, three differentially expressed lncRNAs were selected for validation in PA samples by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). The diagnostic values of these three lncRNAs were further evaluated by a receiver operating characteristic (ROC) curve analysis. Results. A total of 8872 lncRNAs were identified in invasive and paired noninvasive PAs via lncRNA microarray analysis. Among these, the differentially expressed lncRNAs included 81 that were upregulated and 165 that were downregulated. GO enrichment and KEGG pathway analysis showed that these differentially expressed lncRNAs were associated with the posttranslational modifications of proteins. Furthermore, we performed target gene prediction and coexpression analysis. The interrelationships between the significantly differentially expressed lncRNAs and mRNAs were identified. Additionally, three differentially expressed lncRNAs were selected for validation in 41 PA samples by qRT-PCR. The expression levels of FAM182B, LOC105371531, and LOC105375785 were significantly lower in the invasive PAs than in the noninvasive PAs ( P < 0.05 ). These results were consistent with the microarray data. ROC curve analysis suggested that the expression levels of FAM182B and LOC105375785 could be used to distinguish invasive PAs from noninvasive PAs. Conclusion. Our findings demonstrated the expression patterns of lncRNAs in invasive PAs. FAM182B and LOC105375785 may be involved in the invasiveness of PAs and serve as new candidate biomarkers for the diagnosis of invasive PAs.

No abstract

Cisplatin-based regimens are commonly used for the treatment of nasopharyngeal carcinoma (NPC) in patients who receive concurrent chemoradiotherapy. The sensitivity of NPC cells to cisplatin is closely associated with the efficacy of radiation therapy. In this study, we established two radioresistant NPC cell lines, HONE1-IR and CNE2-IR, and found that both cell lines showed reduced sensitivity to cisplatin. RNA-sequence analysis showed that SLC1A6 was upregulated in both HONE1-IR and CNE2-IR cell lines. Downregulation of SLC1A6 enhanced cisplatin sensitivity in these two radioresistant NPC cell lines. It was also found that the expression of SLC1A6 was induced during radiation treatment and correlated with poor prognosis of NPC patients. Notably, we observed that upregulation of SLC1A6 led to elevating level of glutamate and the expression of drug-resistant genes, resulted in reduced cisplatin sensitivity. Our findings provide a rationale for developing a novel therapeutic target for NPC patients with cisplatin resistance.