Accumulating evidence indicates that long noncoding RNAs (lncRNAs) act as tumor promoters or suppressors in various types of cancer. Previous investigations suggest that ceramide synthase 6 (CERS6) antisense RNA 1 (CERS6-AS1) acts as an oncogene in breast cancer; however, its role in colorectal cancer is unknown. This study aimed to explore the molecular mechanism of CERS6-AS1 in colorectal cancer. Gene expression in colorectal cancer was examined using reverse transcription-quantitative polymerase chain reaction and western blot analyses. The viability and proliferation of colorectal cancer cells were measured by Cell Counting Kit-8 assays and colony formation assays. The migratory and invasive capacities of the colorectal cancer cells were assessed by Transwell assay. Cell stemness was examined by sphere-formation assay. Mechanistically, RNA pull-down assays, RNA immunoprecipitation assays, and luciferase reporter assays were performed to explore the relationship among CERS6-AS1, miR-15b-5p and spectrin beta, nonerythrocytic 2 (SPTBN2). Moreover, a xenograft tumor model was established to investigate the role of CERS6-AS1 in vivo. We found that CERS6-AS1 and SPTBN2 were highly expressed in colorectal cancer tissues and cells. CERS6-AS1 depletion inhibited cell viability, proliferation, migration, and invasion; the epithelial-mesenchymal transition process and stemness. It suppressed xenograft tumor growth in colorectal cancer. Moreover, SPTBN2 levels were positively regulated by CERS6-AS1 and negatively regulated by miR-15b-5p in colorectal cancer cells. Rescue assays revealed that SPTBN2 reversed the inhibitory effect of CERS6-AS1 deficiency on the malignant behaviors of colorectal cancer cells. Overall, the lncRNA CERS6-AS1 facilitates malignant phenotypes of colorectal cancer cells by targeting miR-15b-5p to upregulate SPTBN2.

Cancer is one of the leading causes of mortality in China, and poses a threat to public health due to its increasing incidence and mortality rates. Concurrent cancer is defined as one or more organs in the same individual having ≥2 primary malignancies occurring simultaneously or successively; however, concurrent cases are rare and poorly studied. The present study recruited a Chinese family presenting multiple cases of concurrent cancer and performed whole exome sequencing in one unaffected and two affected individuals to identify the causative mutations. DNA was extracted from peripheral blood and tumor tissue samples. Following an exome capture and quality test, the qualified library was sequenced as 100 bp paired-end reads on an Ion Torrent platform. Clean data were obtained by filtering out the low-quality reads. Subsequently, bioinformatics analyses were performed using the clean data. After mapping and annotating in 1000 Genomes Project database, the existing SNP database and the Cancer Gene Census (CGC) database, it was revealed that the NADH:ubiquinone oxidoreductase core subunit S7 gene was a candidate gene with somatic mutations, and a subset of 16 genes were candidate genes with germline mutations. The findings of the present study may improve the understanding of the molecular pathogenesis of concurrent cancer.