Previous study indicates that long noncoding RNA NORAD could serve as a competing endogenous RNA to pancreatic cancer metastasis. However, its role in colorectal cancer requires to be investigated. In the present study, we found that the expression of NORAD was significantly upregulated in colorectal cancer (CRC) tissues. Furthermore, the expression of NORAD was positively related with CRC metastasis and patients' poor prognosis. Knockdown of NORAD markedly inhibited CRC cell proliferation, migration and invasion but induced cell apoptosis in vitro. In vivo experiments also indicated an inhibitory effect of NORAD on tumor growth. In mechanism, we found that NORAD served as a competing endogenous RNA for miR-202-5p. We found that there was an inversely relationship between the expression of NORAD and miR-202-5p in CRC tissues. Moreover, overexpression of miR-202-5p in SW480 and HCT116 cells significantly inhibited cellular proliferation, migration and invasion. Taken together, our study demonstrated NORAD/miR-202-5p axis plays a pivot function on CRC progression.

Aptamer of MPT64 as a new detection tool, to a certain extent, is feasible to diagnose Mycobacterium tuberculosis.

Background: Emerging studies have reported that long non-coding RNAs (lncRNAs) were crucial regulators in the progression of colorectal cancer (CRC). LncRNA susceptibility 9 (CASC9) was involved in several cancers; however, its role in CRC remains unknown. Methods: RT-PCR was done to probe the expression of CASC9 and miR-193a-5p in CRC samples. CRC cell lines (HCT116 and SW480) were used as cell models. The biological influence of CASC9 on cancer cells was studied using CCK-8 assay, Transwell assay and TUNEL assay in vitro, and subcutaneous xenotransplanted tumor model in vivo. Interaction between CASC9 and miR-193a-5p was investigated by bioinformatics analysis, RT-PCR, and luciferase reporter assay. The expression level of the downstream gene of miR-193a-5p, erb-b2 receptor tyrosine kinase 2 (ERBB2), was tested by Western blot. Results: CASC9 was significantly up-regulated in CRC samples, while miR-193a-5p was markedly down-regulated. Overexpression of CASC9 promoted viability, migration and invasion of CRC cells, while overexpression of miR-193a-5p had the opposite effect. CASC9 could down-regulate miR-193a-5p via sponging it, and there was a negative relevancy between CASC9 and miR-193a-5p in CRC samples. CASC9 also enhanced the expression levels of ERBB2, while this effect could be reversed by co-transfection with miR-193a-5p. Conclusion: CASC9, an oncogenic lncRNA, was abnormally up-regulated in CRC tissues, and it could indirectly modulate the expression of ERBB2 via reducing the expression level of miR-193a-5p.

Colorectal cancer (CRC), one of the most commonly diagnosed types of cancer worldwide, is the third most prevalent and fourth most frequent cause of cancer‑related mortality. Dysregulated microRNAs (miRNAs) have potential regulatory roles in the development and progression of various cancer types. Therefore, the investigation of the miRNAs involved in CRC formation and progression may lead to the development of highly effective therapeutic strategies for CRC. In the present study, miRNA‑760 (miR‑760) was frequently downregulated in CRC tissues and cell lines. The low levels of miR‑760 expression were significantly correlated with the tumor size, lymph node metastasis and TNM stage of CRC. Functional assays revealed that restoring miR‑760 expression inhibited CRC cell proliferation and invasion in vitro. The results of bioinformatics analysis, luciferase reporter assay, reverse transcription‑quantitative polymerase chain reaction and western blot analysis suggested that specificity protein 1 (SP1) is a direct target of miR‑760 in CRC. The high expression of SP1 in CRC tissues was inversely correlated with the expression of miR‑760. Rescue experiments demonstrated that enforced SP1 expression rescued the tumor‑suppressing effects of miR‑760 on CRC cell proliferation and invasion. In addition, miR‑760 overexpression is involved in the regulation of the PTEN/AKT signalling pathway. Collectively, the present data demonstrated that miR‑760 directly targets SP1 to inactivate the PTEN/AKT signalling pathway, thus implicating miR‑760 in the regulation of CRC cell proliferation and invasion. Therefore, miR‑760 may be a novel biomarker and therapeutic target for CRC.

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