Abstract

Emerging studies indicate that long non-coding RNAs (lncRNAs) play crucial roles in colorectal cancer (CRC). Here, we reported lncRNA CASC21, which is induced by FOXP1, functions as an oncogene in CRC. We systematically elucidated its clinical significance and possible molecular mechanism in CRC. LncRNA expression in CRC was analyzed by RNA-sequencing data in TCGA. The expression level of CASC21 in tissues was determined by qRT-PCR. The functions of CASC21 was investigated by in vitro and in vivo assays (CCK8 assay, colony formation assay, EdU assay, xenograft model, flow cytometry assay, immunohistochemistry (IHC) and Western blot). Chromatin immunoprecipitation (ChIP), RNA immunoprecipitation (RIP) and luciferase reporter assays were utilized to demonstrate the potential mechanisms of CASC21. CASC21 is overexpressed in CRC and high CASC21 expression is associated with poor survival. Functional experiments revealed that CASC21 promotes CRC cell growth. Mechanistically, we found that CASC21 expressed predominantly in the cytoplasm. CASC21 could interact with miR-539-5p and regulate its target CDK6. Together, our study elucidated that CASC21 acted as an oncogene in CRC, which might serve as a novel target for CRC diagnosis and therapy.

Highlights

  • colorectal cancer (CRC) is one of the most common digestive system’s cancers

  • We divided the patients into two groups according to the CASC21 expression level and we found that the patients in the ‘high CASC21expression’ group had poor prognosis (Figure 1D, 1E)

  • We found that CASC21 was abnormally elevated in CRC and confirmed the result by qRT-PCR

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Summary

Introduction

CRC is one of the most common digestive system’s cancers. Its morbidity ranks third in all malignant tumors and it accounts for one-tenth of all tumor-related death worldwide [1, 2]. With the development of diagnostic and therapeutic techniques, the prognosis of CRC has improved significantly. It is necessary to further explore the molecular mechanism regulating the development and progression of CRC. Most lncRNAs are structurally like mRNA, have a 5' end cap structure and a poly-A tail, and are transcribed from RNA polymerase II. They were originally considered to be ‘transcriptional www.aging-us.com noise’ [6, 7]. Recent studies have shown that several lncRNAs, such as CCAT1, CCAT2, H19 and HOTAIR, are abnormally expressed and play a vital role in CRC [10,11,12,13]. The roles of many other lncRNAs in CRC are not clear and further studies are needed

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