Upregulation of long non-coding RNA PRNCR1 in colorectal cancer promotes cell proliferation and cell cycle progression

  • Authors:
    • Liu Yang
    • Mantang Qiu
    • Youtao Xu
    • Jie Wang
    • Yanyan Zheng
    • Ming Li
    • Lin Xu
    • Rong Yin
  • View Affiliations

  • Published online on: October 30, 2015     https://doi.org/10.3892/or.2015.4364
  • Pages: 318-324
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Colorectal cancer (CRC) is one of the most common cancers worldwide. Long non-coding RNAs (lncRNAs) have been confirmed to play a critical regulatory role in various biological processes including carcinogenesis, which indicates that lncRNAs are valuable biomarkers and therapeutic targets. The novel lncRNA prostate cancer non‑coding RNA 1 (PRNCR1) is located in the susceptible genomic area of CRC, however the functional role of PRNCR1 remains unknown. Thus, we aimed to investigate the clinical significance and biological function of PRNCR1 in CRC. Quantitative real‑time polymerase chain reaction (qRT‑PCR) was used to assess the expression profile of PRNCR1 in CRC tissues and cell lines. An antisense oligonucleotide (ASO) was designed to knock down PRNCR1. In a cohort of 63 patients, PRNCR1 was significantly overexpressed in CRC tissues compared with the expression in adjacent tissues, with an average fold increase of 10.55 (P=0.006). Additionally, a high level of PRNCR1 was associated with large tumor volume (P<0.05). Based on receiver operating characteristic curve (ROC), we found that the area under the curve (AUC) of PRNCR1 was 0.799 while the AUC of conventional biomarker CEA‑CA199 was 0.651, indicating that PRNCR1 could be a sensitive diagnostic biomarker of CRC. Compared with the normal human colorectal epithelial cell line (FHC), PRNCR1 was upregulated in most CRC cell lines (HCT116, SW480, LoVo and HT‑29). After knockdown of PRNCR1 by ASO, CRC cell proliferation ability was significantly inhibited. We further found that PRNCR1 knockdown induced cell cycle arrest in the G0/G1 phase and a significant decrease in the proportion of cells in the S phases. In contrast, PRNCR1 knockdown did not affect cell apoptosis or invasive ability. Hence, these data indicate that PRNCR1 promotes the proliferation of CRC cells and is a potential oncogene of CRC.
View Figures
View References

Related Articles

Journal Cover

January-2016
Volume 35 Issue 1

Print ISSN: 1021-335X
Online ISSN:1791-2431

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Yang L, Qiu M, Xu Y, Wang J, Zheng Y, Li M, Xu L and Yin R: Upregulation of long non-coding RNA PRNCR1 in colorectal cancer promotes cell proliferation and cell cycle progression. Oncol Rep 35: 318-324, 2016
APA
Yang, L., Qiu, M., Xu, Y., Wang, J., Zheng, Y., Li, M. ... Yin, R. (2016). Upregulation of long non-coding RNA PRNCR1 in colorectal cancer promotes cell proliferation and cell cycle progression. Oncology Reports, 35, 318-324. https://doi.org/10.3892/or.2015.4364
MLA
Yang, L., Qiu, M., Xu, Y., Wang, J., Zheng, Y., Li, M., Xu, L., Yin, R."Upregulation of long non-coding RNA PRNCR1 in colorectal cancer promotes cell proliferation and cell cycle progression". Oncology Reports 35.1 (2016): 318-324.
Chicago
Yang, L., Qiu, M., Xu, Y., Wang, J., Zheng, Y., Li, M., Xu, L., Yin, R."Upregulation of long non-coding RNA PRNCR1 in colorectal cancer promotes cell proliferation and cell cycle progression". Oncology Reports 35, no. 1 (2016): 318-324. https://doi.org/10.3892/or.2015.4364