Association between polymorphisms in long non-coding RNA PRNCR1 in 8q24 and risk of colorectal cancer

Li, Lijuan; Sun, Ruili; Liang, Yundan; Pan, Xue; Li, Zhaohui; Bai, Peng; Zeng, Xiaofeng; Zhang, Dongxian; Zhang, Lin; Gao, Linbo

doi:10.1186/1756-9966-32-104

Cited by 85 publications

(76 citation statements)

References 61 publications

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“…lncRNAs are involved in every aspect of cancer progression, such as initiation, cancer metastasis, and could function as oncogenes and tumor suppressors (22). PRNCR1 can promote the progression of prostate cancer, yet the function and molecular mechanism in CRC remain unknown (20,21,25,26).…”

Section: Discussionmentioning

confidence: 99%

“…The interactions of these overexpressed lncRNAs may potentially serve as important regulators in prostate cancer (21). For CRC, many researchers have reported that the crucial locus of 8q24 may contribute to susceptibility to CRC (22,23). It has been gradually recognized that aberration of PRNCR1 might be a biological signature of CRC, but its specific expression pattern related to CRC remains unknown.…”

Section: Introductionmentioning

confidence: 99%

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

Liu

Qiu

et al. 2015

Oncology Reports

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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.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Liu

Qiu

et al. 2015

Oncology Reports

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“…Long non-coding RNAs (lncRNAs) are untranslated transcripts longer than 200 nucleotides baring many of the structural characteristics of mRNAs, including a polyA tail, 5′-capping, and a promoter structure, but no conserved open reading frame [1][2][3][4][5][6]. Many lncRNAs are expressed at specific times and in specific tissues during development, and exhibit a variety of slicing patterns.…”

Section: Introductionmentioning

confidence: 99%

Reciprocal regulation of PCGEM1 and miR-145 promote proliferation of LNCaP prostate cancer cells

Zhang

Han

et al. 2014

J Exp Clin Cancer Res

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Prostate cancer gene expression marker 1 (PCGEM1) is a long non-coding RNA (lncRNA) overexpressed in prostate cancer (PCa) cells that promotes PCa initiation and progression, and protects against chemotherapy-induced apoptosis. The microRNA miR-145 functions as a tumor suppressor in PCa. We speculate that reciprocal regulation of PCGEM1 and miR-145 promote proliferation of LNCaP prostate cancer cells. To test this hypothesis, the interaction between PCGEM1 and miR-145 was examined using a luciferase reporter assay. Expression levels were selectively altered in LNCaP cells and noncancerous RWPE-1 prostate cells by transfection of miR-145 or small interfering RNA sequences against (siRNA) PCGEM1. Relative expression levels were detected by RT-PCR, tumor cell growth and early apoptosis by the MTT assay and flow cytometry, respectively, and tumor cell migration and invasion properties by transwell assays. The effect of siRNA PCGEM1 and miR-145 transfection on prostate cancer growth in vivo was examined in the (nu/nu) mouse model. PCGEM1 and miR-145 exhibited reciprocal regulation; downregulation of PCGEM1 expression in LNCaP cells increased expression of miR-145, while overexpression of miR-145 decreased PCGEM1 expression. Transfection of the miR-145 expression vector and siRNA PCGEM1 inhibited tumor cell proliferation, migration, and invasion, and induced early apoptosis both in vitro. In contrast, there was no effect on RWPE-1 cells. We demonstrate a reciprocal negative control relationship between PCGEM1 and miR-145 that regulates both LNCaP cell proliferation and nu/nu PCa tumor growth. The results also identify PCGEM1 and associated regulators as possible targets for PCa therapy.

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“…To date, certain studies have investigated the impact of PRNCR1 polymorphisms on the risk of various cancers, including prostate (26,(28)(29)(30), gastric (31,32) and colorectal cancer (33).…”

Section: Introductionmentioning

confidence: 99%

Association between genetic polymorphisms of long non‑coding RNA PRNCR1 and prostate cancer risk in a sample of the Iranian population

et al. 2017

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Abstract. The aim of the present study was to determine whether there is an association between the long non-coding RNA (lncRNA) prostate cancer-associated non-coding RNA 1 (PRNCR1) polymorphisms and prostate cancer (PCa) risk in a sample of the Iranian population. This case-control study was performed on 178 patients with PCa and 180 subjects with benign prostatic hyperplasia (BPH). Genotyping assay was performed by polymerase chain reaction-restriction fragment length polymorphism. The findings indicated that the GG genotype of the rs13252298 A>G variant significantly increased the risk of PCa (odds ratio=3.49, 95% confidence interval: 1.79-6.81, P=0.0001) compared with AA+AG. As regards the rs1456315 G>A polymorphism, the AG genotype and G allele significantly increased the risk of PCa. As regards the rs7841060 T>G variant, the findings demonstrated that this TG genotype and the G allele significantly increased the risk of PCa. The rs7007694 T>C variant was not found to be associated with the risk of PCa. Haplotype analysis indicated that GTGA and GTGG significantly increased the risk of PCa compared with rs1456315A/rs7007694T/rs7841060T/rs13252298G (ATTG). The PRNCR1 variants were not found to be significantly associated with the clinicopathological characteristics of PCa patients. In conclusion, our findings support an association between PRNCR1 variants and the risk of PCa in a sample of the Iranian population.

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Association between polymorphisms in long non-coding RNA PRNCR1 in 8q24 and risk of colorectal cancer

Cited by 85 publications

References 61 publications

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

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

Reciprocal regulation of PCGEM1 and miR-145 promote proliferation of LNCaP prostate cancer cells

Association between genetic polymorphisms of long non‑coding RNA PRNCR1 and prostate cancer risk in a sample of the Iranian population

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