Genome-wide analysis of long noncoding RNA signature in human colorectal cancer

Xue, Yue; Ma, Gaoxiang; Gu, Dongying; Zhu, Lingjun; Hua, Qiuhan; Du, Mulong; Chu, Haiyan; Tong, Na; Chen, Jinfei; Wang, Meilin

doi:10.1016/j.gene.2014.11.060

Cited by 60 publications

(55 citation statements)

References 37 publications

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“…Recently a global expression profile of lncRNAs was analyzed by microarray technique [25]. We used house-made non-coding RNA expression arrays designed with probes targeting human pre-miRNAs, mouse pre-miRNAs, ultraconserved genes, pyknon probes, and other non-coding RNAs.…”

Section: Discussionmentioning

confidence: 99%

MALAT1 promoted invasiveness of gastric adenocarcinoma

Lee

Ivan

et al. 2017

BMC Cancer

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BackgroundGastric cancer is the second leading cause of cancer globally, and the mechanism of its pathogenesis is still largely unknown. Recently, non-coding RNAs have been recognized to promote metastasis in various cancers, including gastric cancer.MethodsWe found that metastasis associated lung adenocarcinoma transcript-1 (MALAT1) is upregulated in gastric cancer tissue compared to adjacent normal tissue, as determined by microarray and subsequent qRT-PCR, then investigated the impact of MALAT1 on apoptosis, cell proliferation, and the cell cycle to dissect the carcinogenesis of gastric cancer, and examined mechanisms of invasion and metastasis. Expression of MALAT1 and U6 was determined by SYBR qRT-PCR in nine-teen gastric cancer cell lines and fifty fresh samples of cancer tissue and adjacent tissues. Downregulation of MALAT1 was accomplished with two different siRNAs. Cell proliferation was determined after treatment with these siRNAs. FACS using PI/Annexin-V staining was carried out. To analyze the invasiveness, a scratch wound-healing assay and a Matrigel invasion assay were performed. Cancer related gene expression assay was done after transfection of siR- MALAT1.ResultsThe expression of MALAT1 was significantly elevated in various gastric cancer cell lines and gastric cancer tissues compared to normal cell lines and tissues (p < 0.01). siR-MALAT1 significantly reduced viable AGS cell numbers and induced apoptosis (p < 0.05). Deep invasion of tumor (advanced T stages) was more common in the high MALAT1-level group (p = 0.039). siR-MALAT1 significantly decreased AGS cell invasiveness and migration. siR-MALAT1 reduced expression of snail and N-cadherin, and elevated E-cadherin. The Wnt/β-catenin related genes were significantly decreased by transfection of siRNA MALAT1. MALAT1 is involved in gastric carcinogenesis via inhibition of apoptosis and promotes invasiveness via the epithelial-to-mesenchymal transition.ConclusionsIn our study, we found that deregulation of MALAT1 could be involved in both tumorigenesis and invasiveness in gastric cancer cells.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-016-2988-4) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

MALAT1 promoted invasiveness of gastric adenocarcinoma

Lee

Ivan

et al. 2017

BMC Cancer

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“…Non-coding RNAs (ncRNAs) are proven to be the key regulators in the process of transcription and expression, which could be divided into small ncRNAs (<200 nt) and long ncRNAs (lncRNAs) (7,8). An increasing number of studies have focused on the functional hot spot of lncRNAs in their roles as regulators of biological processes, such as genomic imprinting, chromatin modification and post-transcriptional processing (9)(10)(11), displaying more complex regulatory mechanisms than microRNAs (12,13 shown to play important roles in various human diseases, especially in malignant tumors (16)(17)(18)(19). Prostate cancer non-coding RNA 1 (PRNCR1), also known as PCAT8 and CARLo-3, is a ~13 kb intron-less lncRNA, which is transcribed from the 'gene-desert' region of 8q24 (20).…”

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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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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“…carcinogenesis by regulating protein-coding genes involved in specific biological processes associated with colorectal cancer (22). Furthermore, HOTAIR and lncRNA-422 are upregulated when KRAS is overexpressed, but downregulated when Janus-kinase 2 or TANK-binding kinase 1 are knocked out and when platelet-derived growth factor is overexpressed (22).…”

Section: Cancer-related Lncrnasmentioning

confidence: 99%

“…Furthermore, HOTAIR and lncRNA-422 are upregulated when KRAS is overexpressed, but downregulated when Janus-kinase 2 or TANK-binding kinase 1 are knocked out and when platelet-derived growth factor is overexpressed (22). Cancer susceptibility candidate 2 (CASC2) and growth arrest-specific transcript 5 (GAS5) are known tumor suppressors in colorectal cancer (23,24).…”

Section: Cancer-related Lncrnasmentioning

confidence: 99%

LncRNAs and cancer

Zhang

et al. 2016

Oncology Letters

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Abstract. Long non-coding RNAs (lncRNAs) are a group of non-coding RNAs composed of >200 nucleotides. Recent studies have revealed that lncRNAs exert an important role in the development and progression of cancer. In this review, the involvement of the most extensively investigated lncRNAs in cancers of the digestive, respiratory, reproductive, urinary and central nervous systems are discussed. LncRNAs function via molecular and biochemical mechanisms that include cis-and trans-regulation of gene expression, epigenetic modulation in the nucleus and post-transcriptional control in the cytoplasm. Although the detailed biological functions and molecular mechanisms of the majority of lncRNAs remain to be elucidated, this review aims to provide a novel insight into the diagnosis and treatment of cancer using lncRNAs.

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Genome-wide analysis of long noncoding RNA signature in human colorectal cancer

Cited by 60 publications

References 37 publications

MALAT1 promoted invasiveness of gastric adenocarcinoma

MALAT1 promoted invasiveness of gastric adenocarcinoma

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

LncRNAs and cancer

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