Genomic Insight into the Role of lncRNAs in Cancer Susceptibility

Gao, Ping; Wei, Gong-Hong

doi:10.3390/ijms18061239

Cited by 69 publications

(32 citation statements)

References 79 publications

(61 reference statements)

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“…LncRNAs involved in may key biological processes, such as transcription regulation, epigenetic regulation, chromatin remodeling and mRNA processing [ 6 ]. Growing evidence has showed that lncRNAs play important roles in a wide range of human cancers [ 7 , 8 ]. The lncRNA, Colorectal Neoplasia Differentially Expressed (CRNDE) was first identified in colorectal adenomas and adenocarcinomas, and the CRNDE locus spans ∼10 kb and comprises five core exons with an additional exon that is infrequently present in transcripts [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

LncRNA CRNDE promotes cell proliferation, invasion and migration by competitively binding miR-384 in papillary thyroid cancer

Sun

et al. 2017

Oncotarget

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Thyroid cancer is one of the most prevalent endocrine neoplasm. The present study examined the effects of Colorectal Neoplasia Differentially Expressed (CRNDE) on the progression of papillary thyroid cancer (PTC), and explored the underlying molecular mechanisms. Quantitative real-time PCR was used to detect CRNDE, miR-384 and pleiotrophin (PTN) mRNA expression. Western blot was used to measure PTN protein levels. Cell proliferation, cell growth, cell invasion and migration of PTC cells were determined by CCK-8, colony formation, transwell invasion and migration assays, respectively. CRNDE was up-regulated in PTC tissues and cell lines. Overexpression of CRNDE promoted BCPAP cell proliferation, invasion and migration, while knock-down of CRNDE suppressed K1 cell proliferation, invasion and migration. CRNDE negatively regulated the expression of miR-384 in PTC cells, which was further confirmed by luciferase reporter assay. MiR-384 was down-regulated and inversely correlated with CRNDE expression in PTC tissues. MiR-384 suppressed cell proliferation, invasion and migration in PTC cells, and enforced expression of miR-384 attenuated the oncogenic effects of CRNDE in PTC cells. PTN was predicted as a downstream target of miR-384, which was confirmed by luciferase reporter assay, and PTN was up-regulated in PTC tissues, and was negatively correlated with miR-384 expression and positively correlated with CRNDE expression in PTC tissues. In summary, our results suggested that the CRNDE/miR-384/PTN axis may play an important role in the regulation of PTC progression, which provides us with new insights into understanding the PTC.

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Section: Introductionmentioning

confidence: 99%

LncRNA CRNDE promotes cell proliferation, invasion and migration by competitively binding miR-384 in papillary thyroid cancer

Sun

et al. 2017

Oncotarget

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“…Recent research has suggested that lncRNAs, as oncogenes or tumour suppressor genes, could be involved in the development of cancer and be associated with tumour metastasis and prognosis (Song et al, 2017;Weidle et al, 2017). Given that the majority of the GWAS-identified cancer risk SNPs are located in the noncoding region, the expression and function of lncRNAs are more likely to be impacted by the SNPs (Gao & Wei, 2017). Moreover, GWAS have identified 8q24 as a hotspot for cancer-associated SNPs on account of the strength, density and high allele frequency of these SNPs (Sur et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA polymorphisms on 8q24 are associated with the prognosis of gastric cancer in a Chinese population

Zhang

Jia

et al. 2020

PeerJ

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Background Gastric cancer (GC) remains the third leading cause of cancer death in China. Although genome-wide association studies have identified the association between several single nucleotide polymorphisms (SNPs) on 8q24 and the risk of GC, the role of these SNPs in the prognosis of GC in Chinese populations has not yet been fully evaluated. Therefore, this study was conducted to explore the association between long non-coding RNA (lncRNA) polymorphisms on 8q24 and the prognosis of GC. Methods We genotyped 726 surgically resected GC patients to explore the association between eight SNPs in the lncRNAs CCAT1 (rs10087719, rs7816475), PCAT1 (rs1026411), PRNCR1 (rs12682421, rs13252298), and CASC8 (rs1562430, rs4871789, rs6983267) transcribed from the 8q24 locus and the prognosis of GC in a Chinese population. Results We found that the patients carrying rs12682421 AA genotypes survived for a shorter time than those with the GG/GA genotype (HR = 1.39, 95% confidence interval (CI) [1.09–1.78]). Compared with the CC/CT genotype, the TT genotype of rs1562430 was associated with an increased risk of death (HR = 1.38, 95% CI [1.06–1.80]). Furthermore, the results also identified the rs1026411 SNP as an independent prognostic factor for poor survival in GC patients. Patients carrying AA/AG variant genotypes had a 36% increased risk of death compared to those carrying the GG genotype (HR = 1.36, 95% CI [1.06–1.74]). These findings suggested that the rs12682421, rs1026411 and rs1562430 SNPs may contribute to the survival of GC and be prognostic markers for GC.

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“…LncRNA regulates the expression of genes at the level of transcription, posttranscription and translation, affecting various physiological and pathological processes of cells 6–9 . Current studies have shown that variable abnormal expression of lncRNA is closely related to the occurrence of various diseases, including tumors 10–12 . Emerging studies have found that long noncoding RNA cancer susceptibility candidate 9 ( CASC9 ) is highly expressed in various cancers, such as esophageal squamous cell carcinoma, nasopharyngeal carcinoma and hepatocellular carcinoma, implying a crucial carcinogenic effect of this lncRNA 13–19 .…”

Section: Introductionmentioning

confidence: 99%

Increased expression of lncRNA CASC9 promotes tumor progression by suppressing autophagy-mediated cell apoptosis via the AKT/mTOR pathway in oral squamous cell carcinoma

et al. 2019

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Recent studies showed that lncRNA CASC9 was upregulated and acted as an oncogene in a variety of tumors. However, the expression and biological functions of CASC9 in oral squamous cell carcinoma (OSCC) remain unknown. In this study, we found for the first time that CASC9 was remarkably upregulated in OSCC tissues and cell lines compared with paired noncancerous tissues and normal oral epithelial cells. Highly expressed CASC9 is strongly associated with tumor size, clinical stage, regional lymph node metastasis and overall survival time in OSCC patients. In vitro, CASC9 knockdown in OSCC cells SCC15 and CAL27 significantly promotes autophagy and apoptosis, while inhibiting proliferation. Moreover, the expression levels of p-AKT, p-mTOR, P62 and BCL-2 were significantly decreased, while the expression levels of BAX and the LC3BII/LC3BI ratio were increased in CASC9-knockdown SCC15 and CAL27 cells. After the addition of the AKT activator SC79 in CASC9-knockdown SCC15 and CAL27 cells, we found that the increased autophagy and apoptosis were remarkably rescued. Furthermore, the increased apoptosis was remarkably rescued in CASC9-knockdown OSCC cells treated with the autophagy inhibitor Autophinib. In addition, CASC9 depletion suppressed tumor growth in vivo. In conclusion, our findings demonstrate that lncRNA CASC9 promotes OSCC progression through enhancing cell proliferation and suppressing autophagy-mediated cell apoptosis via the AKT/mTOR pathway. CASC9 could potentially be used as a valuable biomarker for OSCC diagnosis and prognosis.

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Genomic Insight into the Role of lncRNAs in Cancer Susceptibility

Cited by 69 publications

References 79 publications

LncRNA CRNDE promotes cell proliferation, invasion and migration by competitively binding miR-384 in papillary thyroid cancer

LncRNA CRNDE promotes cell proliferation, invasion and migration by competitively binding miR-384 in papillary thyroid cancer

Long non-coding RNA polymorphisms on 8q24 are associated with the prognosis of gastric cancer in a Chinese population

Increased expression of lncRNA CASC9 promotes tumor progression by suppressing autophagy-mediated cell apoptosis via the AKT/mTOR pathway in oral squamous cell carcinoma

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