Long noncoding RNA CCAT1 polymorphisms are associated with the risk of colorectal cancer

Li, Yingjun; Jing, Fangyuan; Ding, Ye; He, Qin; Zhong, Yaohong; Fan, Chunhong

doi:10.1016/j.cancergen.2018.02.003

Cited by 27 publications

(28 citation statements)

References 41 publications

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“…For example, the expression of lncRNA CCAT1 in various digestive system tumors is abnormal. CCAT1 was significantly upregulated in colorectal cancer, which was closely related to the prognosis of patients [8]. In addition, the expression of CCTA1 is also regulated by the oncogene c-Myc to promote the proliferation of cancer cells [9].…”

Section: Introductionmentioning

confidence: 99%

LncRNA CAR10 Upregulates PDPK1 to Promote Cervical Cancer Development by Sponging miR-125b-5p

Zhang

Gao

2020

BioMed Research International

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Cervical cancer is one of the malignant tumors that seriously threaten women’s health. The mechanism of development needs to be deeply studied. In recent years, lncRNA has been identified as one of the important factors affecting the malignant progression of tumors. In this study, we illustrated the important mechanism of lncRNA CAR10 in the development of cervical cancer. We found that CAR10 is significantly increased in4 cervical cancer tissues and cells, which can promote the proliferation of cervical cancer cells in vitro and in vivo, indicating that CAR10 is involved in the progression of cervical cancer as an oncogene. Further studies showed that CAR10 is a target gene of miR-125b-5p, and miR-125b-5p can inhibit the effect of CAR10 on the proliferation of cervical cancer cells. In addition, we also found that 3-phosphoinositide-dependent protein kinase 1 (PDPK1) is also a target gene of miR-125b-5p, and CAR10 can upregulate the expression level of PDPK1. The results showed that CAR10 acts as a ceRNA to upregulate the expression of PDPK1 by sponging miR-125b-5p. Knockdown of PDPK1 can inhibit the effect of CAR10 on cervical cancer cells. Our study demonstrates that, based on ceRNA mechanism, CAR10/miR-125b-5p/PDPK1 network can regulate the proliferation of cervical cancer cells and play an important role in the development of cervical cancer. In addition, our study also suggests that intervention of CAR10/miR-125b-5p/PDPK1 network may be a new strategy for targeted therapy of cervical cancer.

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Section: Introductionmentioning

confidence: 99%

LncRNA CAR10 Upregulates PDPK1 to Promote Cervical Cancer Development by Sponging miR-125b-5p

Zhang

Gao

2020

BioMed Research International

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“…In fact, the polymorphism of rs67085638 was discovered to be associated with an elevated colon cancer risk but not an elevated rectal cancer risk [21]. Another research showed in line results by revealing that the polymorphism of rs67085638 in the 3'UTR of CCAT1 was linked to elevated colon cancer and rectal cancer risks [21]. One team of scientists presented that as compared to healthy cells, CCAT1 was con rmed to become overexpressed in colon tumor cells to enhance the invasion as well as proliferation of colon tumor cells.…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that a single nucleotide polymorphism (rs67085638) in lncRNA-CCAT1 was associated with the risk of tumorigenesis [21]. It was additionally presented that the rs67085638 C > T SNP in lncRNA CCAT1 was linked to an enhanced risk of colon cancer [21]. Another study showed that CCAT1 may affect the chemoresistance of ovary cancer cells to PTX via regulating miR-24-3p and FSCN1 [17].…”

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confidence: 97%

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Effect of rs67085638 in long non-coding RNA (CCAT1) on colon cancer chemoresistance to paclitaxel through modulating the microRNA-24-3p and FSCN1 signaling

Zhang

Wang

2020

Preprint

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BackgroundIt has been reported that rs67085638 in lncRNA-CCAT1 was associated with the risk of tumorigenesis. Also, CCAT1 could affect chemoresistance of cancer cells to PTX via regulating miR-24-3p and FSCN1 expression. In this study, we aimed to investigate the effect of rs67085638 on the expression of CCAT1/miR-24-3p/FSCN1 and the response of colon cancer to the treatment of PTX.Method48 colon cancer patients were recruited and grouped by their genotypes of rs67085638 polymorphism as a CC group (N=28) and a CT group (N=20). Colon cancer cells were collected from the patients and cancer cell xenografts were transplanted into mice. PCR analysis, IHC assay and Western blot were performed to observe the expression of lncRNA-CCAT1, miR-24-3p and FSCN1 in vivo and in vitro, and the relationships among the expression of lncRNA-CCAT1, miR-24-3p and FSCN1 were validated by computational analysis and luciferase assay. TUNEL assay and flow cytometry were conducted to observe tumor cell apoptosis and survival.ResultLncRNA-CCAT1 and FSCN1 mRNA/protein were over-expressed while miR-24-3p was down-regulated in the CT-genotyped patients and cells compared with those in the CC-genotyped patients and cells. The survival of colon cancer cells was decreased while the apoptosis of colon cancer cells was increased by PTX treatment in a dose-dependent manner. However, the survival rate of CT-genotyped cells was higher while the apoptosis rate of CT-genotyped cells was lower than that of the CC-genotyped cells, and the difference was partly eliminated by the knockdown of lncRNA-CCAT1. MiR-24-3p was validated to target lncRNA-CCAT1 and FSCN1 mRNA, and the over-expression of CCAT1 could reduce the expression of miR-24-3p while elevating the expression of FSCN1. The growth of CT-genotyped tumors in mice was more suppressed in compared with the growth of CC-genotyped tumors, while the knockdown of lncRNA-CCAT1 partly reversed the effect of the CT genotype. Furthermore, compared with the rs67085638-CC mice, the lncRNA-CCAT1 and FSCN1 mRNA/protein levels in the rs67085638-CT+NC shRNA mice were increased while their miR-24-3p level was decreased, and the knockdown of lncRNA-CCAT1 partly reversed the dysregulation of these genes.ConclusionThe findings of this study demonstrated that the presence of the minor allele of rs67085638 increased the expression of CCAT1 and accordingly enhanced the resistance to PTX. Downregulation of CCAT1 partially, but significantly, re-stored the sensitivity to PTX of colon cancer cells.

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“…Many studies have investigated the correlation between lncRNAs and the pathogenesis of various diseases, 15 including tumors, 16,17 and the results suggest that SNPs in lncRNA are associated with the susceptibility to cancer. [18][19][20] Cancer susceptibility candidate 8 (CASC8) is an lncRNA with no protein-coding potential that is located in the 8q24 region. 21 LncRNAs originating from the 8q24 region including CASC8 play a critical role in the regulation of MYC, which is important for the development of multiple tumors, and the expression of CASC8 is regulated by longrange interaction of the MYC enhancer with the CASC8 promoter.…”

Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA CASC8 polymorphisms are associated with the risk of esophageal cancer in a Chinese population

Sang

Chen

et al. 2020

Thoracic Cancer

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Background: Esophageal cancer (EC) is an important disease that threatens public health and safety. Although there are numerous treatment options for esophageal cancer including surgery, radiation therapy, and chemotherapy, these treatments have limited effects. Its morbidity and mortality vary widely among countries and regions. Esophageal cancer is classified into squamous cell carcinoma (ESCC) and esopheageal adenocarcinoma (EADC). Here, we examined the genetic susceptibility to ESCC in relation to functional single nucleotide polymorphisms (SNPs) in the long non-coding RNA (lncRNA) CASC8. Methods: To detect the susceptibility to ESCC in relation to functional polymorphisms in CASC8, a hypothesis-driven study was performed to identify CASC8 SNPs in 949 patients with ESCC and 1369 control subjects. Results: The CASC8 rs1562430 GG genotype was significantly associated with increased ESCC risk in men, patients younger than 63 years, non-smokers, and nondrinkers. Conclusions: CASC8 rs1562430 A > G may cause susceptibility to ESCC and CASC8 SNPs may play a vital role in ESCC risk, thereby serving as a potential biomarker for diagnosing ESCC. A larger sample size and multifactor information are needed to confirm these results.

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Long noncoding RNA CCAT1 polymorphisms are associated with the risk of colorectal cancer

Cited by 27 publications

References 41 publications

LncRNA CAR10 Upregulates PDPK1 to Promote Cervical Cancer Development by Sponging miR-125b-5p

LncRNA CAR10 Upregulates PDPK1 to Promote Cervical Cancer Development by Sponging miR-125b-5p

Effect of rs67085638 in long non-coding RNA (CCAT1) on colon cancer chemoresistance to paclitaxel through modulating the microRNA-24-3p and FSCN1 signaling

Long non‐coding RNA CASC8 polymorphisms are associated with the risk of esophageal cancer in a Chinese population

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