Coding-noncoding gene expression in intrahepatic cholangiocarcinoma

Wang, Jianguo; Xie, Haiyang; Ling, Qi; Lu, Di; Lv, Zhen; Zhuang, Runzhou; Liu, Zhikun; Wei, Xuyong; Zhou, Lin; Xu, Xiao; Zheng, Shusen

doi:10.1016/j.trsl.2015.07.007

Cited by 34 publications

(42 citation statements)

References 44 publications

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“…For instance, Wang et al (2) performed a lncRNA microarray using ICC tissues and paired adjacent non-tumour tissues, and identified 2,773 lncRNAs that were significantly upregulated and 2,392 lncRNAs that were downregulated in ICC tissues. They then observed a positive correlation between 4 lncRNA-mRNA pairs in ICC tissues, including RNA43085 and sulfatase 1, RNA47504 and lysine demethylase 8, RNA58630 and proprotein convertase subtilisin/kexin type 6, and RNA40057 and cytochrome P450 family 2 subfamily D member 6 (CYP2D6) (2). Furthermore, the ICC patients with high CYP2D6 and RNA40057 expression had a better prognosis (2).…”

Section: Uca1 Expressionmentioning

confidence: 99%

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Long non‑coding RNA UCA1 promotes proliferation and invasion of intrahepatic cholangiocarcinoma cells through targeting microRNA‑122

Yang

et al. 2019

Exp Ther Med

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Long non-coding RNA urothelial carcinomaassociated 1 (UCA1) has a role in various common types of human malignancy, including cholangiocarcinoma; however, the expression and function of UCA1 in intrahepatic cholangiocarcinoma (ICC) has remained elusive. In the present study, it was observed that UCA1 expression was significantly upregulated in ICC tissues and cell lines compared with that in the adjacent non-tumour tissues and a human intrahepatic biliary epithelial cell line, respectively. The increased expression of UCA1 was significantly associated with lymph node metastasis and clinical T-stage in ICC. Furthermore, the ICC patients with high expression of UCA1 had a shorter survival time when compared with that of patients with low UCA1 expression. Knockdown of UCA1 caused a significant decrease in ICC cell proliferation and invasion, while ectopic overexpression of UCA1 significantly promoted the proliferation and invasion of ICC cells. Furthermore, it was revealed that UCA1 directly binds to microRNA (miR)-122 to negatively regulate its expression in ICC cells. In addition, miR-122 mimics abrogated the promoting effects of UCA1 on ICC cell proliferation and invasion. In addition, an inverse correlation between miR-122 and UCA1 expression in ICC tissues was observed.In conclusion, the present study demonstrates that the lncRNA UCA1 promotes ICC cell proliferation and invasion at least in part by targeting miR-122, suggesting that the UCA1/miR-122 interaction may become a potential therapeutic target for the treatment of ICC.

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Section: Uca1 Expressionmentioning

confidence: 99%

“…Cholangiocarcinomas originate from cholangiocytes of small intrahepatic bile ducts or bile ductules, or of large hilar or extrahepatic bile ducts (1,2). Intrahepatic cholangiocarcinoma (ICC) is the second most common type of primary liver cancer (3,4).…”

Section: Introductionmentioning

confidence: 99%

Long non‑coding RNA UCA1 promotes proliferation and invasion of intrahepatic cholangiocarcinoma cells through targeting microRNA‑122

Yang

et al. 2019

Exp Ther Med

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“…CCA usually metastasize and cause relapse because it is commonly diagnosed in the advanced stage of the disease, and leads to poor prognosis [2][3][4]. Many studies have revealed that numerous genes are involved in CCA [5][6][7][8][9] and many therapeutic strategies have been developed to treat CCA [10][11][12]; however, the survival rate for CCA patients is still low [13]. In this case, the pathogenesis and progression of this malignancy remains to be investigated and new therapeutic targets need to be explored.…”

Section: Introductionmentioning

confidence: 99%

miR-191 Inhibition Induces Apoptosis Through Reactivating Secreted Frizzled-Related Protein-1 in Cholangiocarcinoma

Kang

Leng

Liu

et al. 2018

Cell Physiol Biochem

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Background/Aims: Cholangiocarcinoma (CCA) is one of the most common malignant tumors of the biliary tract originating from biliary epithelial cells. Although many therapeutic strategies have been developed to treat CCA, the survival rate for CCA patients is still quite low. Thus it is urgent to elucidate the pathogenesis of CCA and to explore novel therapeutic targets. miR-191 has been shown to be associated with many human solid cancers, but the function of miR-191 in CCA is still poorly understood. Methods: We first investigated the expression level of miR-191 in human CCA tissues and cell lines with quantitative real-time PCR (qRT-PCR). The effects of miR-191 on CCA cells were determined by Cell Counting Kit-8 assay, colony formation assay and acridine orange/ethidium bromide staining. Finally, we utilized qRT-PCR, western blot and luciferase reporter assays to verify the miR-191 target gene. Results: We showed that miR-191 was up-regulated in CCA cell lines and patients. Knockdown of miR-191 by transfection of its inhibitor sequence blocked RBE cells viability and induced apoptosis of RBE cells. Both qRT-PCR and western blot analysis showed that the secreted frizzled-related protein-1 (sFRP1) level was negatively correlated with that of miR-191. Luciferase assay validated that sFRP1 was a direct target of miR-191. Moreover, knockdown of miR-191 led to suppression of Wnt/β-catenin signaling activation. Co-transfection of sFRP1 small interfering RNA (siRNA) and miR-191 inhibitor re-activated the Wnt/β-catenin signaling pathway as detected by an increased level of β-catenin and phosphorylation of GSK-3β, and restored the expression of survivin and c-myc in RBE cells. Co-transfection of sFRP1 siRNA with miR-191 inhibitor restored the colony formation ability and viability of RBE cells. Conclusion: Taken together, our results demonstrate a novel insight into miR-191 biological function in CCA. Our findings suggest that miR-191 is a potential therapeutic target of CCA treatment.

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“…Lv, L. and his colleagues reported that 2148 lncRNAs were upregulated while 568 lncRNAs were downregulated in ICC tissues compared with normal tissues [26]. Jianguo Wang's report showed a similar result with 2773 lncRNAs upregulated and 2392 lncRNAs downregulated in ICC tissues [27]. Another study by Zhang, F., et al identified that 268 lncRNAs were differentially expressed in ECC(78 lncRNAs upregulated, 190 lncRNAs downregulated) [28].…”

Section: Lncrna Is Abnormally Expressed In Cca Tissuesmentioning

confidence: 88%

The Advancement of Long Non-Coding RNAs in Cholangiocarcinoma Development

Jiang¹,

Ling²

2019

J. Cancer

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Cholangiocarcinoma (CCA) is a malignancy with increasing incidence in recent years. CCA patients are usually diagnosed at advanced stage due to lack of apparent symptoms and specifically diagnostic markers. Nowadays, surgical removal is the only effective method for CCA whereas overall 5-year-survival rate keeps around 10%. Long-noncoding RNA (lncRNA), a subtype of noncoding RNA, is widely studied to be abnormally expressed in multiple cancers including CCA. LncRNA can promote proliferation, migration, invasion and inhibit apoptosis of CCA. Moreover, lncRNA is negatively correlated with the prognosis of CCA. LncRNA may contribute to the development of CCA via modulating gene transcription, sponging microRNA, regulating CCA-related signaling pathways or protein expression. LncRNA is thought to be potential diagnostic markers and therapeutic targets for CCA.

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Coding-noncoding gene expression in intrahepatic cholangiocarcinoma

Cited by 34 publications

References 44 publications

Long non‑coding RNA UCA1 promotes proliferation and invasion of intrahepatic cholangiocarcinoma cells through targeting microRNA‑122

Long non‑coding RNA UCA1 promotes proliferation and invasion of intrahepatic cholangiocarcinoma cells through targeting microRNA‑122

miR-191 Inhibition Induces Apoptosis Through Reactivating Secreted Frizzled-Related Protein-1 in Cholangiocarcinoma

The Advancement of Long Non-Coding RNAs in Cholangiocarcinoma Development

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