Long non‐coding ribonucleic acid zinc finger antisense 1 promotes the progression of colonic cancer by modulating ZEB1 expression

Fang, Changyi; Zan, Jianbao; Yue, Bing; Liu, Chenchen; He, Chenglong; Yan, Dongwang

doi:10.1111/jgh.13646

Cited by 63 publications

(58 citation statements)

References 32 publications

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“…Some transcriptional factors could bind to the promoter region of E-Cadherin to suppress its expression, and further trigger the EMT conversion and metastasis of tumor cells, including SNAIL, SLUG, ZEB1 and ZEB2 [33, 34]. Among them, ZEB1 (characterized by the presence of 2 zinc finger clusters) is a well investigated transcriptional factor to act as a driver of EMT and cancer progression toward metastasis and invasion [35].…”

Section: Discussionmentioning

confidence: 99%

PIK3R3 Promotes Metastasis of Pancreatic Cancer via ZEB1 Induced Epithelial-Mesenchymal Transition

Peng

Zhu

Yin

et al. 2018

Cell Physiol Biochem

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Background/Aims: PIK3R3 is a regulatory subunit of phosphatidylinositol 3-kinase (PI3K) which plays an essential role in the metastasis of several types of cancer. However, whether PIK3R3 can promote the metastasis of pancreatic cancer (PC) is still unclear. In this study, we characterized the role of PIK3R3 in metastasis of PC and underlying potential mechanisms. Methods: RT-PCR, western blot, immunofluorescence (IF) and immunohistochemistry (IHC) were applied to investigate the expression of genes and proteins in different cell lines and tissues. To assess the function of PIK3R3 and related mechanisms, the cells with RNAi-mediated knockdown or overexpression were used to perform a series of in vitro and in vivo assays. Results: PIK3R3 was significantly overexpressed in pancreatic cancer tissues, especially in metastatic cancer tissues, as well as in pancreatic cancer cells. Functional assays suggested that overexpression or knockdown of PIK3R3 could respectively promote or suppress the migration and invasion of PC cells in vitro and in vivo. Further mechanism related studies demonstrated that ERK1/2-ZEB1 pathway-triggered epithelial-mesenchymal transition (EMT) might be responsible for the PIK3R3-induced PC cell migration and invasion. Conclusion: PIK3R3 could promote the metastasis of PC by facilitating ZEB1 induced EMT, and could act as a potential therapeutic target to limit PC metastasis.

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Section: Discussionmentioning

confidence: 99%

PIK3R3 Promotes Metastasis of Pancreatic Cancer via ZEB1 Induced Epithelial-Mesenchymal Transition

Peng

Zhu

Yin

et al. 2018

Cell Physiol Biochem

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“…Then they found ZFAS1 inhibition could markedly suppress CRC cell lines proliferation and invasion both in cell lines and mouse models of proliferation and metastasis. Another study by Fang et al [33] found ZFAS1 was up-regulated in colonic cancer tissues compared with adjacent mucosa, and its expression level was significantly correlated with TNM stage, vascular invasion, and lymph node metastasis. In addition, they found knockdown of ZFAS1 impeded proliferation, invasion, and promoted apoptosis of colonic cancer cell lines.…”

Section: Zfas1 In Various Cancersmentioning

confidence: 99%

ZFAS1: a novel tumor-related long non-coding RNA

Dong

Zhao

et al. 2018

Cancer Cell Int

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Long non-coding RNAs (lncRNA) are classified as a kind of RNA, which are longer than 200 nucleotides in length and cannot be translated into proteins. Multiple studies have demonstrated that lncRNAs are involved in various cellular processes, including proliferation, differentiation, cell death, and metastasis. In addition, aberrant expression of lncRNAs has been discovered in human tumors, where they function as either oncogenes or tumor suppressor genes. Among numerous lncRNAs, we focus on ZNFX1 antisense RNA 1 (ZFAS1), a well-known lncRNA that is aberrant overexpression in various tumors, including melanoma, esophageal squamous cell carcinoma, non-small cell lung cancer, gastric cancer, colon cancer, and Hepatocellular carcinoma, in which it functions as oncogene. In contrast, ZFAS1 is downregulated in breast cancer, which may function as tumor suppressor gene. In this review, we provide an overview of current evidence concerning the role and potential clinical utilities of ZFAS1 in human cancers.

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“…Nie et al also revealed that lncRNA ZFAS1 could mediate the carcinogenic effects in GC partially through silencing the KLF2 and NKD2 expression by binding with PRC2 and LSD1 [19]. Epithelial-Mesenchymal Transition (EMT) was mentioned in one study that the author suggested that lncRNA ZFAS1 induce EMT by elevating ZEB1 expression [12].…”

Section: Publication Biasmentioning

confidence: 99%

“…However, there were opposite findings that elevated lncRNA ZFAS1 occurred in gastric cancer, hepatocellular carcinoma and glioma. The function of lncRNA ZFAS1 in cancer cells might be cell type-dependent [12][13][14][15][16][17][18][19][20]. Therefore, we need a systematical and comprehensive meta-analysis to explore whether overexpression of ZFAS1 in tumor are related to worse outcome.…”

Section: Oncotarget 2 Wwwimpactjournalscom/oncotargetmentioning

confidence: 99%

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Prognostic and clinicopathological role of long non-coding RNA ZFAS1 in various carcinomas

Ren¹,

Zhi²,

Shen³

et al. 2017

Oncotarget

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Long non‐coding ribonucleic acid zinc finger antisense 1 promotes the progression of colonic cancer by modulating ZEB1 expression

Abstract: Long non-coding RNA ZFAS1 may function as an oncogene by modulating ZEB1 to induce EMT. Manipulation of ZFAS1 level may be a novel approach to suppress colonic cancer progression. In addition, ZFAS1 in plasma has the potential to be a diagnostic biomarker of colonic cancer.

Cited by 63 publications

References 32 publications

PIK3R3 Promotes Metastasis of Pancreatic Cancer via ZEB1 Induced Epithelial-Mesenchymal Transition

PIK3R3 Promotes Metastasis of Pancreatic Cancer via ZEB1 Induced Epithelial-Mesenchymal Transition

ZFAS1: a novel tumor-related long non-coding RNA

Prognostic and clinicopathological role of long non-coding RNA ZFAS1 in various carcinomas

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