Long non‐coding RNA PlncRNA‐1 promotes cell proliferation and hepatic metastasis in colorectal cancer

Ge, Jia; Zhang, Mingming; Wang, Kang; Zhao, Gaoping; Pang, Ming; Chen, Zheyu

doi:10.1002/jcb.27031

Cited by 20 publications

(14 citation statements)

References 38 publications

(72 reference statements)

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“…Thirty-one studies demonstrated that increased lncRNA expression was associated with increased cellular proliferation in vitro. 37,38,[40][41][42][43][44][45]49,50,54,58,59,[61][62][63][65][66][67]69,72,73,77,79,80,83,84,[86][87][88][89][90][94][95][96][97] In contrast, decreased expression of four lncRNAs was associated with increased cellular proliferation. 46,68,75,85…”

Section: Cell Proliferationmentioning

confidence: 99%

Long non-coding RNA (lncRNA) and epithelial-mesenchymal transition (EMT) in colorectal cancer: a systematic review

O’Brien

Bishop

Hallion

et al. 2020

Cancer Biology & Therapy

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Background: Colorectal cancer (CRC) is a leading cause of cancer-related death. Epithelial-mesenchymal transition (EMT) is a major process in tumor metastasis development. This systematic review aims to describe the role of long non-coding RNA (lncRNA) in EMT in CRC. Methods: The electronic databases, PubMed, Cochrane, and EMBASE, were searched from January1990 to June 2019 to identify studies examining lncRNA and their role in mediating EMT in CRC. Studies examining clinical specimens and/or in vitro experiments were included. Results: In 61 identified studies, 54 lncRNAs were increased in CRC compared to normal colorectal epithelium. Increased lncRNA expression was frequently associated with worse survival. Many lncRNAs mediate their effect through competitive endogenous RNA or transcription factor regulation. The ZEB1, 2/ E-cadherin, Wnt/β-catenin signaling, and chromatin remodeling pathways are discussed in particular. Conclusions: lncRNAs are major regulators of EMT and predictor adverse outcome in CRC patients. Future research must focus on delineating lncRNA function prior to potential clinical use.

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Section: Cell Proliferationmentioning

confidence: 99%

Long non-coding RNA (lncRNA) and epithelial-mesenchymal transition (EMT) in colorectal cancer: a systematic review

O’Brien

Bishop

Hallion

et al. 2020

Cancer Biology & Therapy

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“…LncRNAs have become a hot topic as diagnostic markers of diseases. The transcriptional level of PlncRNA-1 is signi cantly elevated in multiple malignancies, and PlncRNA-1 acts as a transcriptional regulator of various developmental processes [17][18][19][20][21][22][23][24][25]. In several human tumours, overexpression of PlncRNA-1 is related to poor OS, high TNM classi cation, advanced clinical stage, low histological differentiation, and poor vital status [20,22,24,[32][33][34].…”

Section: Discussionmentioning

confidence: 99%

“…PlncRNA-1 is ubiquitously expressed in the prostate, salivary glands and 25 other tissues. It has been shown that PlncRNA-1 plays an important role in various cancer types, including prostate cancer, colorectal cancer, osteosarcoma, glioma and oesophageal squamous carcinoma [17][18][19][20][21][22][23][24][25][26]. Accumulating evidence has demonstrated that PlncRNA-1 acts as a transcriptional regulator to modify various developmental processes.…”

Section: Introductionmentioning

confidence: 99%

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The prognostic value of long non-coding RNA PlncRNA-1 in patients with cancers: a systematic review and meta-analysis

Lei

Sheng

et al. 2020

Preprint

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Background We performed this meta-analysis to elucidate whether the expression of PlncRNA-1 might serve as an effective prognostic marker for various cancers. Methods We conducted a database search of PubMed, ScienceDirect, Embase, Web of Science and CNKI database (up to Oct 31, 2019). The pooled hazard ratio (HR), odds ratio (OR) and 95% confidence interval (CI) were used to estimate the strength of the relationship between PlncRNA-1 expression and the clinical prognosis of cancer patients. Results The results showed that elevated PlncRNA-1 expression predicted a poor OS with pooled HRs of 1.43 (95% CI: 1.25-1.63, I 2 =63.1%, P=0.004). Likewise, we found that advanced tumour stages were associated with upregulated PlncRNA-1 expression in various cancer types (III–IV vs I–II: OR=2.79, 95% CI: 1.76-4.41, I 2 =0%, P=0.822),patients with high PlncRNA-1 expression might have an increased risk of large tumours (OR=2.03, 95% CI: 1.31-3.14, I 2 =67.1%, P=0.028). Conclusions PlncRNA-1 might be used as a prognostic biomarker and as a tool for the early detection of various tumours.

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“…PlncRNA-1 targets β-catenin through a competitive endogenous RNA mechanism with miR-204 to mediate EMT. 77 In contrast, H19 and TUG1 target β-catenin indirectly by targeting molecules that interact with β-catenin. 66,[78][79][80] H19 targets PGRN and TUG1 targets KIAA1199, through miR-29b binding and miR-600 binding respectively.…”

Section: Wnt/β-catenin Signalingmentioning

confidence: 99%

The identification of long non-coding RNA ZFAS1 through an exploratory RNA-sequencing analysis and its association with epithelial-to-mesenchymal transition in colon cancer adenocarcinoma.

O’Brien¹

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Colorectal adenocarcinoma is the fourth most common cancer diagnosed worldwide and is a significant cause of morbidity and mortality. This dissertation performed an exploratory RNA-sequencing analysis comparing gene expression between colon adenocarcinoma tissue and paired normal colon epithelium. After identification of a number of lncRNAs that were increased in expression in colon adenocarcinoma compared to normal colon epithelium, we aimed to validate the expression and investigate their function in vitro. Specifically, we focused on the lncRNA ZFAS1 and its association with epithelial-to-mesenchymal transition. These studies found the following: 1. Seven candidate lncRNAs were identified from the exploratory RNA-sequencing analysis to be significantly increased in expression in colon adenocarcinoma, three of viii which ZFAS1, GAS5, and PVT1 were found to be significantly increased in colon adenocarcinoma compared to paired normal colon epithelium as examined by laser capture microdissection. 2. Both ZFAS1 and GAS5 are significantly increased in cytoplasm of cell lines compared to the nucleus, whereas PVT1 was more represented in the nucleus. As such there was significant knockdown of both ZFAS1 and GAS5 following transfection with siRNA. 3. Knockdown of ZFAS1 leads to decreased proliferation and migration in colon adenocarcinoma cell lines. In contrast, knockdown of GAS5 did not lead to a change in proliferation. We focused our subsequent investigation on ZFAS1. 4. ZFAS1 has a reciprocal relationship with miR-200b and miR-200c expression in vitro but not with three of the other experimentally verified miRNAs that bind ZFAS1. We also validated the functional effect of miR-200b and miR-200c mimics on decreasing cell migration. 5. ZFAS1 knockdown is associated with the functional changes on cellular phenotype through decreasing ZEB1 expression through miR-200 signaling, causing a subsequent increase in the expression of the epithelial marker, E-cadherin, and a decrease in the expression of the mesenchymal marker, vimentin. These findings demonstrate an association between ZFAS1 and miR-200/ZEB1/Ecadherin, vimentin signaling in EMT signaling in colon adenocarcinoma. In contrast to typical EMT signaling, ZFAS1 knockdown also leads to decreased cell proliferation suggesting its potential value as a therapeutic agent.

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Long non‐coding RNA PlncRNA‐1 promotes cell proliferation and hepatic metastasis in colorectal cancer

Cited by 20 publications

References 38 publications

Long non-coding RNA (lncRNA) and epithelial-mesenchymal transition (EMT) in colorectal cancer: a systematic review

Long non-coding RNA (lncRNA) and epithelial-mesenchymal transition (EMT) in colorectal cancer: a systematic review

The prognostic value of long non-coding RNA PlncRNA-1 in patients with cancers: a systematic review and meta-analysis

The identification of long non-coding RNA ZFAS1 through an exploratory RNA-sequencing analysis and its association with epithelial-to-mesenchymal transition in colon cancer adenocarcinoma.

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