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image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Journal of Cellular ...arrow_drop_down
image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao
Journal of Cellular Biochemistry
Article . 2019 . Peer-reviewed
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LncRNA NOC2L‐4.1 functions as a tumor oncogene in cervical cancer progression by regulating the miR‐630/YAP1 pathway

Authors: Qingwei Wang; Jin Ding; Guo Nan; Yuanyuan Lyu; Guantai Ni;

LncRNA NOC2L‐4.1 functions as a tumor oncogene in cervical cancer progression by regulating the miR‐630/YAP1 pathway

Abstract

AbstractLong noncoding RNA (lncRNA) is a new class of noncoding RNA playing an indispensable role in different diseases by regulating miRNA. Our previous studies have suggested that miR‐630 was decreased in patients with cervical cancer. Recently, studies have shown that lncRNA NOC2L‐4.1 was abnormally expressed in patients with cervical cancer and can target miR‐630. Therefore, we wanted to identify the integrated relationship between lncRNA NOC2L‐4.1 and miR‐630 in the pathological processes regarding cervical cancer either in vitro or in vivo. Quantitative reverse transcription‐polymerase chain reaction detection shows that compared with human normal cervical epithelial cell, the expression of lncRNA NOC2L‐4.1 was significantly increased and the expression of miR‐630 was decreased in cell lines of cervical cancer. Moreover, luciferase reporter assay showed that miR‐630 was a target of lncRNA NOC2L‐4.1. The in vitro study found that downregulation of lncRNA NOC2L‐4.1 suppressed cervical cancer cell migration (transwell assays) and proliferation (cell counting kit‐8 and cloning formation assays). miR‐630 specific inhibitor treatment reversed the inhibitory effect of lncRNA NOC2L‐4.1 on cell proliferation and migration. Further studies also found that yes‐associated protein 1 (YAP1) was the target of miR‐630. Overexpression YAP1 suppressed miR‐630 overexpression induced cell proliferation and inhibition of migration. Tumors induced by implantation of lncRNA NOC2L‐4.1‐knockdown Hela cells in nude mice showed that lncRNA NOC2L‐4.1 silencing decreased the growth of tumors in both volume and weight by regulation of miR‐630/YAP1. Taken together, our study reveals the important role of lncRNA NOC2L‐4.1/miR‐630/YAP1 regulatory network in cervical cancer, which provides new insights concerning the pathogenesis of cervical cancer.

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Keywords

Mice, Inbred BALB C, Mice, Nude, Oncogenes, Gene Expression Regulation, Neoplastic, Repressor Proteins, Mice, MicroRNAs, Cell Movement, Cell Line, Tumor, Gene Knockdown Techniques, Disease Progression, Animals, Humans, Female, RNA, Long Noncoding, Adaptor Proteins, Signal Transducing, Cell Proliferation, HeLa Cells, Signal Transduction, Transcription Factors

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
22
Top 10%
Average
Top 10%
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