LncRNA NCK1-AS1 promotes proliferation and induces cell cycle progression by crosstalk NCK1-AS1/miR-6857/CDK1 pathway

Li, Haiyu; Jia, Yongqin; Cheng, Jun; Liu, Geli; Song, Fangzhou

doi:10.1038/s41419-017-0249-3

Cited by 52 publications

(50 citation statements)

References 34 publications

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“…In recent years, many studies have reported that lncRNAs can function as ceRNA to regulate the expression of miRNAs in many cancers . For example, Li et al reported that lncRNA NCK1‐AS1 promotes proliferation and induces cell cycle progression by regulating the NCK1‐AS1/miR‐6857/CDK1 pathway in CC cells. In addition, Yu et al reported that lncRNA HCP5 promotes the development of cervical cancer by regulating MACC1 by suppression of miRNA‐15a.…”

Section: Discussionmentioning

confidence: 99%

DANCR‐mediated microRNA‐665 regulates proliferation and metastasis of cervical cancer through the ERK/SMAD pathway

et al. 2019

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Emerging evidence has indicated that microRNAs (miRNAs) play an important role in cervical cancer (CC). However, the role of miRNA (miR)‐665 in cervical cancer remains unclear. The aim of the present study was to investigate the potential functions of miR‐665 in CC and to identify the underlying mechanisms of action. Herein, we show that miR‐665 was downregulated in CC tissues and cell lines, which is negatively correlated with tumor size, distant metastasis, advanced TNM stage and poor prognosis. Functionally, miR‐665 inhibited cell proliferation, migration and invasion and resistance of cisplatin for CC cells, as well as tumor growth. We validated that transforming growth factor beta receptor 1 (TGFBR1) was a direct target of miR‐665 and mediated the ERK/SMAD pathway. In addition, we identified miR‐665 as the competing endogenous RNA for long noncoding (lnc)‐DANCR. These observations suggested that lnc‐DANCR‐mediated miR‐665 downregulation regulates the malignant phenotype of CC cells by targeting TGFBR1 through the ERK/SMAD pathway, which may present a pathway for novel therapeutic stratagems for CC therapy.

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Section: Discussionmentioning

confidence: 99%

DANCR‐mediated microRNA‐665 regulates proliferation and metastasis of cervical cancer through the ERK/SMAD pathway

et al. 2019

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“…reported that up‐regulation of lncRNA C5orf66‐AS1 contributed to CC cell proliferation both in vitro and in vivo . Li et al . reported the oncogenic function of lncRNA NCK1‐AS1 in CC progression.…”

Section: Discussionmentioning

confidence: 99%

ELK1‐activated GPC3‐AS1/GPC3 axis promotes the proliferation and migration of cervical cancer cells

Zhu

2019

The Journal of Gene Medicine

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Background Long non‐coding RNA (lncRNA) is reported to be involved in multiple biological processes in numerous human tumors. Furthermore, an increasing number of studies have confirmed the involvement of lncRNA in the initiation and development of human cancers, including cervical cancer (CC). Methods The present study explored the potential role of lncRNA glypican 3 antisense transcript 1 (GPC3‐AS1) with respect to regulating CC cell proliferation and migration. Results A quantitative reverse transcriptase‐polymerase chain reaction confirmed that GPC3‐AS1 was up‐regulated in CC cells compared to normal CRL‐2614 cells. Loss‐of‐function assays demonstrated the negative effect of GPC3‐AS1 depletion on CC cell proliferation and migration. GPC3‐AS1 positively regulated its nearby gene glypican 3 (GPC3). Significant up‐regulation of GPC3 was also observed in CC cells, consistently with GPC3‐AS1. In addition, GPC3‐AS1 and GPC3 synergistically promoted the proliferative and migratory abilities of CC cells. Mechanistic investigation showed that ELK1 acted as the transcription activator of GPC3‐AS1 and GPC3, thus contributing to their up‐regulation in CC cells. Rescue assays indicated that the ELK1‐induced GPC3‐AS1/GPC3 axis promoted cell proliferation and migration in CC. Conclusions The results of the present study have revealed a novel molecular pathway that can regulate CC cell proliferation and migration, thus providing a new basis for investigating the molecular mechanism associated with CC progression.

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“…The expression of these genes is not only regulated at the transcriptional level but also at the post-transcriptional level. Recent studies have revealed that lncRNAs are involved in the occurrence and development of various tumors, including cervical cancer [17][18][19][20], attracting increasing attention from researchers. In the present study, lncRNA chip analysis was performed using 10 pairs of cervical cancer and para-carcinoma tissue samples, and 20 lncRNAs with significant differences in their expression were further verified.…”

Section: Discussionmentioning

confidence: 99%

lncRNA DLG1-AS1 Promotes Cell Proliferation by Competitively Binding with miR-107 and Up-Regulating ZHX1 Expression in Cervical Cancer

Xin

Huang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Recent studies have revealed that long non-coding RNAs (lncRNAs) are involved in the occurrence and development of various tumors, thereby attracting increasing attention from researchers. The important biological functions of lncRNAs have been recognized gradually, but their mechanism in cervical cancer remains unclear. Methods: Differentially expressed lncRNAs in cervical cancer and para-carcinoma tissues were identified by screening using an lncRNA array, and candidate lncRNAs were verified by quantitative real-time PCR. A series of bioinformatics and molecular biological methods were adopted to investigate the interactions among lncRNAs, microRNAs (miRNAs), and miRNA target genes in cervical cancer. Cell viability was measured using a Cell Counting Kit-8 assay. Results: DLG1-AS1 was the most significantly up-regulated lncRNA in cervical cancer tissues, and it was confirmed that cervical cancer patients with high DLG1-AS1 expression had a poor prognosis. Down-regulation of DLG1-AS1 expression suppressed the proliferation of cervical cancer cells. Further investigation revealed that DLG1-AS1 eliminated the inhibition of miR-107 on the expression of its target gene ZHX1 by competitively binding to miR-107. Moreover, rescue assays proved that the effect of DLG1-AS1 on the proliferation of cervical cancer cells was dependent on miR-107. Conclusion: DLG1-AS1/miR-107/ZHX1 can form a competitive endogenous RNA network that regulates the proliferation of cervical cancer cells, resulting in tumor progression.

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LncRNA NCK1-AS1 promotes proliferation and induces cell cycle progression by crosstalk NCK1-AS1/miR-6857/CDK1 pathway

Cited by 52 publications

References 34 publications

DANCR‐mediated microRNA‐665 regulates proliferation and metastasis of cervical cancer through the ERK/SMAD pathway

DANCR‐mediated microRNA‐665 regulates proliferation and metastasis of cervical cancer through the ERK/SMAD pathway

ELK1‐activated GPC3‐AS1/GPC3 axis promotes the proliferation and migration of cervical cancer cells

lncRNA DLG1-AS1 Promotes Cell Proliferation by Competitively Binding with miR-107 and Up-Regulating ZHX1 Expression in Cervical Cancer

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