Evidence map›Paper›PMID 29416014›Full record

ArticleCell death & disease2018

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

Haiyu Li, Yongqin Jia, Junning Cheng, Geli Liu, Fangzhou Song

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.2field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 71 citations in OpenAlex.

  1. Long noncoding RNAs in female malignancies: critical review of molecular mechanisms, clinical gaps, and therapeutic perspectives.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  13. Long Non-coding RNAs in Cisplatin Resistance in Osteosarcoma.Current treatment options in oncology · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Haiyu LiMolecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, 400016, China.
Yongqin JiaMolecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, 400016, China.
Junning ChengMolecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, 400016, China.
Geli LiuMolecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, 400016, China.
Fangzhou SongMolecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, 400016, China. fzsongcq@163.com.
Chongqing Medical University · CNDalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The purpose of this study was to develop an lncRNA signature to improve the prediction of the prognosis of cervical cancer through integration bioinformatics and analysis of TCGA RNA sequencing data. In this study, we established a set of four lncRNA signatures that was significantly associated with recurrence-free survival using the Cox regression model. Functionally, we screened the CC-associated lncRNA NCK1-AS1 as a new candidate lncRNA and regulator which promotes development and progression in CC. qRT-PCR and RNA in situ hybridization (RISH) results showed that NCK1-AS1 was significantly up-regulated in 77.4% (24/31) of the CC tissue group compared with the normal group (P < 0.01). Interestingly, we demonstrated that transcription factor SP1 directly binds to the promoter to activate NCK1-AS1 expression in SiHa cells. In vitro and in vivo assays of silencing NCK1-AS1 significantly inhibited cell proliferation and invasion, with induction of cell arrest in S phase of the cell cycle. Furthermore, Human Transcriptome Array 2.0 analysis after NCK1-AS1 silencing highlighted alterations in cell proliferation and cell cycle pathways. NCK1-AS1 functioned as a molecular sponge for miR-6857, antagonizing its ability to repress CDK1/6 protein translation. In conclusion, these findings suggest that NCK1-AS1/miR-6857/CDK1 crosstalk serve as a critical effector in cervical cancer progression and may serve as a potential target in cervical cancer.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCDC2 Protein KinaseCell CycleCell Line, TumorCell ProliferationDisease ProgressionFemaleHumansMiceMice, Inbred BALB CMice, NudeMiddle AgedOncogene ProteinsPromoter Regions, GeneticRNA, AntisenseAdaptor Proteins, Signal TransducingCDC2 Protein KinaseCDK1 protein, humanNck proteinOncogene ProteinsRNA, AntisenseRNA, Long Noncoding

Identifiers

PMID29416014
PMCPMC5833418
OpenAlexW2791566014

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.