Evidence map›Paper›PMID 33493519›Full record

ArticleThe Journal of biological chemistry

Suppression of the NTS-CPS1 regulatory axis by AFF1 in lung adenocarcinoma cells.

Junjie Yue, Qian Dai, Shaohua Hao, Shiqi Zhu, Xiaoxu Liu, Zhiqun Tang, Meng Li, Haitong Fang, Chengqi Lin, Zhuojuan Luo

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.9field-weighted citation impact, top 32% 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

4 citing papers in PubMed, 14 citations in OpenAlex.

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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

10 authors at 3 institutions in 2 countries.

Junjie YueThe Key Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China.
Qian DaiThe Key Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China.
Shaohua HaoThe Key Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China.
Shiqi ZhuThe Key Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China.
Xiaoxu LiuThe Key Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China.
Zhiqun TangSingapore Eye research Institute, Singapore, Singapore.
Meng LiThe Key Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China.
Haitong FangThe Key Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China.
Chengqi LinThe Key Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China; Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China. Electronic address: cqlin@seu.edu.cn.
Zhuojuan LuoThe Key Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China; Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China. Electronic address: zjluo@seu.edu.cn.
Southeast University · CNNantong University · CNSingapore Eye Research Institute · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Upregulation of the neuropeptide neurotensin (NTS) in a subgroup of lung cancers has been linked to poor prognosis. However, the regulatory pathway centered on NTS in lung cancer remains unclear. Here we identified the NTS-specific enhancer in lung adenocarcinoma cells. The AF4/FMR2 (AFF) family protein AFF1 occupies the NTS enhancer and inhibits NTS transcription. Clustering analysis of lung adenocarcinoma gene expression data demonstrated that NTS expression is highly positively correlated with the expression of the oncogenic factor CPS1. Detailed analyses demonstrated that the IL6 pathway antagonizes NTS in regulating CPS1. Thus, our analyses revealed a novel NTS-centered regulatory axis, consisting of AFF1 as a master transcription suppressor and IL6 as an antagonist in lung adenocarcinoma cells.

Indexed as

A549 CellsAdenocarcinoma of LungCarbamoyl-Phosphate Synthase (Ammonia)Cell ProliferationDNA-Binding ProteinsEnhancer Elements, GeneticFemaleGene Expression Regulation, NeoplasticHumansInterleukin-6MaleNeurotensinPrognosisSignal TransductionTranscriptional Elongation FactorsAFF1 protein, humanCarbamoyl-Phosphate Synthase (Ammonia)CPS1 protein, humanDNA-Binding ProteinsIL6 protein, humanInterleukin-6NeurotensinTranscriptional Elongation FactorsAFF1enhancerlung adenocarcinomaneurotensintranscription regulation

Identifiers

PMID33493519
PMCPMC7949158
OpenAlexW3121374469

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.