Evidence map›Paper›PMID 36978001›Full record

ArticleBMC cancer2023

NPAS2 promotes aerobic glycolysis and tumor growth in prostate cancer through HIF-1A signaling.

Shuaijun Ma, Yafan Chen, Penghe Quan, Jingliang Zhang, Shichao Han, Guohui Wang, Ruochen Qi, Xiaoyan Zhang, Fuli Wang, Jianlin Yuan and 3 more

Open access · goldFull text read
In one paragraph

Article in BMC cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

21 citing papers in PubMed, 42 citations in OpenAlex.

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  7. Circadian clock and cancer.Military Medical Research · 2026
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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

13 authors at 2 institutions in 1 country.

Shuaijun Ma *Department of Urology, The First Affiliated Hospital of Air Force Medical University, 127 Changle West Road, 710032, Xi 'an, Shaanxi, China.
Yafan Chen *Department of Human Movement Science, Xi'an Physical Education University, Xi'an, China.
Penghe Quan *Department of Urology, The First Affiliated Hospital of Air Force Medical University, 127 Changle West Road, 710032, Xi 'an, Shaanxi, China.
Jingliang ZhangDepartment of Urology, The First Affiliated Hospital of Air Force Medical University, 127 Changle West Road, 710032, Xi 'an, Shaanxi, China.
Shichao HanDepartment of Urology, The First Affiliated Hospital of Air Force Medical University, 127 Changle West Road, 710032, Xi 'an, Shaanxi, China.
Guohui WangDepartment of Urology, The First Affiliated Hospital of Air Force Medical University, 127 Changle West Road, 710032, Xi 'an, Shaanxi, China.
Ruochen QiDepartment of Urology, The First Affiliated Hospital of Air Force Medical University, 127 Changle West Road, 710032, Xi 'an, Shaanxi, China.
Xiaoyan ZhangDepartment of Urology, The First Affiliated Hospital of Air Force Medical University, 127 Changle West Road, 710032, Xi 'an, Shaanxi, China.
Fuli WangDepartment of Urology, The First Affiliated Hospital of Air Force Medical University, 127 Changle West Road, 710032, Xi 'an, Shaanxi, China.
Jianlin YuanDepartment of Urology, The First Affiliated Hospital of Air Force Medical University, 127 Changle West Road, 710032, Xi 'an, Shaanxi, China. jianliny@fmmu.edu.cn.
Xiaojian YangDepartment of Urology, The First Affiliated Hospital of Air Force Medical University, 127 Changle West Road, 710032, Xi 'an, Shaanxi, China. yangxiaojianxjh@163.com.
Weijing JiaDepartment of Hematology, The First Affiliated Hospital of Air Force Medical University, 127 Changle West Road, 710032, Xi 'an, Shaanxi, China. jiaweijing1989@yeah.net.
Weijun QinDepartment of Urology, The First Affiliated Hospital of Air Force Medical University, 127 Changle West Road, 710032, Xi 'an, Shaanxi, China. qinweij@fmmu.edu.cn.
Air Force Medical University · CNXi'an Physical Education University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProstate cancer (PCa), one of the common malignant tumors, is the second leading cause of cancer-related deaths in men. The circadian rhythm plays a critical role in disease. Circadian disturbances are often found in patients with tumors and enable to promote tumor development and accelerate its progression. Accumulating evidence suggests that the core clock gene NPAS2 (neuronal PAS domain-containing protein 2) has been implicated in tumors initiation and progression. However, there are few studies on the association between NPAS2 and prostate cancer. The purpose of this paper is to investigate the impact of NPAS2 on cell growth and glucose metabolism in prostate cancer.

methodsQuantitative real-time PCR (qRT-PCR), immunohistochemical (IHC) staining, western blot, GEO (Gene Expression Omnibus) and CCLE (Cancer Cell Line Encyclopedia) databases were used to analyze the expression of NPAS2 in human PCa tissues and various PCa cell lines. Cell proliferation was assessed using MTS, clonogenic assays, apoptotic analyses, and subcutaneous tumor formation experiments in nude mice. Glucose uptake, lactate production, cellular oxygen consumption rate and medium pH were measured to examine the effect of NPAS2 on glucose metabolism. The relation of NPAS2 and glycolytic genes was analyzed based on TCGA (The Cancer Genome Atlas) database.

resultsOur data showed that NPAS2 expression in prostate cancer patient tissue was elevated compared with that in normal prostate tissue. NPAS2 knockdown inhibited cell proliferation and promoted cell apoptosis in vitro and suppressed tumor growth in a nude mouse model in vivo. NPAS2 knockdown led to glucose uptake and lactate production diminished, oxygen consumption rate and pH elevated. NPAS2 increased HIF-1A (hypoxia-inducible factor-1A) expression, leading to enhanced glycolytic metabolism. There was a positive correlation with the expression of NPAS2 and glycolytic genes, these genes were upregulated with overexpression of NPAS2 while knockdown of NPAS2 led to a lower level.

conclusionNPAS2 is upregulated in prostate cancer and promotes cell survival by promoting glycolysis and inhibiting oxidative phosphorylation in PCa cells.

Indexed as

Prostatic NeoplasmsAnimalsBasic Helix-Loop-Helix ProteinsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticGlucoseGlycolysisHumansHypoxia-Inducible Factor 1, alpha SubunitLactic AcidMaleMiceMice, NudeNerve Tissue ProteinsBasic Helix-Loop-Helix ProteinsGlucoseHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitLactic AcidNerve Tissue ProteinsNPAS2 protein, humanGlycolysisHIF-1ANPAS2Oxidative phosphorylationProstate cancer (PCa)

Identifiers

PMID36978001
PMCPMC10045944
OpenAlexW4361223414

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read53
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.