Evidence map›Paper›PMID 34132347›Full record

ArticleBioscience reports2021

Hypoxia-induced PTTG3P contributes to colorectal cancer glycolysis and M2 phenotype of macrophage.

Yue Wang, Guilin Yu, Yiyang Liu, Longfei Xie, Jinnian Ge, Guohua Zhao, Jie Lin

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2021. 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
2.2field-weighted citation impact, top 12% 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, 31 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

7 authors at 4 institutions in 2 countries.

Yue Wang *Department of General Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Liaoning 110042, P.R. China.
Guilin Yu *Department of General Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Liaoning 110042, P.R. China.
Yiyang LiuDepartment of Surgery, Affiliated Hospital of Youjiang Medical University for Nationalities, 533000, Guangxi Zhuang Autonomous Region, P.R. China.
Longfei XieDepartment of Physics and Integrative Biology, University of California, Berkeley, CA 94720, U.S.A.
Jinnian GeDepartment of General Surgery, The Central Hospital of Shenyang Medical College, Liaoning 110031, P.R. China.
Guohua ZhaoDepartment of General Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Liaoning 110042, P.R. China.
Jie LinDepartment of General Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Liaoning 110042, P.R. China.ORCID 0000-0002-5167-2814
Liaoning Cancer Hospital & Institute · CNAffiliated Hospital of Youjiang Medical University for Nationalities · CNCentral Hospital Affiliated to Shenyang Medical College · CNUniversity of California, Berkeley · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long noncoding RNAs (lncRNAs) play critical factors in tumor progression and are ectopically expressed in malignant tumors. Until now, lncRNA pituitary tumor-transforming 3, pseudogene (PTTG3P) biological function in colorectal cancer (CRC) further needs to be clarified. qRT-PCR was used to measure the PTTG3P level and CCK-8, glucose uptake, lactate assay, adenosine triphosphate (ATP) assay, extracellular acidification rate (ECAR) assay, and xenograft mice model were adopted to evaluate the glycolysis and proliferation, and macrophage polarization were determined in CRC cells. Xenograft experiments were utilized to analyze tumor growth. Ectopic expression of PTTG3P was involved in CRC and related to dismal prognosis. Through gain- and loss-of-function approaches, PTTG3P enhanced cell proliferation and glycolysis through YAP1. Further, LDHA knockdown or glycolysis inhibitor (2-deoxyglucose (2-DG), 3-BG) recovered from PTTG3P-induced proliferation. And PTTG3P overexpression could facilitate M2 polarization of macrophages. Silenced PTTG3P decreased the level of inflammatory cytokines TNF-α, IL-1β and IL-6, and low PTTG3P expression related with CD8+ T, NK, and TFH cell infiltration. Besides, hypoxia-inducible factor-1α (HIF1A) could increase PTTG3P expression by binding to the PTTG3P promoter region. Hypoxia-induced PTTG3P contributes to glycolysis and M2 phenotype of macrophage, which proposes a novel approach for clinical treatment.

Indexed as

GlycolysisPseudogenesTumor HypoxiaAnimalsCell ProliferationColorectal NeoplasmsCytokinesDatabases, GeneticFemaleGene Expression Regulation, NeoplasticHCT116 CellsHT29 CellsHumansInflammation MediatorsMaleMiceCytokinesInflammation MediatorsRNA, Long NoncodinghypoxiapseudogenePTTG3PYAP1

Identifiers

PMID34132347
PMCPMC8264182
OpenAlexW3158653173

What OpenQuestion holds

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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.