Evidence map›Paper›PMID 35847493›Full record

ArticleActa pharmaceutica Sinica. B2022

Nuclear TIGAR mediates an epigenetic and metabolic autoregulatory loop

Hong Wang, Qianqian Wang, Guodi Cai, Zhijian Duan, Zoann Nugent, Jie Huang, Jianwei Zheng, Alexander D Borowsky, Jian Jian Li, Peiqing Liu and 4 more

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

Article in Acta pharmaceutica Sinica. B, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. TIGAR Suppresses ER Stress-Induced Neuronal Injury through Targeting ATF4 Signaling in Cerebral Ischemia/Reperfusion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
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  12. Review
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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

14 authors at 5 institutions in 3 countries.

Hong WangSchool of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
Qianqian WangSchool of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
Guodi CaiSchool of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
Zhijian DuanDepartment of Biochemistry and Molecular Medicine, University of California, Davis, Sacramento, CA 95817, USA.
Zoann NugentResearch Institute in Oncology and Hematology, University of Manitoba and CancerCare Manitoba, Winnipeg R3E 0V9, Canada.
Jie HuangGuangdong Lung Cancer Institute, Guangdong Provincial Key Laboratory of Translational Medicine in Lung Cancer, Guangdong Provincial People's Hospital and Guangdong Academy of Medical Sciences, Guangzhou 510080, China.
Jianwei ZhengSchool of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
Alexander D BorowskyDepartment of Pathology and Laboratory Medicine, University of California, Davis, Sacramento, CA 95817, USA.
Jian Jian LiDepartment of Radiation Oncology, University of California, Davis, Sacramento, CA 95817, USA.
Peiqing LiuSchool of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
Hsing-Jien KungDepartment of Biochemistry and Molecular Medicine, University of California, Davis, Sacramento, CA 95817, USA.
Leigh MurphyResearch Institute in Oncology and Hematology, University of Manitoba and CancerCare Manitoba, Winnipeg R3E 0V9, Canada.
Hong-Wu ChenDepartment of Biochemistry and Molecular Medicine, University of California, Davis, Sacramento, CA 95817, USA.
Junjian WangSchool of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
Sun Yat-sen University · CNUniversity of California, Davis · USCancerCare Manitoba · CAUC Davis Comprehensive Cancer CenterGuangdong Academy of Medical Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic and epigenetic reprogramming play important roles in cancer therapeutic resistance. However, their interplays are poorly understood. We report here that elevated TIGAR (TP53-induced glycolysis and apoptosis regulator), an antioxidant and glucose metabolic regulator and a target of oncogenic histone methyltransferase NSD2 (nuclear receptor binding SET domain protein 2), is mainly localized in the nucleus of therapeutic resistant tumor cells where it stimulates NSD2 expression and elevates global H3K36me2 mark. Mechanistically, TIGAR directly interacts with the antioxidant master regulator NRF2 and facilitates chromatin recruitment of NRF2, H3K4me3 methylase MLL1 and elongating Pol-II to stimulate the expression of both new (NSD2) and established (

Indexed as

ARE, antioxidant response elementDoxR, doxorubicin resistantEpigenetic reprogrammingF2,6bPase, fructose-2,6-bisphosphataseFBS, fetal bovine serumMetabolismNLS, nuclear localization signalNRF2NRF2, NF-E2-related factor-2NSCLC, non-small-cell lung carcinomaNSD2NSD2, nuclear receptor binding SET domain protein 2Oxidative stressPGC1α, PPARG coactivator 1 alphaPPP, pentose phosphate pathwayRadR, ionizing radiation-resistanceRedox homeostasisTamR, tamoxifen resistantTherapeutic resistanceTIGARTIGAR, TP53-induced glycolysis and apoptosis regulator

Identifiers

PMID35847493
PMCPMC9279715
OpenAlexW3209800860

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.