Evidence map›Paper›PMID 36114745›Full record

ArticleCancer science2022

Gankyrin and TIGAR cooperatively accelerate glucose metabolism toward the PPP and TCA cycle in hepatocellular carcinoma.

Chun Yang, Xiao-Wen Cui, Zhi-Wen Ding, Tian-Yi Jiang, Xiao-Fan Feng, Yu-Fei Pan, Yun-Kai Lin, Tai-Yu Shang, Qing Wang, Jian Pan and 3 more

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

Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 13 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

13 authors at 4 institutions in 2 countries.

Chun YangInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Hospital, The Naval Medical University, Shanghai, China.
Xiao-Wen CuiInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Hospital, The Naval Medical University, Shanghai, China.
Zhi-Wen DingDepartment of Hepatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Tian-Yi JiangNational Center for Liver Cancer, The Naval Medical University, Shanghai, China.
Xiao-Fan FengNational Center for Liver Cancer, The Naval Medical University, Shanghai, China.
Yu-Fei PanNational Center for Liver Cancer, The Naval Medical University, Shanghai, China.
Yun-Kai LinNational Center for Liver Cancer, The Naval Medical University, Shanghai, China.
Tai-Yu ShangNational Center for Liver Cancer, The Naval Medical University, Shanghai, China.
Qing WangNational Center for Liver Cancer, The Naval Medical University, Shanghai, China.
Jian PanInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Jian WangInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Hong-Yang WangInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Hospital, The Naval Medical University, Shanghai, China.ORCID https://orcid.org/0000-0002-4709-3334
Li-Wei DongInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Hospital, The Naval Medical University, Shanghai, China.ORCID https://orcid.org/0000-0003-2116-1674
Naval University of Engineering · CNSecond Military Medical University · CNSoochow University · CNFudan University Shanghai Cancer Center · CN

Funding

Applied Foundational Research of Medical and Health Care of Suzhou City SYS2019079Applied Foundational Research of Medical and Health Care of Suzhou City SYSD2018206Jiangsu Commission of Health supported program M2021041National Natural Science Foundation of China 81802311National Natural Science Foundation of China 82172895National Natural Science Foundation of China 82203586the Clinical Research Plan of SHDC SHDC2020CR2011A
6 · The paper itself

Abstract

Oncogene-derived metabolic reprogramming is important for anabolic growth of cancer cells, which is now considered to be not simply rely on glycolysis. Pentose phosphate pathway and tricarboxylic acid cycle also play pivotal roles in helping cancer cells to meet their anabolic and energy demands. The present work focused on gankyrin, a relatively specific oncogene in hepatocellular carcinoma (HCC), and its impact on glycolysis and mitochondrial homeostasis. Metabolomics, RNA-seq analysis, and subsequent conjoint analysis illustrated that gankyrin regulated the pentose phosphate pathway (PPP), tricarboxylic acid (TCA) cycle, and mitochondrial function and homeostasis, which play pivotal roles in tumor development. Mechanistically, gankyrin was found to modulate HCC metabolic reprogramming via TIGAR. Gankyrin positively regulated the transcription of TIGAR through Nrf2, which bound to the antioxidant response elements (AREs) in the promoter of TIGAR. Interestingly, TIGAR feedback regulated the transcription of Nrf2 and subsequently gankyrin by promoting nuclear importation of PGC1α. The loop between gankyrin, Nrf2, and TIGAR accelerated glucose metabolism toward the PPP and TCA cycle, which provided vital building blocks, such as NADPH, ATP, and ribose of tumor and further facilitated the progression of HCC.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsCitric Acid CycleGlucoseGlycolysisHumansGlucosegankyrinmetabolism reprogrammitochondrial functionpentose phosphate pathwayTIGAR

Identifiers

PMID36114745
PMCPMC9746032
OpenAlexW4296120343

What OpenQuestion holds

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Registered trials

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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.