Evidence map›Paper›PMID 36849569›Full record

ArticleNature communications2023

mcPGK1-dependent mitochondrial import of PGK1 promotes metabolic reprogramming and self-renewal of liver TICs.

Zhenzhen Chen, Qiankun He, Tiankun Lu, Jiayi Wu, Gaoli Shi, Luyun He, Hong Zong, Benyu Liu, Pingping Zhu

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
13.4field-weighted citation impact, top 1% 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

42 citing papers in PubMed, 56 citations in OpenAlex.

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  5. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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  13. The Immune Microenvironment in Liver Cancer: From Analysis to Targeting.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    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

9 authors at 3 institutions in 1 country.

Zhenzhen Chen *School of Life Sciences, Zhengzhou University, 100 Kexue Road, Zhengzhou, Henan, 450001, China. chenzz2015@zzu.edu.cn.ORCID 0000-0003-2093-4639
Qiankun He *School of Life Sciences, Zhengzhou University, 100 Kexue Road, Zhengzhou, Henan, 450001, China.ORCID 0000-0001-6252-7818
Tiankun Lu *School of Life Sciences, Zhengzhou University, 100 Kexue Road, Zhengzhou, Henan, 450001, China.ORCID 0000-0002-8483-2087
Jiayi Wu *School of Medicine, Nankai University, 94 Weijin Road, Tianjin, 300071, China.ORCID 0000-0002-4819-2190
Gaoli ShiSchool of Life Sciences, Zhengzhou University, 100 Kexue Road, Zhengzhou, Henan, 450001, China.
Luyun HeDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, 450001, China.ORCID 0000-0001-9602-010X
Hong ZongDepartment of Oncology, The First Affiliated Hospital of Zhengzhou University, NO.1 Eastern Jianshe Road, Zhengzhou, 450052, Henan, China.
Benyu LiuResearch Center of Basic Medicine, Academy of Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China. benyuliu@zzu.edu.cn.ORCID 0000-0001-5812-7221
Pingping ZhuSchool of Life Sciences, Zhengzhou University, 100 Kexue Road, Zhengzhou, Henan, 450001, China. zhup@zzu.edu.cn.ORCID 0000-0002-8009-2923
Zhengzhou University · CNFirst Affiliated Hospital of Zhengzhou University · CNNankai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver tumour-initiating cells (TICs) contribute to tumour initiation, metastasis, progression and drug resistance. Metabolic reprogramming is a cancer hallmark and plays vital roles in liver tumorigenesis. However, the role of metabolic reprogramming in TICs remains poorly explored. Here, we identify a mitochondria-encoded circular RNA, termed mcPGK1 (mitochondrial circRNA for translocating phosphoglycerate kinase 1), which is highly expressed in liver TICs. mcPGK1 knockdown impairs liver TIC self-renewal, whereas its overexpression drives liver TIC self-renewal. Mechanistically, mcPGK1 regulates metabolic reprogramming by inhibiting mitochondrial oxidative phosphorylation (OXPHOS) and promoting glycolysis. This alters the intracellular levels of α-ketoglutarate and lactate, which are modulators in Wnt/β-catenin activation and liver TIC self-renewal. In addition, mcPGK1 promotes PGK1 mitochondrial import via TOM40 interactions, reprogramming metabolism from oxidative phosphorylation to glycolysis through PGK1-PDK1-PDH axis. Our work suggests that mitochondria-encoded circRNAs represent an additional regulatory layer controlling mitochondrial function, metabolic reprogramming and liver TIC self-renewal.

Indexed as

LiverOxidative PhosphorylationCarcinogenesisHumansLactic AcidMitochondriaPhosphoglycerate KinaseRNA, CircularRNA, MitochondrialLactic AcidPGK1 protein, humanPhosphoglycerate KinaseRNA, CircularRNA, Mitochondrial

Identifiers

PMID36849569
PMCPMC9971191
OpenAlexW4322490075

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.