Evidence map›Paper›PMID 35757841›Full record

ArticleCancer medicine2023

Mitochondrial phosphoenolpyruvate carboxykinase promotes tumor growth in estrogen receptor-positive breast cancer via regulation of the mTOR pathway.

Hui-Ping Hsu, Pei-Yi Chu, Tsung-Ming Chang, Kuo-Wei Huang, Wen-Chun Hung, Shih Sheng Jiang, Hui-You Lin, Hui-Jen Tsai

Abstract read
In one paragraph

Article in Cancer medicine, 2023. 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
–field-weighted citation impact
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.

  1. Review
  2. Review
  3. Mitochondrial control of glycerolipid synthesis by a PEP shuttle.bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Cancer biology & therapy · 2025
    Article
  6. 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

8 authors.

Hui-Ping HsuDepartment of Surgery, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Pei-Yi ChuDepartment of Pathology, Show Chwan Memorial Hospital, Changhua, Taiwan.
Tsung-Ming ChangNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan.
Kuo-Wei HuangNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan.
Wen-Chun HungNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan.
Shih Sheng JiangNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan.
Hui-You LinNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan.
Hui-Jen TsaiNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan.ORCID 0000-0001-5246-5748

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTumor cells may aberrantly express metabolic enzymes to adapt to their environment for survival and growth. Targeting cancer-specific metabolic enzymes is a potential therapeutic strategy. Phosphoenolpyruvate carboxykinase (PEPCK) catalyzes the conversion of oxaloacetate to phosphoenolpyruvate and links the tricarboxylic acid cycle and glycolysis/gluconeogenesis. Mitochondrial PEPCK (PEPCK-M), encoded by PCK2, is an isozyme of PEPCK and is distributed in mitochondria. Overexpression of PCK2 has been identified in many human cancers and demonstrated to be important for the survival program initiated upon metabolic stress in cancer cells. We evaluated the expression status of PEPCK-M and investigated the function of PEPCK-M in breast cancer.

methodsWe checked the expression status of PEPCK-M in breast cancer samples by immunohistochemical staining. We knocked down or overexpressed PCK2 in breast cancer cell lines to investigate the function of PEPCK-M in breast cancer.

resultsPEPCK-M was highly expressed in estrogen receptor-positive (ER

conclusionPEPCK-M promotes proliferation and cell cycle progression in ER

Indexed as

Breast NeoplasmsReceptors, EstrogenFemaleGlutamineHumansMechanistic Target of Rapamycin Complex 1MitochondriaPhosphoenolpyruvatePhosphoenolpyruvate Carboxykinase (ATP)TOR Serine-Threonine KinasesGlutamineMechanistic Target of Rapamycin Complex 1MTOR protein, humanPhosphoenolpyruvatePhosphoenolpyruvate Carboxykinase (ATP)Receptors, EstrogenTOR Serine-Threonine KinasesE2F1estrogen receptor positive (ER+) breast cancermitochondrial phosphoenolpyruvate carboxykinase (PEPCK-M)mTORC1PCK2

Identifiers

PMID35757841
PMCPMC9883444

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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.