Evidence map›Paper›PMID 38774408›Full record

ReviewFrontiers in oncology2024

From metabolism to malignancy: the multifaceted role of PGC1α in cancer.

Yue Wang, Jianing Peng, Dengyuan Yang, Zhongjie Xing, Bo Jiang, Xu Ding, Chaoyu Jiang, Bing Ouyang, Lei Su

Abstract readReview
In one paragraph

Review in Frontiers in oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Article
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  3. Oxidative Phosphorylation and Fatty Acid Oxidation Are Central to Mitochondrial Metabolism Rewiring in CML Stem/Progenitor Cell Survival.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
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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.

Yue Wang *Department of Surgery, Nanjing Central Hospital, Nanjing, China.
Jianing Peng *Division of Biosciences, University College London, London, United Kingdom.
Dengyuan Yang *Department of Surgery, Nanjing Central Hospital, Nanjing, China.
Zhongjie XingDepartment of Surgery, Nanjing Central Hospital, Nanjing, China.
Bo JiangDepartment of General Surgery, Nanjing Drum Tower Hospital, Clinical College of Nanjing Medical University, Nanjing, China.
Xu DingDepartment of Surgery, Nanjing Central Hospital, Nanjing, China.
Chaoyu JiangDepartment of General Surgery, Nanjing Drum Tower Hospital, Clinical College of Nanjing Medical University, Nanjing, China.
Bing OuyangDepartment of Surgery, Nanjing Central Hospital, Nanjing, China.
Lei SuDepartment of General Surgery, Nanjing Drum Tower Hospital, Clinical College of Nanjing Medical University, Nanjing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PGC1α, a central player in mitochondrial biology, holds a complex role in the metabolic shifts seen in cancer cells. While its dysregulation is common across major cancers, its impact varies. In some cases, downregulation promotes aerobic glycolysis and progression, whereas in others, overexpression escalates respiration and aggression. PGC1α's interactions with distinct signaling pathways and transcription factors further diversify its roles, often in a tissue-specific manner. Understanding these multifaceted functions could unlock innovative therapeutic strategies. However, challenges exist in managing the metabolic adaptability of cancer cells and refining PGC1α-targeted approaches. This review aims to collate and present the current knowledge on the expression patterns, regulators, binding partners, and roles of PGC1α in diverse cancers. We examined PGC1α's tissue-specific functions and elucidated its dual nature as both a potential tumor suppressor and an oncogenic collaborator. In cancers where PGC1α is tumor-suppressive, reinstating its levels could halt cell proliferation and invasion, and make the cells more receptive to chemotherapy. In cancers where the opposite is true, halting PGC1α's upregulation can be beneficial as it promotes oxidative phosphorylation, allows cancer cells to adapt to stress, and promotes a more aggressive cancer phenotype. Thus, to target PGC1α effectively, understanding its nuanced role in each cancer subtype is indispensable. This can pave the way for significant strides in the field of oncology.

Indexed as

cancer metabolismmetabolic heterogeneityPGC1αsignaling pathwaystherapeutic targettumor progression

Identifiers

PMID38774408
PMCPMC11106418

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.