Evidence map›Paper›PMID 35589683›Full record

ArticleOncogenesis2022

Tumor suppressor p53 restrains cancer cell dissemination by modulating mitochondrial dynamics.

Trinh T T Phan, Yu-Chun Lin, Yu-Ting Chou, Chien-Wei Wu, Lih-Yuan Lin

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  6. Dysregulation of Mitochondrial Function in Cancer Cells.International journal of molecular sciences · 2025
    Review
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  17. A comparative assessment ofInternational journal of reproductive biomedicine · 2022
    Article
  18. Review
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

5 authors at 1 institution in 1 country.

Trinh T T PhanInstitute of Molecular and Cellular Biology, College of Life Science, National Tsing Hua University, Hsinchu, 300044, Taiwan ROC. s107080893@m107.nthu.edu.tw.ORCID http://orcid.org/0000-0002-5850-0855
Yu-Chun LinInstitute of Molecular Medicine, College of Life Science, National Tsing Hua University, Hsinchu, 300044, Taiwan ROC.ORCID http://orcid.org/0000-0002-9629-7560
Yu-Ting ChouInstitute of Biotechnology, College of Life Science, National Tsing Hua University, Hsinchu, 300044, Taiwan ROC.ORCID http://orcid.org/0000-0001-9274-8603
Chien-Wei WuInstitute of Molecular and Cellular Biology, College of Life Science, National Tsing Hua University, Hsinchu, 300044, Taiwan ROC.
Lih-Yuan LinInstitute of Molecular and Cellular Biology, College of Life Science, National Tsing Hua University, Hsinchu, 300044, Taiwan ROC. lylin@life.nthu.edu.tw.ORCID http://orcid.org/0000-0001-9827-3434
National Tsing Hua University · TW

Funding

Ministry of Science and Technology, Taiwan (Ministry of Science and Technology of Taiwan) 107-2514-S-007-001Ministry of Science and Technology, Taiwan (Ministry of Science and Technology of Taiwan) 109-2320-B-007-003-MY3Ministry of Science and Technology, Taiwan (Ministry of Science and Technology of Taiwan) 109-2636-B-007-003 and 108-26
6 · The paper itself

Abstract

Tumor suppressor p53 plays a central role in preventing tumorigenesis. Here, we unravel how p53 modulates mitochondrial dynamics to restrain the metastatic properties of cancer cells. p53 inhibits the mammalian target of rapamycin complex 1 (mTORC1) signaling to attenuate the protein level of mitochondrial fission process 1 (MTFP1), which fosters the pro-fission dynamin-related protein 1 (Drp1) phosphorylation. This regulatory mechanism allows p53 to restrict cell migration and invasion governed by Drp1-mediated mitochondrial fission. Downregulating p53 expression or elevating the molecular signature of mitochondrial fission correlates with aggressive tumor phenotypes and poor prognosis in cancer patients. Upon p53 loss, exaggerated mitochondrial fragmentation stimulates the activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling resulting in epithelial-to-mesenchymal transition (EMT)-like changes in cell morphology, accompanied by accelerated matrix metalloproteinase 9 (MMP9) expression and invasive cell migration. Notably, blocking the activation of mTORC1/MTFP1/Drp1/ERK1/2 axis completely abolishes the p53 deficiency-driven cellular morphological switch, MMP9 expression, and cancer cell dissemination. Our findings unveil a hitherto unrecognized mitochondria-dependent molecular mechanism underlying the metastatic phenotypes of p53-compromised cancers.

Identifiers

PMID35589683
PMCPMC9120037
OpenAlexW4280540572

What Socratic holds

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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 Socratic graph.