Evidence map›Paper›PMID 34206503›Full record

ReviewBiomedicines2021

The Pathways Underlying the Multiple Roles of p62 in Inflammation and Cancer.

Paulina Hennig, Gabriele Fenini, Michela Di Filippo, Tugay Karakaya, Hans-Dietmar Beer

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
10.5field-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

69 citing papers in PubMed, 106 citations in OpenAlex.

  1. Review
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  3. The SQSTM1/Animals : an open access journal from MDPI · 2026
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  5. Article
  6. Article
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  9. The Roles of SQSTM1/p62 in Selective Autophagy and Oncogenic Signaling.International journal of molecular sciences · 2026
    Review
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  11. Review
  12. Article
  13. Review
  14. Article
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  20. Article

9 more citing papers are in PubMed but not listed here.

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.

Paulina HennigDepartment of Dermatology, University Hospital Zurich, Wagistrasse 18, CH-8952 Schlieren, Switzerland.ORCID 0000-0003-2633-452X
Gabriele FeniniDepartment of Dermatology, University Hospital Zurich, Wagistrasse 18, CH-8952 Schlieren, Switzerland.ORCID 0000-0002-5778-936X
Michela Di FilippoDepartment of Dermatology, University Hospital Zurich, Wagistrasse 18, CH-8952 Schlieren, Switzerland.
Tugay KarakayaDepartment of Dermatology, University Hospital Zurich, Wagistrasse 18, CH-8952 Schlieren, Switzerland.
Hans-Dietmar BeerDepartment of Dermatology, University Hospital Zurich, Wagistrasse 18, CH-8952 Schlieren, Switzerland.ORCID 0000-0002-8085-713X
University of Zurich · CH

Funding

Bangerter-Rhyner-Stiftung 8472Dr. Hans Altschüler-Stiftung 2019Monika Kutzner Stiftung 2019Monique Dornonville de la Cour-Stiftung 2019Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung 310030_197426Swiss Cancer Research Foundation KFS-3940-08-2016Swiss Cancer Research Foundation KFS-5087-08-2020Wilhelm Sander-Stiftung 2019.075.1Wolfermann-Nägeli-Stiftung 2019
6 · The paper itself

Abstract

p62 is a highly conserved, multi-domain, and multi-functional adaptor protein critically involved in several important cellular processes. Via its pronounced domain architecture, p62 binds to numerous interaction partners, thereby influencing key pathways that regulate tissue homeostasis, inflammation, and several common diseases including cancer. Via binding of ubiquitin chains, p62 acts in an anti-inflammatory manner as an adaptor for the auto-, xeno-, and mitophagy-dependent degradation of proteins, pathogens, and mitochondria. Furthermore, p62 is a negative regulator of inflammasome complexes. The transcription factor Nrf2 regulates expression of a bundle of ROS detoxifying genes. p62 activates Nrf2 by interaction with and autophagosomal degradation of the Nrf2 inhibitor Keap1. Moreover, p62 activates mTOR, the central kinase of the mTORC1 sensor complex that controls cell proliferation and differentiation. Through different mechanisms, p62 acts as a positive regulator of the transcription factor NF-κB, a central player in inflammation and cancer development. Therefore, p62 represents not only a cargo receptor for autophagy, but also a central signaling hub, linking several important pro- and anti-inflammatory pathways. This review aims to summarize knowledge about the molecular mechanisms underlying the roles of p62 in health and disease. In particular, different types of tumors are characterized by deregulated levels of p62. The elucidation of how p62 contributes to inflammation and cancer progression at the molecular level might promote the development of novel therapeutic strategies.

Indexed as

autophagycancerinflammasomesinflammationmTORC1NF-κBNrf2/Keap1p62

Identifiers

PMID34206503
PMCPMC8301319
OpenAlexW3174419361

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.