Evidence map›Paper›PMID 33894381›Full record

ReviewSeminars in cancer biology2021

p62 functions as a signal hub in metal carcinogenesis.

Zhuo Zhang, Max Costa

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 38% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Zhuo ZhangDepartment of Environmental Medicine, NYU School of Medicine, 341 East 25th Street, New York, NY 10010, USA.
Max CostaDepartment of Environmental Medicine, NYU School of Medicine, 341 East 25th Street, New York, NY 10010, USA. Electronic address: max.costa@nyumc.org.
New York University · US

Funding

RESEARCH IN ENVIRONMENTAL HEALTH SCIENCES (CENTER GRANT)P30ES000260 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ZELIKOFF, JUDITH TERRY · 1985 to 2020
$26.1M
Arsenic carcinogenesis and disruption of histone variant H3.3 assemblyR01ES030583 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI COSTA, MAX, JIN, CHUNYUAN · 2019 to 2023
$2.7M
MEG3 deletion drives lung tumorigenesis due to environmental nickel exposureR01CA229234 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI COSTA, MAX · 2019 to 2024
$2.4M
Epigenetic Stress and Chromate CarcinogenesisR01ES029359 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI COSTA, MAX, JIN, CHUNYUAN · 2018 to 2022
$2.4M
SESN2 and therapeutic effect of Isohapontigenin (ISO)R01CA217923 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI COSTA, MAX, SUN, HONG · 2018 to 2022
$2.1M
Arsenic and Nickel Carcinogenesis in Human Lung CellsR01ES030572 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI COSTA, MAX · 2019 to 2023
$2.0M
NCI NIH HHS R01 CA217923NCI NIH HHS R01 CA229234NIEHS NIH HHS P30 ES000260NIEHS NIH HHS R01 ES029359NIEHS NIH HHS R01 ES030572NIEHS NIH HHS R01 ES030583
6 · The paper itself

Abstract

A number of metals are toxic and carcinogenic to humans. Reactive oxygen species (ROS) play an important role in metal carcinogenesis. Oxidative stress acts as the converging point among various stressors with ROS being the main intracellular signal transducer. In metal-transformed cells, persistent expression of p62 and erythroid 2-related factor 2 (Nrf2) result in apoptosis resistance, angiogenesis, inflammatory microenvironment, and metabolic reprogramming, contributing to overall mechanism of metal carcinogenesis. Autophagy, a conserved intracellular process, maintains cellular homeostasis by facilitating the turnover of protein aggregates, cellular debris, and damaged organelles. In addition to being a substrate of autophagy, p62 is also a crucial molecule in a myriad of cellular functions and in molecular events, which include oxidative stress, inflammation, apoptosis, cell proliferation, metabolic reprogramming, that modulate cell survival and tumor growth. The multiple functions of p62 are appreciated by its ability to interact with several key components involved in various oncogenic pathways. This review summarizes the current knowledge and progress in studies of p62 and metal carcinogenesis with emphasis on oncogenic pathways related to oxidative stress, inflammation, apoptosis, and metabolic reprogramming.

Indexed as

AnimalsAutophagyCarcinogenesisHumansMetalsSequestosome-1 ProteinMetalsSequestosome-1 ProteinApoptosis resistanceCarcinogenesisInflammationMetabolic reprogrammingMetalsNrf2Oxidative stressp62

Identifiers

PMID33894381
PMCPMC9161642
OpenAlexW3158920157

What OpenQuestion holds

Textmetadata
LicenceTDM
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.