Evidence map›Paper›PMID 32323805›Full record

ArticleOncology reports2020

p62 promotes proliferation, apoptosis‑resistance and invasion of prostate cancer cells through the Keap1/Nrf2/ARE axis.

Ganggang Jiang, Xue Liang, Yiqiao Huang, Ziquan Lan, Zhiming Zhang, Zhengming Su, Zhiyuan Fang, Yuxiong Lai, Wenxia Yao, Ting Liu and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

26 citing papers in PubMed, 34 citations in OpenAlex.

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  6. DHRS9 promotes malignant progression of ovarian cancer through SQSTM1.Journal of cancer research and clinical oncology · 2025
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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

15 authors at 3 institutions in 2 countries.

Ganggang Jiang *Department of Urology, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510700, P.R. China.
Xue Liang *Department of Center Laboratory, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510700, P.R. China.
Yiqiao Huang *Department of Urology, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510700, P.R. China.
Ziquan LanDepartment of Urology, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510700, P.R. China.
Zhiming ZhangDepartment of Urology, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510700, P.R. China.
Zhengming SuDepartment of Urology, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510700, P.R. China.
Zhiyuan FangDepartment of Center Laboratory, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510700, P.R. China.
Yuxiong LaiDepartment of Center Laboratory, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510700, P.R. China.
Wenxia YaoDepartment of Center Laboratory, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510700, P.R. China.
Ting LiuDepartment of Center Laboratory, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510700, P.R. China.
La HuDepartment of Center Laboratory, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510700, P.R. China.
Fen WangCenter for Translational Cancer Research, Texas A&M Institute of Biosciences and Technology, Texas A&M University, Houston, TX 77030, USA.
Hai HuangDepartment of Urology, The Sun Yat‑sen Memorial Hospital, Sun Yat‑sen University, Guangzhou 510120, P.R. China.
Leyuan LiuDepartment of Urology, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510700, P.R. China.
Xianhan JiangDepartment of Urology, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510700, P.R. China.
Guangzhou Medical University · CNSun Yat-sen Memorial Hospital · CNTexas A&M University · US

Funding

Roles of C19ORF5 and LRPPRC in Autophagy and Tumor SuppressionR01CA142862 · NCI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI LIU, LEYUAN · 2010 to 2014
$1.2M
NCI NIH HHS R01 CA142862
6 · The paper itself

Abstract

Prostate cancer poses a public health threat to hundreds of people around the world. p62 has been identified as a tumor suppressor, however, the mechanism by which p62 promotes prostate cancer remains poorly understood. The present study aimed to investigate whether p62 promotes proliferation, apoptosis resistance and invasion of prostate cancer cells via the Kelch‑like ECH‑associated protein 1/nuclear factor erytheroid‑derived 2‑like 2/antioxidant response element (Keap1/Nrf2/ARE) axis. Immunohistochemical staining and immunoblotting were performed to determine the protein levels. Rates of proliferation, invasion and apoptosis of prostate cancer cells were assessed using an RTCA system and flow cytometric assays. Levels of reactive oxygen species (ROS) were assessed using Cell ROX Orange reagent and mRNA levels of Nrf2 target genes were detected by qRT‑PCR. It was revealed that p62 increased the levels and activities of Nrf2 by suppressing Keap1‑mediated proteasomal degradation in prostate cancer cells and tissues, and high levels of p62 promoted growth of prostate cancer through the Keap1/Nrf2/ARE system. Silencing of Nrf2 in DU145 cells overexpressing p62 led to decreases in the rate of cell proliferation and invasion and an increase in the rate of cell apoptosis. p62 activated the Nrf2 pathway, promoted the transcription of Nrf2‑mediated target genes and suppressed ROS in prostate cancer. Therefore, p62 promoted the development of prostate cancer by activating the Keap1/Nrf2/ARE pathway and decreasing p62 may provide a new strategy to ameliorate tumor aggressiveness and suppress tumorigenesis to improve clinical outcomes.

Indexed as

AnimalsAntioxidant Response ElementsCell Line, TumorCell ProliferationCell SurvivalGene Expression Regulation, NeoplasticHumansKelch-Like ECH-Associated Protein 1MaleMiceNeoplasm InvasivenessNF-E2-Related Factor 2Prostatic NeoplasmsReactive Oxygen SpeciesSequestosome-1 ProteinKEAP1 protein, humanKelch-Like ECH-Associated Protein 1NFE2L2 protein, humanNF-E2-Related Factor 2Reactive Oxygen SpeciesSequestosome-1 ProteinSQSTM1 protein, humanapoptosisautophagyKeap1Nrf2p62prostate cancer

Identifiers

PMID32323805
PMCPMC7107779
OpenAlexW3008643496

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.