Evidence map›Paper›PMID 33420365›Full record

ArticleOncogene2021

MAOA promotes prostate cancer cell perineural invasion through SEMA3C/PlexinA2/NRP1-cMET signaling.

Lijuan Yin, Jingjing Li, Jing Wang, Tianjie Pu, Jing Wei, Qinlong Li, Boyang Jason Wu

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
8.0field-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

60 citing papers in PubMed, 98 citations in OpenAlex.

  1. Integrins as key regulators in tumor perineural invasion: mechanisms and clinical implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
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  13. Neuropilin-1: A Multifaceted Target for Cancer Therapy.Current oncology (Toronto, Ont.) · 2025
    Review
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  20. The MET Oncogene Network of Interacting Cell Surface Proteins.International journal of molecular sciences · 2024
    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

7 authors at 2 institutions in 2 countries.

Lijuan Yin *Uro-Oncology Research Program, Samuel Oschin Comprehensive Cancer Institute, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, 90048, USA.
Jingjing Li *Department of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA, 99202, USA.ORCID http://orcid.org/0000-0002-0661-5642
Jing Wang *Department of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA, 99202, USA.
Tianjie PuDepartment of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA, 99202, USA.
Jing WeiDepartment of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA, 99202, USA.
Qinlong LiUro-Oncology Research Program, Samuel Oschin Comprehensive Cancer Institute, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, 90048, USA.
Boyang Jason WuDepartment of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA, 99202, USA. boyang.wu@wsu.edu.ORCID http://orcid.org/0000-0002-2823-3573
Washington State University Spokane · USCedars-Sinai Medical Center · US

Funding

MAOA and AR Reciprocal Crosstalk in Prostate CancerR37CA233658 · NCI · WASHINGTON STATE UNIVERSITY · PI WU, BOYANG · 2019 to 2025
$2.4M
NCI NIH HHS R37 CA233658
6 · The paper itself

Abstract

Perineural invasion (PNI), a pathologic feature defined as cancer cell invasion in, around, and through nerves, is an indicator of poor prognosis and survival in prostate cancer (PC). Despite widespread recognition of the clinical significance of PNI, the molecular mechanisms are largely unknown. Here, we report that monoamine oxidase A (MAOA) is a clinically and functionally important mediator of PNI in PC. MAOA promotes PNI of PC cells in vitro and tumor innervation in an orthotopic xenograft model. Mechanistically, MAOA activates SEMA3C in a Twist1-dependent transcriptional manner, which in turn stimulates cMET to facilitate PNI via autocrine or paracrine interaction with coactivated PlexinA2 and NRP1. Furthermore, MAOA inhibitor treatment effectively reduces PNI of PC cells in vitro and tumor-infiltrating nerve fiber density along with suppressed xenograft tumor growth and progression in mice. Collectively, these findings characterize the contribution of MAOA to the pathogenesis of PNI and provide a rationale for using MAOA inhibitors as a targeted treatment for PNI in PC.

Indexed as

AnimalsCell Line, TumorCell ProliferationHeterograftsHumansMaleMiceMonoamine OxidaseMonoamine Oxidase InhibitorsNeoplasm InvasivenessNerve Tissue ProteinsNeuropilin-1Nuclear ProteinsProstatic NeoplasmsProto-Oncogene Proteins c-metReceptors, Cell SurfaceMET protein, humanMonoamine Oxidasemonoamine oxidase A, humanMonoamine Oxidase InhibitorsNerve Tissue ProteinsNeuropilin-1Nuclear ProteinsPLXNA2 protein, humanProto-Oncogene Proteins c-metReceptors, Cell SurfaceSema3C protein, humanSemaphorinsTWIST1 protein, humanTwist-Related Protein 1

Identifiers

PMID33420365
PMCPMC8604374
OpenAlexW3120036594

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.