Evidence map›Paper›PMID 28844715›Full record

ArticleCancer letters2017

Manumycin A suppresses exosome biogenesis and secretion via targeted inhibition of Ras/Raf/ERK1/2 signaling and hnRNP H1 in castration-resistant prostate cancer cells.

Amrita Datta, Hogyoung Kim, Madhu Lal, Lauren McGee, Adedoyin Johnson, Ahmed A Moustafa, Jennifer C Jones, Debasis Mondal, Marc Ferrer, Asim B Abdel-Mageed

Abstract read
In one paragraph

Article in Cancer letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

142 citing papers in PubMed, 212 citations in OpenAlex.

  1. Exosome trafficking is a key regulator of adipocyte thermogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026
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82 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

10 authors at 2 institutions in 2 countries.

Amrita DattaDepartment of Urology, Tulane University School of Medicine, New Orleans, LA 70112, United States.
Hogyoung KimDepartment of Urology, Tulane University School of Medicine, New Orleans, LA 70112, United States.
Madhu LalDivision of Preclinical Innovation, National Center for Advancing Translational Sciences (NCATS), National Cancer Institute, National Institutes of Health, Bethesda, MD 20850, United States.
Lauren McGeeDivision of Preclinical Innovation, National Center for Advancing Translational Sciences (NCATS), National Cancer Institute, National Institutes of Health, Bethesda, MD 20850, United States.
Adedoyin JohnsonDepartment of Urology, Tulane University School of Medicine, New Orleans, LA 70112, United States.
Ahmed A MoustafaDepartment of Urology, Tulane University School of Medicine, New Orleans, LA 70112, United States; Zoology and Entomology Department, Faculty of Science, Helwan University, Cairo 11790, Egypt.
Jennifer C JonesMolecular Immunogenetics and Vaccine Research Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20850, United States.
Debasis MondalDepartment of Pharmacology, Tulane University School of Medicine, New Orleans, LA 70112, United States; Department of Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA 70112, United States.
Marc FerrerDivision of Preclinical Innovation, National Center for Advancing Translational Sciences (NCATS), National Cancer Institute, National Institutes of Health, Bethesda, MD 20850, United States.
Asim B Abdel-MageedDepartment of Urology, Tulane University School of Medicine, New Orleans, LA 70112, United States; Department of Pharmacology, Tulane University School of Medicine, New Orleans, LA 70112, United States; Department of Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA 70112, United States. Electronic address: amageed@tulane.edu.
Tulane University · USNational Institutes of Health · US

Funding

Trans-NIH RNAi Facility (TNRF)ZICTR000041 · NCATS · NATIONAL CENTER FOR ADVANCING TRANSLATIONAL SCIENCES · PI CHENG, KEN · 2015 to 2025
$9.4M
Development and use of nanoFACS for analysis and sorting of nanoparticlesZIABC011502 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI JONES, JENNIFER · 2013 to 2025
$8.6M
Targeting Tumor-Derived exRNA-Containing Microvesicles by High Throughput ScreeniUH3TR000928 · NCATS · TULANE UNIVERSITY OF LOUISIANA · PI ABDEL-MAGEED, ASIM B · 2016 to 2017
$2.0M
Targeting Tumor-Derived exRNA-Containing Microvesicles by High Throughput ScreeniUH2TR000928 · NCATS · TULANE UNIVERSITY OF LOUISIANA · PI ABDEL-MAGEED, ASIM B · 2013 to 2015
$1.3M
Targeting Tumor-derived exRNA-Containing microvesicles by high throughput screeningZIATR000243 · NCATS · NATIONAL CENTER FOR ADVANCING TRANSLATIONAL SCIENCES · PI FERRER-ALEGRE, MARC · 2015 to 2017
$542k
NCATS NIH HHS UH2 TR000928NCATS NIH HHS UH3 TR000928
6 · The paper itself

Abstract

Emerging evidence links exosomes to cancer progression by the trafficking of oncogenic factors and neoplastic reprogramming of stem cells. This necessitates identification and integration of functionally validated exosome-targeting therapeutics into current cancer management regimens. We employed quantitative high throughput screen on two libraries to identify exosome-targeting drugs; a commercially available collection of 1280 pharmacologically active compounds and a collection of 3300 clinically approved compounds. Manumycin-A (MA), a natural microbial metabolite, was identified as an inhibitor of exosome biogenesis and secretion by castration-resistant prostate cancer (CRPC) C4-2B, but not the normal RWPE-1, cells. While no effect was observed on cell growth, MA attenuated ESCRT-0 proteins Hrs, ALIX and Rab27a and exosome biogenesis and secretion by CRPC cells. The MA inhibitory effect is primarily mediated via targeted inhibition of the Ras/Raf/ERK1/2 signaling. The Ras-dependent MA suppression of exosome biogenesis and secretion is partly mediated by ERK-dependent inhibition of the oncogenic splicing factor hnRNP H1. Our findings suggest that MA is a potential drug candidate to suppress exosome biogenesis and secretion by CRPC cells.

Indexed as

ApoptosisCell ProliferationEnzyme InhibitorsExosomesGene Expression Regulation, NeoplasticHeterogeneous-Nuclear Ribonucleoprotein Group F-HHumansMaleMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PolyenesPolyunsaturated AlkamidesProstatic Neoplasms, Castration-Resistantraf Kinasesras ProteinsSignal TransductionEnzyme InhibitorsHeterogeneous-Nuclear Ribonucleoprotein Group F-HmanumycinMAPK1 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PolyenesPolyunsaturated Alkamidesraf Kinasesras ProteinsExosome biogenesis and secretionhnRNP H1Manumycin AProstate cancerRas signaling

Identifiers

PMID28844715
PMCPMC5628151
OpenAlexW2749972535

What OpenQuestion holds

Textmetadata
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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.