Evidence map›Paper›PMID 30787043›Full record

ArticleEMBO reports2019

HRAS-driven cancer cells are vulnerable to TRPML1 inhibition.

Jewon Jung, Kwang-Jin Cho, Ali K Naji, Kristen N Clemons, Ching On Wong, Mariana Villanueva, Steven Gregory, Nicholas E Karagas, Lingxiao Tan, Hong Liang and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in EMBO reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

53 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
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  6. CaBiophysics reports · 2024
    Article
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  17. Epitranscriptic regulation ofProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  18. Article
  19. Lysosomal Potassium Channels.Handbook of experimental pharmacology · 2023
    Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 4 institutions in 1 country.

Jewon JungDepartment of Integrative Biology and Pharmacology, McGovern Medical School, the University of Texas Health Sciences Center (UTHealth), Houston, TX, USA.
Kwang-Jin ChoDepartment of Biochemistry and Molecular Biology, Boonshoft School of Medicine, Wright State University, Dayton, OH, USA.
Ali K NajiDepartment of Diagnostic and Biomedical Sciences, School of Dentistry, The University of Texas Health Science Center, Houston, TX, USA.
Kristen N ClemonsDepartment of Integrative Biology and Pharmacology, McGovern Medical School, the University of Texas Health Sciences Center (UTHealth), Houston, TX, USA.
Ching On WongDepartment of Integrative Biology and Pharmacology, McGovern Medical School, the University of Texas Health Sciences Center (UTHealth), Houston, TX, USA.
Mariana VillanuevaBobby R. Alford Department of Otolaryngology-Head and Neck Surgery, Baylor College of Medicine, Houston, TX, USA.
Steven GregoryDepartment of Integrative Biology and Pharmacology, McGovern Medical School, the University of Texas Health Sciences Center (UTHealth), Houston, TX, USA.
Nicholas E KaragasDepartment of Integrative Biology and Pharmacology, McGovern Medical School, the University of Texas Health Sciences Center (UTHealth), Houston, TX, USA.
Lingxiao TanDepartment of Integrative Biology and Pharmacology, McGovern Medical School, the University of Texas Health Sciences Center (UTHealth), Houston, TX, USA.
Hong LiangDepartment of Integrative Biology and Pharmacology, McGovern Medical School, the University of Texas Health Sciences Center (UTHealth), Houston, TX, USA.
Morgan A RousseauDepartment of Integrative Biology and Pharmacology, McGovern Medical School, the University of Texas Health Sciences Center (UTHealth), Houston, TX, USA.
Kelly M TomasevichDepartment of Integrative Biology and Pharmacology, McGovern Medical School, the University of Texas Health Sciences Center (UTHealth), Houston, TX, USA.
Andrew G SikoraBobby R. Alford Department of Otolaryngology-Head and Neck Surgery, Baylor College of Medicine, Houston, TX, USA.
Ilya LeventalDepartment of Integrative Biology and Pharmacology, McGovern Medical School, the University of Texas Health Sciences Center (UTHealth), Houston, TX, USA.
Dharini van der HoevenDepartment of Diagnostic and Biomedical Sciences, School of Dentistry, The University of Texas Health Science Center, Houston, TX, USA.
Yong ZhouDepartment of Integrative Biology and Pharmacology, McGovern Medical School, the University of Texas Health Sciences Center (UTHealth), Houston, TX, USA.
John F HancockDepartment of Integrative Biology and Pharmacology, McGovern Medical School, the University of Texas Health Sciences Center (UTHealth), Houston, TX, USA.
Kartik VenkatachalamDepartment of Integrative Biology and Pharmacology, McGovern Medical School, the University of Texas Health Sciences Center (UTHealth), Houston, TX, USA Kartik.venkatachalam@uth.tmc.edu.ORCID 0000-0002-3055-9265
The University of Texas MD Anderson Cancer Center · USThe University of Texas Health Science Center at Houston · USBaylor College of Medicine · USWright State University · US

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
Alterations in synaptic growth and lipid-raft organization in a fly MLIV modelR01NS081301 · NINDS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI VENKATACHALAM, KARTIK · 2014 to 2018
$1.7M
K-Ras plasma membrane interactions: a tractable therapeutic targetR00CA188593 · NCI · WRIGHT STATE UNIVERSITY · PI CHO, KWANGJIN · 2017 to 2019
$747k
GDAP1 mediated cellular damage in MLIVR21NS094860 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KISELYOV, KIRILL, VENKATACHALAM, KARTIK · 2016 to 2017
$428k
NCI NIH HHS P30 CA125123NCI NIH HHS R00 CA188593NINDS NIH HHS R01 NS081301NINDS NIH HHS R21 NS094860
6 · The paper itself

Abstract

By serving as intermediaries between cellular metabolism and the bioenergetic demands of proliferation, endolysosomes allow cancer cells to thrive under normally detrimental conditions. Here, we show that an endolysosomal TRP channel, TRPML1, is necessary for the proliferation of cancer cells that bear activating mutations in

Indexed as

AnimalsCalciumCalcium SignalingCell MembraneCell ProliferationDrosophilaEndosomesExtracellular Signal-Regulated MAP KinasesGene ExpressionGene Regulatory NetworksHumansLysosomesModels, BiologicalMutationNeoplasmsPhosphorylationCalciumExtracellular Signal-Regulated MAP KinasesHRAS protein, humanMCOLN1 protein, humanProto-Oncogene Proteins p21(ras)Transient Receptor Potential ChannelscancercholesterolendolysosomesHRASTRPML1

Identifiers

PMID30787043
PMCPMC6446245
OpenAlexW2917476711

What OpenQuestion holds

Textmetadata
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.