Evidence map›Paper›PMID 34312217›Full record

ArticleMolecular pharmacology2021

Eribulin Activates the cGAS-STING Pathway via the Cytoplasmic Accumulation of Mitochondrial DNA.

Charles S Fermaintt, Leila Takahashi-Ruiz, Huiyun Liang, Susan L Mooberry, April L Risinger

Open access · hybridAbstract read
In one paragraph

Article in Molecular pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Phase II Study of Eribulin plus Pembrolizumab in Metastatic Soft-tissue Sarcomas: Clinical Outcomes and Biological Correlates.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
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  15. Mitochondrial DNA Release in Innate Immune Signaling.Annual review of biochemistry · 2023
    Review
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  20. cGAS/STING cross-talks with cell cycle and potentiates cancer immunotherapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    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

5 authors at 2 institutions in 1 country.

Charles S FermainttDepartment of Pharmacology (C.S.F., L.T.-R., H.L., S.L.M., A.L.R.), and Mays Cancer Center (C.S.F., S.L.M., A.L.R.), University of Texas Health Science Center San Antonio, San Antonio, Texas.
Leila Takahashi-RuizDepartment of Pharmacology (C.S.F., L.T.-R., H.L., S.L.M., A.L.R.), and Mays Cancer Center (C.S.F., S.L.M., A.L.R.), University of Texas Health Science Center San Antonio, San Antonio, Texas.
Huiyun LiangDepartment of Pharmacology (C.S.F., L.T.-R., H.L., S.L.M., A.L.R.), and Mays Cancer Center (C.S.F., S.L.M., A.L.R.), University of Texas Health Science Center San Antonio, San Antonio, Texas.
Susan L MooberryDepartment of Pharmacology (C.S.F., L.T.-R., H.L., S.L.M., A.L.R.), and Mays Cancer Center (C.S.F., S.L.M., A.L.R.), University of Texas Health Science Center San Antonio, San Antonio, Texas.
April L RisingerDepartment of Pharmacology (C.S.F., L.T.-R., H.L., S.L.M., A.L.R.), and Mays Cancer Center (C.S.F., S.L.M., A.L.R.), University of Texas Health Science Center San Antonio, San Antonio, Texas Risingera@uthscsa.edu.
Mays Cancer Center at UT Health San AntonioThe University of Texas Health Science Center at San Antonio · US

Funding

TISSUE CULTURE---COREP30CA054174 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Lei Zheng · 1991 to 2026
$59.1M
Institute for Integration of Medicine & Science: A Partnership to Improve HealthUL1TR002645 · NCATS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARK, ROBERT A, HARGREAVES, KENNETH M · 2018 to 2022
$20.4M
San Antonio Biomedical Education and ResearchK12GM111726 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI LECHLEITER, JAMES D, OYAJOBI, BABATUNDE OLUKAYODE · 2015 to 2024
$7.6M
NCATS NIH HHS UL1 TR002645NCI NIH HHS P30 CA054174NIGMS NIH HHS K12 GM111726
6 · The paper itself

Abstract

Microtubule-targeting agents (MTAs), including both microtubule stabilizers and destabilizers are highly effective chemotherapeutic drugs used in the treatment of solid tumors and hematologic malignancies. In addition to the shared ability of all MTAs to block cell cycle progression, growing evidence shows that different agents of this class can also have mechanistically distinct effects on nonmitotic microtubule-dependent cellular processes, including cellular signaling and transport. Herein, we test the biologic hypothesis that MTAs used in the treatment of triple-negative breast cancer (TNBC) can differentially affect innate immune signaling pathways independent of their antimitotic effects. Our data demonstrate that the microtubule destabilizer eribulin, but not the microtubule stabilizer paclitaxel, induces cGAS-STING-dependent expression of interferon-

Indexed as

AnimalsCell Line, TumorCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseCytoplasmDNA, MitochondrialFuransHumansImmunity, InnateKetonesMembrane ProteinsMiceMice, Inbred BALB CMice, Inbred C57BLMice, TransgenicMicrotubulesNucleotidyltransferasescGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNA, MitochondrialeribulinFuransKetonesMembrane ProteinsNucleotidyltransferasesPolyether PolyketidesSTING1 protein, humanSTING Protein

Identifiers

PMID34312217
PMCPMC8626644
OpenAlexW3186881769

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.