Evidence map›Paper›PMID 36119107›Full record

ArticleFrontiers in immunology2022

Lipopolysaccharide sensitizes the therapeutic response of breast cancer to IAP antagonist.

Xin Liu, Jimmy J Yao, Zhongxuan Chen, Wei Lei, Rong Duan, Zhenqiang Yao

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 15 citations in OpenAlex.

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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

6 authors at 2 institutions in 2 countries.

Xin LiuDepartment of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, United States.
Jimmy J YaoDepartment of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, United States.
Zhongxuan ChenDepartment of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, United States.
Wei LeiDepartment of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, United States.
Rong DuanDepartment of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, United States.
Zhenqiang YaoDepartment of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, United States.
University of Rochester Medical Center · USUniversity of Rochester · US

Funding

Role of Macrophage in Osteoimmunology with AgingR01AG076731 · NIA · UNIVERSITY OF ROCHESTER · PI Zhenqiang Yao · 2022 to 2026
$2.1M
Studies of TRAF3 in age-related low-level chronic inflammation and osteoporosisR01AG049994 · NIA · UNIVERSITY OF ROCHESTER · PI BOYCE, BRENDAN F, YAO, ZHENQIANG · 2016 to 2020
$1.6M
NIA NIH HHS R01 AG076731
6 · The paper itself

Abstract

Inhibitor of apoptosis protein (IAP) is a class of E3 ubiquitin ligases functioning to support cancer survival and growth. Many small-molecule IAP antagonists have been developed, aiming to degrade IAP proteins to kill cancer. We have evaluated the effect of lipopolysaccharide (LPS), a component of the bacterial outer membrane, on IAP antagonists in treating breast cancer in a mouse model to guide future clinical trials. We show that LPS promotes IAP antagonist-induced regression of triple-negative breast cancer (TNBC) from MDA-MB-231 cells in immunodeficient mice. IAP antagonists such as SM-164, AT-406, and BV6, do not kill MDA-MB-231 cells alone, but allow LPS to induce cancer cell apoptosis rapidly. The apoptosis caused by LPS plus SM-164 is blocked by toll-like receptor 4 (TLR4) or MyD88 inhibitor, which inhibits LPS-induced TNFα production by the cancer cells. Consistent with this, MDA-MB-231 cell apoptosis induced by LPS plus SM-164 is also blocked by the TNF inhibitor. LPS alone does not kill MDA-MB-231 cells because it markedly increases the protein level of cIAP1/2, which is directly associated with and stabilized by MyD88, an adaptor protein of TLR4. ER

Indexed as

NeoplasmsToll-Like Receptor 4AnimalsAnti-Bacterial AgentsInhibitor of Apoptosis ProteinsLipopolysaccharidesMiceMyeloid Differentiation Factor 88Tumor Necrosis Factor-alphaTumor Necrosis Factor InhibitorsUbiquitinsAnti-Bacterial AgentsInhibitor of Apoptosis ProteinsLipopolysaccharidesMyeloid Differentiation Factor 88Toll-Like Receptor 4Tumor Necrosis Factor-alphaTumor Necrosis Factor InhibitorsUbiquitinsapoptosisbreast cancerinhibitor of apoptosis proteinlipopolysaccharideMyD88TNF-αTolllike receptor 4

Identifiers

PMID36119107
PMCPMC9471085
OpenAlexW4293724424

What OpenQuestion holds

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LicenceCC BY
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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.