Evidence map›Paper›PMID 30603685›Full record

ArticleHeliyon2018

Targeting B7-H1 (PD-L1) sensitizes cancer cells to chemotherapy.

Xiaosheng Wu, Yanli Li, Xin Liu, Chunhua Chen, Susan M Harrington, Siyu Cao, Tiancheng Xie, Tu Pham, Aaron S Mansfield, Yiyi Yan and 4 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Heliyon, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.5field-weighted citation impact, top 14% 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

34 citing papers in PubMed, 58 citations in OpenAlex.

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  14. Old Dog, New Trick: A Tumor-Intrinsic Role for PD-1 in Chemoresistant Tumor Subclones.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 1 country.

Xiaosheng WuDepartment of Medicine Division of Hematology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Yanli LiDepartment of Urology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Xin LiuDepartment of Urology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Chunhua ChenDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Susan M HarringtonDepartment of Urology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Siyu CaoDepartment of Urology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Tiancheng XieDepartment of Urology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Tu PhamDepartment of Immunology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Aaron S MansfieldDivision of Medical Oncology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Yiyi YanDivision of Medical Oncology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Eugene D KwonDepartment of Urology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Liewei WangDepartment of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic College of Medicine, Rochester, MN, USA.
Kun LingDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Haidong DongDepartment of Urology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Mayo Clinic · USMayo Clinic in Arizona · US

Funding

The Role of CHFR in Tumorigenesis and Paclitaxel-Sensitivity in Breast CancerP50CA116201 · NCI · MAYO CLINIC ROCHESTER · PI PETER C LUCAS · 2005 to 2026
$49.9M
NCI NIH HHS P50 CA116201
6 · The paper itself

Abstract

Development of resistance to chemotherapy is a major obstacle in extending the survival of patients with cancer. Although originally defined as an immune checkpoint molecule, B7-H1 (also named as PD-L1 or CD274) was found to play a role in cancer chemoresistance; however, the underlying mechanism of action of B7-H1 in regulation of chemotherapy sensitivity remains unclear in cancer cells. Here we show that development of chemoresistance depends on an increased activation of ERK in cancer cells overexpressing B7-H1. Conversely, B7-H1 knockout (KO) by CRISPR/Cas9 renders human cancer cells susceptible to chemotherapy in a cell-context dependent manner through a reduced activation of p38 MAPK. B7-H1 was found to associate with the catalytic subunit of DNA-dependent protein kinase (DNA-PKcs) and this association promoted or maintained the activation of ERK or p38 MAPK in cancer cells. Importantly, we found that targeting B7-H1 by anti-B7-H1 monoclonal antibody (H1A) increased the sensitivity of human triple negative breast cancer cells to cisplatin therapy in vivo. Our results suggest that targeting B7-H1 by an antibody capable of disrupting B7-H1 signals may be a new approach to sensitize cancer cells to chemotherapy.

Indexed as

Cancer researchOncology

Identifiers

PMID30603685
PMCPMC6300616
OpenAlexW2904458868

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.