Evidence map›Paper›PMID 27870715›Full record

ArticleInternational journal of gynecological cancer : official journal of the International Gynecological Cancer Society2017

Posttranscriptional Control of PD-L1 Expression by 17β-Estradiol via PI3K/Akt Signaling Pathway in ERα-Positive Cancer Cell Lines.

Lingyun Yang, Feng Huang, Jiandong Mei, Xun Wang, Qiuyang Zhang, Hongjing Wang, Mingrong Xi, Zongbing You

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Article in International journal of gynecological cancer : official journal of the International Gynecological Cancer Society, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 5% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

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  19. Generation, secretion and degradation of cancer immunotherapy target PD-L1.Cellular and molecular life sciences : CMLS · 2022
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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

8 authors at 1 institution in 1 country.

Lingyun Yang*Department of Structural and Cellular Biology, Tulane University School of Medicine, New Orleans, LA; †Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Chengdu; ‡Department of Clinical Medicine, the First Affiliated Hospital, Shanxi University of Chinese Medicine, Xianyang; §Department of Thoracic Surgery, West China Hospital, Sichuan University, Chengdu; and ∥Department of Gastroenterology, Wuchang Hospital, Wuhan, China.
Feng Huang
Jiandong Mei
Xun Wang
Qiuyang Zhang
Hongjing Wang
Mingrong Xi
Zongbing You
Tulane University · US

Funding

UNCOVERING THE MECHANISMS OF OSTEOSARCOMA METASTASIS SUPPRESSION BY MTBPP20RR020152 · NCRR · TULANE UNIVERSITY OF LOUISIANA · PI DEININGER, PRESCOTT L. · 2004 to 2011
$17.0M
Mentoring a Cancer Genetics ProgramP20GM103518 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI DEININGER, PRESCOTT L. · 2012 to 2013
$4.3M
The role of IL-17 in prostate cancerR01CA174714 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI YOU, ZONGBING · 2013 to 2017
$1.6M
NCI NIH HHS R01 CA174714NCRR NIH HHS P20 RR020152NIGMS NIH HHS P20 GM103518
6 · The paper itself

Abstract

objectiveEstrogen is a well-known oncogenic driver in endometrial (ECs) and breast cancers (BCs). Programmed cell death protein 1 (PD-1) and its ligands PD-1 Ligand 1 (PD-L1) and PD-L2 have been shown to mediate immune evasion of the tumor cells. The purpose of the present study was to assess the effects of estrogen on PD-L1 and PD-L2 expression in EC and BC cell lines.

methods17β-Estradiol (E2)-induced expression of PD-L1 and PD-L2 and possible signaling pathway were investigated in EC and BC cells. Coculture of T cells and cancer cells with E2 stimulation was performed to assess the functions of T cells.

resultsWe found that E2 increased expression of PD-L1, but not PD-L2, protein via activation of phosphoinositide 3-kinase (PI3K)/Akt pathway in Ishikawa and Michigan Cancer Foundation-7 (MCF-7) cells. Phosphoinositide 3-kinase and Akt inhibitors could block E2's effects. 17β-Estradiol did not increase PD-L1 mRNA transcription, but stabilized PD-L1 mRNA. 17β-Estradiol's effects were only observed in estrogen receptor α (ERα)-positive Ishikawa and MCF-7 cells, but not in ERα-negative MDA-MB-231 cells. Coculture of Ishikawa or MCF-7 cells with T cells inhibited expression of interferon-γ and interleukin-2 and increased BCL-2-interacting mediator of cell death expression in the presence of E2.

conclusionsThis study provides the first evidence that estrogen upregulates PD-L1 protein expression in ERα-positive EC and BC cells to suppress immune functions of T cells in the tumor microenvironment, demonstrating a new mechanism of how estrogen drives cancer progression.

Indexed as

B7-H1 AntigenBreast NeoplasmsCell Line, TumorEndometrial NeoplasmsEstradiolEstrogen Receptor alphaFemaleHumansJurkat CellsMCF-7 CellsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, MessengerRNA Processing, Post-TranscriptionalSignal TransductionT-LymphocytesB7-H1 AntigenCD274 protein, humanESR1 protein, humanEstradiolEstrogen Receptor alphaPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Messenger

Identifiers

PMID27870715
PMCPMC5258765
OpenAlexW2551403261

What OpenQuestion holds

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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.