Evidence map›Paper›PMID 29706653›Full record

ArticleOncogene2018

Programmed death ligand 1 promotes lymph node metastasis and glucose metabolism in cervical cancer by activating integrin β4/SNAI1/SIRT3 signaling pathway.

Shaojia Wang, Jiajia Li, Jie Xie, Fei Liu, Yachen Duan, Yong Wu, Shenglin Huang, Xianghuo He, Ziliang Wang, Xiaohua Wu

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 2 pooled it
5.9field-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

87 citing papers in PubMed, 2 syntheses or guidelines pooled it, 125 citations in OpenAlex.

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  18. Translational lung cancer research · 2024
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27 more citing papers are in PubMed but not listed here.

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

10 authors at 2 institutions in 1 country.

Shaojia WangDepartment of Gynecological Oncology and Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Jiajia LiDepartment of Gynecological Oncology and Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Jie XieDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Fei LiuDepartment of Gynecological Oncology and Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Yachen DuanDepartment of Gynecological Oncology and Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Yong WuDepartment of Gynecological Oncology and Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Shenglin HuangDepartment of Gynecological Oncology and Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.ORCID http://orcid.org/0000-0003-1279-0794
Xianghuo HeDepartment of Gynecological Oncology and Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.ORCID http://orcid.org/0000-0001-8872-668X
Ziliang WangDepartment of Gynecological Oncology and Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. huf_zlwang@126.com.
Xiaohua WuDepartment of Gynecological Oncology and Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. wu.xh@fudan.edu.cn.
Shanghai Medical College of Fudan University · CNFudan University Shanghai Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although PD-L1 has been shown to play a well-characterized role in inhibiting antitumor immunity via engagement of its receptor PD-1 in T lymphocytes, little is known about the tumor cell-intrinsic function of PD-L1 and its association with prognosis. Here, we investigate this issue and dissect the molecular mechanisms underlying the role of PD-L1 in glucose metabolism, proliferation, migration, and invasion in human cervical cancer cells. As a result, we found that PD-L1 overexpression in cervical cancer cells increases glucose metabolism and metastasis-related behaviors. Mechanistically, PD-L1 bound directly to integrin β4 (ITGB4), activating the AKT/GSK3β signaling pathway and consequently inducing the expression of the transcriptional repressor SNAI1. SNAIL in turn influenced the expression of genes involved in the epithelial-to-mesenchymal transition and regulated glucose metabolism by inhibiting SIRT3 promoter activity. High expression of PD-L1 and ITGB4 in human cervical carcinomas was significantly associated with lymph node metastasis and poor prognosis. Finally,

Indexed as

AdultAgedAnimalsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFemaleGlucoseGlycogen Synthase Kinase 3 betaHeLa CellsHumansIntegrin beta4Lymphatic MetastasisLymph NodesMiceGlucoseGlycogen Synthase Kinase 3 betaIntegrin beta4PDCD1 protein, humanProgrammed Cell Death 1 ReceptorProto-Oncogene Proteins c-aktSIRT3 protein, humanSirtuin 3SNAI1 protein, humanSnail Family Transcription Factors

Identifiers

PMID29706653
OpenAlexW2799522453

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.