Evidence map›Paper›PMID 35092121›Full record

ArticleCancer science2022

Exosomes from M1-polarized macrophages promote apoptosis in lung adenocarcinoma via the miR-181a-5p/ETS1/STK16 axis.

Xuan Wang, Renhong Huang, Zhouyi Lu, Zheng Wang, Xiaofeng Chen, Dayu Huang

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.9field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 59 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 1 country.

Xuan WangDepartment of Thoracic Surgery, Huashan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0002-3528-5785
Renhong HuangDepartment of General Surgery, Comprehensive Breast Health Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Zhouyi LuDepartment of Thoracic Surgery, Huashan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0001-5502-3830
Zheng WangDepartment of General Surgery, Comprehensive Breast Health Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiaofeng ChenDepartment of Thoracic Surgery, Huashan Hospital, Fudan University, Shanghai, China.
Dayu HuangDepartment of Thoracic Surgery, Huashan Hospital, Fudan University, Shanghai, China.
Fudan University · CNShanghai Jiao Tong University · CN

Funding

The National Natural Science Foundation of China 82002773The special project of clinical research of Shanghai Health Commission 202040454
6 · The paper itself

Abstract

Serine/threonine kinase 16 (STK16) is crucial in on regulating tumor cell proliferation, apoptosis, and prognosis. Activated M1 macrophages regulate lung adenocarcinoma (LUAD) growth by releasing exosomes. This study aims to investigate the role of STK16 and then focus on the possible mechanisms through which exosomes derived from M1 macrophages play their roles in LUAD cells by targeting STK16. Clinical LUAD samples were used to evaluate the expression of STK16 and its association with prognosis. Exosomes were isolated from M0 and M1 macrophages by ultracentrifugation and were then identified by electron microscopy and western blotting. In vitro gain- and loss-of-function experiments with LUAD cells were performed to elucidate the functions of miR-181a-5p, ETS1, and STK16, and mouse xenograft models were used to verify the function of STK16 in vivo. Western blotting, quantitative real-time PCR, CCK-8 assay, cell apoptosis, immunohistochemistry staining, luciferase assay, ChIP assay, and bioinformatics analysis were performed to reveal the underlying mechanisms. High expression of STK16 was observed in LUAD tissues and cells, and higher expression of STK16 was associated with worse prognosis. Silencing STK16 expression inhibited cell proliferation and promoted apoptosis via the AKT1 pathway. Exosomes from M1 macrophages inhibited viability and promoted apoptosis by inhibiting STK16. Moreover, miR-181a-5p is the functional molecule in M1 macrophage-derived exosomes and plays a vital role in inhibiting cell proliferation and promoting apoptosis by targeting ETS1 and STK16. Hence, exosomes derived from M1 macrophages were capable of inhibiting viability and promoting apoptosis in LUAD via the miR-181a-5p/ETS1/STK16 axis.

Indexed as

Adenocarcinoma of LungAnimalsApoptosisCell SurvivalExosomesFemaleGene Expression Regulation, NeoplasticHumansLung NeoplasmsMacrophage ActivationMacrophagesMaleMiceMicroRNAsMiddle AgedPrognosisAKT1 protein, humanETS1 protein, humanMicroRNAsMIrn181 microRNA, humanProtein Serine-Threonine KinasesProto-Oncogene Protein c-ets-1Proto-Oncogene Proteins c-aktSTK16 protein, humanTranscription Factorsapoptosisexosomelung adenocarcinomamacrophageSTK16

Identifiers

PMID35092121
PMCPMC8898733
OpenAlexW4205805960

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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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.