Evidence map›Paper›PMID 33748098›Full record

ArticleFrontiers in cell and developmental biology2020

Exosomes Derived From Macrophages Enhance Aerobic Glycolysis and Chemoresistance in Lung Cancer by Stabilizing c-Myc via the Inhibition of NEDD4L.

Huan Wang, Lie Wang, Haiyan Pan, Yaona Wang, Miao Shi, Hang Yu, Chaoye Wang, Xinfu Pan, Zhijun Chen

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.1field-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

53 citing papers in PubMed, 72 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

9 authors at 2 institutions in 1 country.

Huan WangDepartment of Cardiothoracic Surgery, Zhoushan Hospital, Zhejiang University, Zhoushan, China.
Lie WangDepartment of Cardiothoracic Surgery, Zhoushan Hospital, Zhejiang University, Zhoushan, China.
Haiyan PanDepartment of Internal Medicine, Zhoushan Hospital, Zhejiang University, Zhoushan, China.
Yaona WangDepartment of Cardiothoracic Surgery, Zhoushan Hospital, Zhejiang University, Zhoushan, China.
Miao ShiDepartment of Cardiothoracic Surgery, Zhoushan Hospital, Zhejiang University, Zhoushan, China.
Hang YuDepartment of Cardiothoracic Surgery, Zhoushan Hospital, Zhejiang University, Zhoushan, China.
Chaoye WangDepartment of Cardiothoracic Surgery, Zhoushan Hospital, Zhejiang University, Zhoushan, China.
Xinfu PanDepartment of Cardiothoracic Surgery, Zhoushan Hospital, Zhejiang University, Zhoushan, China.
Zhijun ChenDepartment of Cardiothoracic Surgery, Zhoushan Hospital, Zhejiang University, Zhoushan, China.
Zhejiang University · CNZhoushan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As one of the most common and lethal cancer, lung cancer severely threatens the health of human. It has been reported that tumor-associated macrophages promote initiation, progression, as well as chemoresistance in human cancers. However, the underneath molecular mechanism that drives chemoresistance in lung cancer is yet not fully characterized. In this article, we demonstrated that M2 macrophage-derived exosomes (MDE) is the key factor to promote cisplatin-resistance in lung cancer. MDE exhibited high expression level of several miRNA including miR-3679-5p. Mechanistically, miR-3679-5p was delivered to lung cancer cells by MDE, downregulating the expression of a known E3 ligase, NEDD4L, which has been identified as a key regulator controlling the stability of c-Myc. Such decreased NEDD4L expression level resulted in the stabilization of c-Myc and elevated glycolysis. The enhanced glycolysis drives the chemoresistance in lung cancer. Taken together, our findings not only show that M2 macrophage induce chemoresistance in lung cancer through MDE mediated miR-3679-5R/NEDD4L/c-Myc signaling cascade, but also shed the light on the mechanism of the cross-talk between M2 macrophage and lung cancers. By pinpointing a potential novel survival signaling pathway, our data could provide a new potential therapeutic target for lung cancer treatment and management.

Indexed as

chemoresistanceglycolysislung cancerM2 macrophage-derived exosomesNEDD4L

Identifiers

PMID33748098
PMCPMC7969980
OpenAlexW3135058320

What OpenQuestion holds

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LicenceCC BY
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.