Evidence map›Paper›PMID 35168607›Full record

ArticleCancer cell international2022

Exosomes derived from M2 type tumor-associated macrophages promote osimertinib resistance in non-small cell lung cancer through MSTRG.292666.16-miR-6836-5p-MAPK8IP3 axis.

Xiaoying Wan, Boxiong Xie, Hui Sun, Weiqing Gu, Chunyan Wang, Qinfang Deng, Songwen Zhou

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. METTL14-Mediated lncRNA MSTRG.292666.16 mInternational journal of molecular sciences · 2026
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  19. Overcoming EGFR-TKI resistance by targeting the tumor microenvironment.Chinese medical journal pulmonary and critical care medicine · 2024
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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

7 authors at 1 institution in 1 country.

Xiaoying WanDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, No.507, Zhengmin Road, Yangpu District, Shanghai, 200433, China.
Boxiong XieDepartment of Thoracic, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, 200433, China.
Hui SunDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, No.507, Zhengmin Road, Yangpu District, Shanghai, 200433, China.
Weiqing GuDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, No.507, Zhengmin Road, Yangpu District, Shanghai, 200433, China.
Chunyan WangDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, No.507, Zhengmin Road, Yangpu District, Shanghai, 200433, China.
Qinfang DengDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, No.507, Zhengmin Road, Yangpu District, Shanghai, 200433, China. dengqinfang@hotmail.com.
Songwen ZhouDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, No.507, Zhengmin Road, Yangpu District, Shanghai, 200433, China. zhou_songwen@aliyun.com.ORCID http://orcid.org/0000-0002-4820-6724
Tongji University · CN

Funding

Key projects of Shanghai Zhangjiang High Tech Park 2016-08
6 · The paper itself

Abstract

backgroundOsimertinib resistance limits the treatment of epidermal growth factor receptor-(EGFR)-mutated non-small-cell lung carcinoma (NSCLC). The mechanisms of osimertinib resistance need to be elucidated to determine alternative treatment strategies. This study explores the role of M2 type tumor-associated macrophage (TAM)-derived exosomal MSTRG.292666.16 in osimertinib resistance, and its related competing endogenous RNA (ceRNA) mechanism.

methodsM2 type TAMs were induced with 200 ng/mL phorbol 12-myristate 13-acetate, 20 ng/mL IL-4 and IL-13, and M2 type macrophage markers were measured by RT-qPCR. Next, the exosomes were isolated and characterized. Tumor formation in nude mice was conducted using H1975 cells under different treatment conditions. Small RNA sequencing was performed on exosomes derived from sensitive and resistant plasma, and ceRNA networks were constructed. Fluorescence in situ hybridization was used to observe the localization of MSTRG.292666.16, and a ceRNA network (MSTRG.292666.16-miR-6836-5p-MAPK8IP3) was selected for further validation.

resultsM2 type TAMs, and M2 type TAM-derived exosomes were successfully induced and isolated. Nude mice results showed that M2 type TAM-derived exosomes and MSTRG.292666.16 overexpression significantly increased tumor volume after administration of osimertinib for 4 weeks. M2 type TAMs were found in the resistant plasma, and MSTRG.292666.16 localized in the cytoplasm of H1975 cells. In addition, the genes in the ceRNA networks were significantly enriched in eight GO terms and seven KEGG pathways, including the MAPK signaling pathway. Subsequently, the levels of MSTRG.292666.16 and MAPK8IP3 significantly increased in both resistant plasma-derived exosomes and M2 type TAM-derived exosomes, while miR-6836-5p levels were significantly reduced. Finally, MSTRG.292666.16, miR-6836-5p, and MAPK8IP3 were part of the same network.

conclusionsM2 type TAM-derived exosomes promoted osimertinib resistance in NSCLC by regulating the MSTRG.292666.16/miR-6386-5p/MAPK8IP3 axis.

Indexed as

ExosomesM2-type TAMMAPK8IP3miR-6836-5pMSTRG.292666.16NSCLCOsimertinib resistance

Identifiers

PMID35168607
PMCPMC8845243
OpenAlexW4212995405

What OpenQuestion holds

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LicenceCC BY
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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.