Evidence map›Paper›PMID 35980503›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2022

Cancer cell-derived exosomal LINC00313 induces M2 macrophage differentiation in non-small cell lung cancer.

Wencui Kong, Lei Zhang, Ying Chen, Zongyang Yu, Zhongquan Zhao

Abstract read
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In one paragraph

Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 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

5 authors at 1 institution in 1 country.

Wencui Kong *Department of Pulmonary and Critical Care Medicine, 900TH Hospital of Joint Logistics Support Force, Fuzhou, 350025, Fujian, China.
Lei Zhang *Department of Pulmonary and Critical Care Medicine, 900TH Hospital of Joint Logistics Support Force, Fuzhou, 350025, Fujian, China.
Ying ChenDepartment of Pulmonary and Critical Care Medicine, 900TH Hospital of Joint Logistics Support Force, Fuzhou, 350025, Fujian, China.
Zongyang YuDepartment of Pulmonary and Critical Care Medicine, 900TH Hospital of Joint Logistics Support Force, Fuzhou, 350025, Fujian, China.
Zhongquan ZhaoDepartment of Pulmonary and Critical Care Medicine, 900TH Hospital of Joint Logistics Support Force, Fuzhou, 350025, Fujian, China. zhaozhonquan@163.com.ORCID http://orcid.org/0000-0002-2040-3734
Fuzhou Pulmonary Hospital of Fujian · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeNon-small cell lung cancer (NSCLC) is the major subtype of lung cancer, which is the leading cause of cancer death worldwide. Tumor-associated macrophages (TAMs) are one of the main non-tumor cells in the tumor microenvironment. Here, we investigated the effect of cancer cell-derived exosomal LINC00313 on the M2 macrophage differentiation in NSCLC and clarified its underlying mechanism.

methodsFlow cytometry, Western blotting, ELISA and immunohistochemical staining were performed to identify the macrophage phenotype by detecting the expression of M2 markers. The expression levels of LINC00313 and miR-135a-3p were measured by qRT-PCR, and luciferase reporter assay was used to validate the binding of lncRNA to miRNA, and miRNA to the target gene STAT6. The mouse-xenograft models were established by subcutaneous injection of the NCl-H1299 cells with stable overexpression or knockdown of LINC00313. GW4869 was injected intra-tumorally after tumor implantation.

resultsIt was found that the cancer cells promoted M2 macrophage differentiation by secreting exosomes. LINC00313 was overexpressed in H1299-derived exosomes, and its knockdown abolished the effect of H1299-induced M2 macrophage differentiation. LINC00313 sponged miR-135a-3p to increase the STAT6 expression, resulting in the M2 macrophage differentiation. LINC00313 promoted tumor progression and promoted the expression of M2 markers in isolated tumor macrophages. A novel regulatory mechanism of M2 macrophage differentiation in NSCLC was revealed. It was found that cancer cell-derived exosomal LINC00313 promoted M2 macrophage differentiation in NSCLC by up-regulating STAT6 as miR-135a-3p sponge.

conclusionsThis study provides a new mechanism and direction to prevent the M2 macrophage differentiation in NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungExosomesLung NeoplasmsMicroRNAsRNA, Long NoncodingAnimalsCell Line, TumorCell MovementHumansMacrophagesMiceTumor MicroenvironmentMicroRNAsRNA, Long NoncodingExosomeLncRNAMacrophage differentiationmicroRNANon-small cell lung cancer

Identifiers

PMID35980503
OpenAlexW4292481172

What OpenQuestion holds

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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.