Evidence map›Paper›PMID 32956565›Full record

ArticleThoracic cancer2020

M2 macrophages reduce the effect of gefitinib by activating AKT/mTOR in gefitinib-resistant cell lines HCC827/GR.

Fengqi Xiao, Ni Liu, Xinchun Ma, Jing Qin, Yanguo Liu, Xiuwen Wang

Open access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
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 1 institution in 1 country.

Fengqi XiaoDepartment of Medical Oncology, Qilu Hospital of Shandong University, Jinan, China.
Ni LiuDepartment of Medical Oncology, Qilu Hospital of Shandong University, Jinan, China.
Xinchun MaDepartment of Medical Oncology, Qilu Hospital of Shandong University, Jinan, China.
Jing QinDepartment of Medical Oncology, Qilu Hospital of Shandong University, Jinan, China.
Yanguo LiuDepartment of Medical Oncology, Qilu Hospital of Shandong University, Jinan, China.
Xiuwen WangDepartment of Medical Oncology, Qilu Hospital of Shandong University, Jinan, China.ORCID 0000-0001-6494-122X
Qilu Hospital of Shandong University · CN

Funding

National Natural Science Foundation of China 81874044Natural Science Foundation of Shandong Province ZR2019MH050Wu Jieping Medical Foundation 320.6750.12129Wu Jieping Medical Foundation 320.6750.19088-25
6 · The paper itself

Abstract

backgroundThe biological behavior of cells change after they develop drug resistance, and the degree of resistance will be affected by the tumor microenvironment. Here, we aimed to explore the changes in the biological behavior of tumors and to observe the differences in the release of cytokines and chemokines which can influence the tumor microenvironment. We also aimed to study how TKIs-resistant cell lines recruit macrophages to reduce the sensitivity of the cells following gefitinib administration.

methodsWe generated and maintained gefitinib-resistant cell lines to study the differences between gefitinib-sensitive cell lines according to clone formation, cell growth curve analysis, whole-exome sequencing, and qPCR ARRAY technology. We used the WNT/β-catenin inhibitor, WNT/β-catenin activator and overexpression β-catenin lentivirus to observe the changes in CCL2. M2 macrophages and gefitinib-resistant cell lines HCC827/GR were cocultured to detect the viability gefitinib for inducing cell death.

resultsThe proliferation and migratory activities were much more pronounced in HCC827/GR cells. CCL2 expression was also enhanced and regulated by β-catenin in HCC827/GR. CCL2 promoted the chemotactic ability of M2 macrophages. M2 macrophages reduced the antitumor effect of gefitinib treatment by activating AKT/mTOR.

conclusionsGefitinib-resistant cell lines have stronger proliferation and migration capabilities, and attract macrophages by releasing more CCL2 to reduce the sensitivity of cells to gefitinib.

Indexed as

Antineoplastic AgentsCell Line, TumorGefitinibGene Expression Regulation, NeoplasticHumansMacrophagesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesTransfectionAntineoplastic AgentsGefitinibMTOR protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesCCL2epidermal growth factor receptorgefitinib resistancenon-small cell lung cancerβ-catenin

Identifiers

PMID32956565
PMCPMC7606002
OpenAlexW3087571032

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.