Evidence map›Paper›PMID 31610280›Full record

ArticleInternational journal of pharmaceutics2019

Effects of gefitinib treatment on cellular uptake of extracellular vesicles in EGFR-mutant non-small cell lung cancer cells.

Tomoya Takenaka, Shinya Nakai, Miku Katayama, Mami Hirano, Natsumi Ueno, Kosuke Noguchi, Tomoka Takatani-Nakase, Ikuo Fujii, Susumu S Kobayashi, Ikuhiko Nakase

Open access · greenAbstract read
In one paragraph

Article in International journal of pharmaceutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

26 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  8. Cellular Regulation of Macropinocytosis.International journal of molecular sciences · 2024
    Review
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  12. NOTCH4Nature communications · 2023
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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

10 authors at 3 institutions in 2 countries.

Tomoya TakenakaNanoSquare Research Institute, Research Center for the 21st Century, Organization for Research Promotion, Osaka Prefecture University, Sakai, Osaka 599-8570, Japan; Graduate School of Science, Osaka Prefecture University, Sakai, Osaka 599-8570, Japan.
Shinya NakaiNanoSquare Research Institute, Research Center for the 21st Century, Organization for Research Promotion, Osaka Prefecture University, Sakai, Osaka 599-8570, Japan; Graduate School of Science, Osaka Prefecture University, Sakai, Osaka 599-8570, Japan.
Miku KatayamaNanoSquare Research Institute, Research Center for the 21st Century, Organization for Research Promotion, Osaka Prefecture University, Sakai, Osaka 599-8570, Japan; Graduate School of Science, Osaka Prefecture University, Sakai, Osaka 599-8570, Japan.
Mami HiranoNanoSquare Research Institute, Research Center for the 21st Century, Organization for Research Promotion, Osaka Prefecture University, Sakai, Osaka 599-8570, Japan; Graduate School of Science, Osaka Prefecture University, Sakai, Osaka 599-8570, Japan.
Natsumi UenoNanoSquare Research Institute, Research Center for the 21st Century, Organization for Research Promotion, Osaka Prefecture University, Sakai, Osaka 599-8570, Japan; Graduate School of Science, Osaka Prefecture University, Sakai, Osaka 599-8570, Japan.
Kosuke NoguchiNanoSquare Research Institute, Research Center for the 21st Century, Organization for Research Promotion, Osaka Prefecture University, Sakai, Osaka 599-8570, Japan; Graduate School of Science, Osaka Prefecture University, Sakai, Osaka 599-8570, Japan.
Tomoka Takatani-NakaseDepartment of Pharmaceutics, School of Pharmacy and Pharmaceutical Sciences, Mukogawa Women's University, Nishinomiya, Hyogo 663-8179, Japan.
Ikuo FujiiGraduate School of Science, Osaka Prefecture University, Sakai, Osaka 599-8570, Japan.
Susumu S KobayashiBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA; Division of Translational Genomics, Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Kashiwa, Chiba 277-8577, Japan. Electronic address: sukobaya@east.ncc.go.jp.
Ikuhiko NakaseNanoSquare Research Institute, Research Center for the 21st Century, Organization for Research Promotion, Osaka Prefecture University, Sakai, Osaka 599-8570, Japan; Graduate School of Science, Osaka Prefecture University, Sakai, Osaka 599-8570, Japan. Electronic address: i-nakase@21c.osakafu-u.ac.jp.
Osaka Prefecture University · JPBeth Israel Deaconess Medical Center · USMukogawa Women's University · JP

Funding

Overcoming resistance to tyrosine kinase inhibitors in lung cancerR01CA169259 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KOBAYASHI, SUSUMU · 2013 to 2018
$1.8M
Emergence of drug resistant mutations in lung cancerR21CA178301 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KOBAYASHI, SUSUMU · 2015 to 2016
$435k
NCCDPHP CDC HHS R01 DP000110NCI NIH HHS R01 CA169259NCI NIH HHS R21 CA178301
6 · The paper itself

Abstract

Extracellular vesicles (exosomes, EVs) are cell membrane particles (30-200 nm) secreted by virtually all cells. During intercellular communication in the body, secreted EVs play crucial roles by carrying functional biomolecules (e.g., microRNAs and enzymes) into other cells to affect cellular function, including disease progression. We previously reported that the macropinocytosis pathway contributes greatly to the efficient cellular uptake of EVs. The activation of growth factor receptors, such as epidermal growth factor receptor (EGFR), induces macropinocytosis. In this study, we demonstrated the effects of gefitinib, a tyrosine kinase inhibitor of EGFR, on the cellular uptake of EVs. In EGFR-mutant HCC827 non-small cell lung cancer (NSCLC) cells, which are sensitive to gefitinib, macropinocytosis was suppressed by gefitinib treatment. However, the cellular uptake of EVs was increased by gefitinib treatment, whereas that of liposomes was reduced. In accordance with the results of the cellular uptake studies, the anti-cancer activity of doxorubicin (DOX)-loaded EVs in HCC827 cells was significantly increased in the presence of gefitinib, whereas the activity of DOX-loaded liposomes was reduced. The digestion of EV proteins by trypsin did not affect uptake, suggesting that the cellular uptake of EVs might not be mediated by EV proteins. These results suggest that gefitinib can enhance cell-to-cell communication via EVs within the tumor microenvironment. In addition, EVs show potential as drug delivery vehicles in combination with gefitinib for the treatment of patients harboring EGFR-mutant NSCLC tumors.

Indexed as

A549 CellsCarcinoma, Non-Small-Cell LungCell Line, TumorDoxorubicinErbB ReceptorsExtracellular VesiclesGefitinibHeLa CellsHumansLung NeoplasmsMutationProtein Kinase InhibitorsTumor MicroenvironmentDoxorubicinEGFR protein, humanErbB ReceptorsGefitinibProtein Kinase InhibitorsEGFRExosomesExtracellular vesiclesGefitinibNon-small cell lung cancer

Identifiers

PMID31610280
PMCPMC6899172
OpenAlexW2979321351

What OpenQuestion holds

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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.