Evidence map›Paper›PMID 31073278›Full record

ArticleCancer cell international2019

Apatinib preferentially inhibits PC9 gefitinib-resistant cancer cells by inducing cell cycle arrest and inhibiting VEGFR signaling pathway.

Yong-An Song, Ting Ma, Xue-Yan Zhang, Xiang-Song Cheng, Ayobami-Matthew Olajuyin, Zhi-Fu Sun, Xiao-Ju Zhang

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

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  13. AhR and Cancer: From Gene Profiling to Targeted Therapy.International journal of molecular sciences · 2021
    Review
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  17. Neoantimycin F, aFrontiers in pharmacology · 2019
    Article
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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 2 institutions in 2 countries.

Yong-An Song *1The People's Hospital of Zhengzhou University, Zhengzhou, 450000 China.
Ting Ma *2Key Laboratory of Technology of Drug Preparation, Zhengzhou University, Zhengzhou, China.
Xue-Yan Zhang2Key Laboratory of Technology of Drug Preparation, Zhengzhou University, Zhengzhou, China.
Xiang-Song Cheng1The People's Hospital of Zhengzhou University, Zhengzhou, 450000 China.
Ayobami-Matthew Olajuyin1The People's Hospital of Zhengzhou University, Zhengzhou, 450000 China.
Zhi-Fu Sun4Department of Health Sciences Research, Mayo Clinic, Rochester, MN 55905 USA.
Xiao-Ju Zhang1The People's Hospital of Zhengzhou University, Zhengzhou, 450000 China.
Zhengzhou University · CNMayo Clinic in Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLung cancer is one of the most common and deadly tumors around the world. Targeted therapy for patients with certain mutations, especially by use of tyrosine kinase inhibitors (TKIs) targeting epidermal growth factor receptor (EGFR), has provided significant benefit to patients. However, gradually developed resistance to the therapy becomes a major challenge in clinical practice and an alternative to treat such patients is needed. Herein, we report that apatinib, a novel anti-angiogenic drug, effectively inhibits obtained gefitinib-resistant cancer cells but has no much effect on their parental sensitive cells.

methodsGefitinib-resistant lung cancer cell line (PC9GR) was established from its parental sensitive line (PC9) with a traditional EGFR mutation after long time exposure to gefitinib. Different concentrations of apatinib were used to treat PC9, PC9GR, and other two lung cancer cell lines for its anti-growth effects. RNA sequencing was performed on PC9, PC9GR, and both after apatinib treatment to detect differentially expressed genes and involved pathways. Protein expression of key cycle regulators p57, p27, CDK2, cyclin E2, and pRb was detected using Western blot. Xenograft mouse model was used to assess the anti-tumor activity of apatinib in vivo.

resultsThe established PC9GR cells had over 250-fold increased resistance to gefitinib than its sensitive parental PC9 cells (IC

conclusionsApatinib demonstrated strong anti-proliferation and anti-growth effects on gefitinib resistant lung cancer cells but not its parental sensitive cells. The anti-tumor effect was mostly due to apatinib induced cell cycle arrest and VEGFR signaling pathway inhibition. These data suggested that apatinib may provide a benefit to patients with acquired resistance to EGFR-TKI treatment.

Indexed as

ApatinibCell cycle arrestGefitinib-resistancePC9 cellsVEGF2 pathway

Identifiers

PMID31073278
PMCPMC6498592
OpenAlexW2942593273

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.