Apatinib has anti-tumor effects and induces autophagy in lung cancer cells with high expression of VEGFR-2

Objective(s): This study investigated the inhibitory effect of apatinib on lung cancer cells with high expression of vascular endothelial growth factor-2 (VEGFR-2) and on inducing cellular autophagy and drug resistance. Materials and Methods: The expression of VEGFR-2 was detected using western blot...

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Main Authors: Mingtao Liu, Hui Li
Format: Article
Language:English
Published: Mashhad University of Medical Sciences 2024-11-01
Series:Iranian Journal of Basic Medical Sciences
Subjects:
Online Access:https://ijbms.mums.ac.ir/article_24603_042710fff0c5ea2b30e872e327837733.pdf
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author Mingtao Liu
Hui Li
author_facet Mingtao Liu
Hui Li
author_sort Mingtao Liu
collection DOAJ
description Objective(s): This study investigated the inhibitory effect of apatinib on lung cancer cells with high expression of vascular endothelial growth factor-2 (VEGFR-2) and on inducing cellular autophagy and drug resistance. Materials and Methods: The expression of VEGFR-2 was detected using western blotting and RT-PCR. Cell proliferation was measured using the CCK8 and colony formation assays. The cell apoptosis rate was determined using flow cytometry and tunnel assay. Cellular autophagy was detected by measuring the expression of LC3-II using Western blotting and cellular immunofluorescence. The inhibitory effect of apatinib on lung cancer cells and transplanted tumors was observed after treatment with the autophagy inhibitor chloroquine. Results: Apatinib dose-dependently inhibited the proliferation of H1975 and H446 cells; it induced apoptosis via the PARP and caspase 3 pathways in H1975 and H446 cells and effectively inhibited the growth of transplanted tumors. Apatinib induced autophagy in a dose-dependent manner in H1975 and H446 cells. The inhibitory effect of apatinib on cells and the promotion of apoptosis were significantly enhanced after treatment with chloroquine. Immunohistochemistry showed that combining apatinib with chloroquine could reduce the expression of CD31 and Ki67 and increase the expression of caspase 3. Conclusion: Apatinib inhibits proliferation and induces apoptosis in H1975 and H1446 lung cancer cells with high VEGFR2 expression and autophagy in H1975 and H446 cells.
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publishDate 2024-11-01
publisher Mashhad University of Medical Sciences
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spelling doaj-art-25468b2d64ce4d6dab19cc2d3d95d4f82025-08-20T03:34:26ZengMashhad University of Medical SciencesIranian Journal of Basic Medical Sciences2008-38662008-38742024-11-0127111370137910.22038/ijbms.2024.74820.1624624603Apatinib has anti-tumor effects and induces autophagy in lung cancer cells with high expression of VEGFR-2Mingtao Liu0Hui Li1Department of Pulmonary Medicine, Binzhou People’s Hospital, Binzhou, Shandong, ChinaDepartment of Pulmonary Medicine, Binzhou People’s Hospital, Binzhou, Shandong, ChinaObjective(s): This study investigated the inhibitory effect of apatinib on lung cancer cells with high expression of vascular endothelial growth factor-2 (VEGFR-2) and on inducing cellular autophagy and drug resistance. Materials and Methods: The expression of VEGFR-2 was detected using western blotting and RT-PCR. Cell proliferation was measured using the CCK8 and colony formation assays. The cell apoptosis rate was determined using flow cytometry and tunnel assay. Cellular autophagy was detected by measuring the expression of LC3-II using Western blotting and cellular immunofluorescence. The inhibitory effect of apatinib on lung cancer cells and transplanted tumors was observed after treatment with the autophagy inhibitor chloroquine. Results: Apatinib dose-dependently inhibited the proliferation of H1975 and H446 cells; it induced apoptosis via the PARP and caspase 3 pathways in H1975 and H446 cells and effectively inhibited the growth of transplanted tumors. Apatinib induced autophagy in a dose-dependent manner in H1975 and H446 cells. The inhibitory effect of apatinib on cells and the promotion of apoptosis were significantly enhanced after treatment with chloroquine. Immunohistochemistry showed that combining apatinib with chloroquine could reduce the expression of CD31 and Ki67 and increase the expression of caspase 3. Conclusion: Apatinib inhibits proliferation and induces apoptosis in H1975 and H1446 lung cancer cells with high VEGFR2 expression and autophagy in H1975 and H446 cells.https://ijbms.mums.ac.ir/article_24603_042710fff0c5ea2b30e872e327837733.pdfapatinib mesylateapoptosisautophagylung neoplasmscell proliferationvegfr2
spellingShingle Mingtao Liu
Hui Li
Apatinib has anti-tumor effects and induces autophagy in lung cancer cells with high expression of VEGFR-2
Iranian Journal of Basic Medical Sciences
apatinib mesylate
apoptosis
autophagy
lung neoplasms
cell proliferation
vegfr2
title Apatinib has anti-tumor effects and induces autophagy in lung cancer cells with high expression of VEGFR-2
title_full Apatinib has anti-tumor effects and induces autophagy in lung cancer cells with high expression of VEGFR-2
title_fullStr Apatinib has anti-tumor effects and induces autophagy in lung cancer cells with high expression of VEGFR-2
title_full_unstemmed Apatinib has anti-tumor effects and induces autophagy in lung cancer cells with high expression of VEGFR-2
title_short Apatinib has anti-tumor effects and induces autophagy in lung cancer cells with high expression of VEGFR-2
title_sort apatinib has anti tumor effects and induces autophagy in lung cancer cells with high expression of vegfr 2
topic apatinib mesylate
apoptosis
autophagy
lung neoplasms
cell proliferation
vegfr2
url https://ijbms.mums.ac.ir/article_24603_042710fff0c5ea2b30e872e327837733.pdf
work_keys_str_mv AT mingtaoliu apatinibhasantitumoreffectsandinducesautophagyinlungcancercellswithhighexpressionofvegfr2
AT huili apatinibhasantitumoreffectsandinducesautophagyinlungcancercellswithhighexpressionofvegfr2