Antrodia cinnamomea Inhibits Growth and Migration of Lung Cancer Cells through Regulating p53-Bcl2 and MMPs Pathways.

Tan, Y; Johnson, M; Zhou, J; Zhao, Y; Kamal, MA; Qu, X

Antrodia cinnamomea Inhibits Growth and Migration of Lung Cancer Cells through Regulating p53-Bcl2 and MMPs Pathways.

Tan, Y

Johnson, M Zhou, J Zhao, Y Kamal, MA Qu, X

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Publisher:: World Scientific Publishing
Publication Type:: Journal Article
Citation:: The American Journal Of Chinese Medicine, 2020, 48, (8), pp. 1941-1953
Issue Date:: 2020-12-09

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Field	Value	Language
dc.contributor.author	Tan, Y https://orcid.org/0000-0001-9221-330X
dc.contributor.author	Johnson, M
dc.contributor.author	Zhou, J
dc.contributor.author	Zhao, Y
dc.contributor.author	Kamal, MA
dc.contributor.author	Qu, X
dc.date.accessioned	2022-04-29T23:58:55Z
dc.date.available	2022-04-29T23:58:55Z
dc.date.issued	2020-12-09
dc.identifier.citation	The American Journal Of Chinese Medicine, 2020, 48, (8), pp. 1941-1953
dc.identifier.issn	0192-415X
dc.identifier.issn	1793-6853
dc.identifier.uri	http://hdl.handle.net/10453/156831
dc.description.abstract	<i>Antrodia cinnamomea</i> has been shown to possess antitumor activity. This study investigated the effects and mechanisms of Antrodia cinnamomea extract (ACE) on growth and migration of human non-small cell lung cancer A549 cells. The effect of ACE on cell viability was determined by MTT assay and fluorescent live-cell imaging. The apoptotic effect of ACE was determined by cell cycle distribution using flow cytometry. A P53-mediated apoptosis pathway was identified by measuring protein expression of p53 and Bcl-2 with Western blotting. Additionally, mRNA expression of p53 and Bcl-2 and Bax was detected by qRT-PCR. The effect of ACE on cancer cell migration was confirmed by a wound-healing assay. Expression of MMP-2 and MMP-9 at the protein and gene levels was determined by western blot and qRT-PCR analysis. This study demonstrates the inhibitory effect of ACE on A549 cell proliferation in a dose-response manner with an [Formula: see text]. It was determined that ACE concentration at [Formula: see text] induced cell cycle arrest at S phase in A549 cells. The apoptosis-regulating protein p53 expression was enhanced and also associated with the downregulation of Bcl-2 in ACE treatment cells. The mRNA expression of p53 and <i>Bcl-2</i> associated with <i>Bxa</i> was consistent with protein expression. The inhibition of migration of cancer cells treated with ACE was clearly evident. At the same time, suppression of expression of MMP-2 and MMP-9 at protein and mRNA levels was observed. The findings of this study highlight ACE as a potential agent of adjuvant therapy for lung cancer.
dc.format	Print-Electronic
dc.language	eng
dc.publisher	World Scientific Publishing
dc.relation.ispartof	The American Journal Of Chinese Medicine
dc.relation.isbasedon	10.1142/s0192415x20500974
dc.rights	info:eu-repo/semantics/closedAccess
dc.subject	11 Medical and Health Sciences
dc.subject.classification	Complementary & Alternative Medicine
dc.subject.mesh	Antrodia
dc.subject.mesh	Cell Line, Tumor
dc.subject.mesh	Cell Movement
dc.subject.mesh	Cell Proliferation
dc.subject.mesh	Chemotherapy, Adjuvant
dc.subject.mesh	Gene Expression Regulation, Neoplastic
dc.subject.mesh	Humans
dc.subject.mesh	Lung Neoplasms
dc.subject.mesh	Matrix Metalloproteinase 2
dc.subject.mesh	Matrix Metalloproteinase 9
dc.subject.mesh	Phytotherapy
dc.subject.mesh	Plant Extracts
dc.subject.mesh	Proto-Oncogene Proteins c-bcl-2
dc.subject.mesh	Signal Transduction
dc.subject.mesh	Tumor Suppressor Protein p53
dc.subject.mesh	Cell Line, Tumor
dc.subject.mesh	Humans
dc.subject.mesh	Lung Neoplasms
dc.subject.mesh	Proto-Oncogene Proteins c-bcl-2
dc.subject.mesh	Plant Extracts
dc.subject.mesh	Chemotherapy, Adjuvant
dc.subject.mesh	Phytotherapy
dc.subject.mesh	Signal Transduction
dc.subject.mesh	Cell Proliferation
dc.subject.mesh	Cell Movement
dc.subject.mesh	Gene Expression Regulation, Neoplastic
dc.subject.mesh	Tumor Suppressor Protein p53
dc.subject.mesh	Matrix Metalloproteinase 2
dc.subject.mesh	Matrix Metalloproteinase 9
dc.subject.mesh	Antrodia
dc.title	Antrodia cinnamomea Inhibits Growth and Migration of Lung Cancer Cells through Regulating p53-Bcl2 and MMPs Pathways.
dc.type	Journal Article
utslib.citation.volume	48
utslib.location.activity	Singapore
utslib.for	11 Medical and Health Sciences
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Strength - CHT - Health Technologies
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
pubs.organisational-group	/University of Technology Sydney/Centre for Health Technologies (CHT)
utslib.copyright.status	closed_access	*
pubs.consider-herdc	true
dc.date.updated	2022-04-29T23:58:52Z
pubs.issue	8
pubs.publication-status	Published
pubs.volume	48
utslib.citation.issue	8

Abstract:

Antrodia cinnamomea has been shown to possess antitumor activity. This study investigated the effects and mechanisms of Antrodia cinnamomea extract (ACE) on growth and migration of human non-small cell lung cancer A549 cells. The effect of ACE on cell viability was determined by MTT assay and fluorescent live-cell imaging. The apoptotic effect of ACE was determined by cell cycle distribution using flow cytometry. A P53-mediated apoptosis pathway was identified by measuring protein expression of p53 and Bcl-2 with Western blotting. Additionally, mRNA expression of p53 and Bcl-2 and Bax was detected by qRT-PCR. The effect of ACE on cancer cell migration was confirmed by a wound-healing assay. Expression of MMP-2 and MMP-9 at the protein and gene levels was determined by western blot and qRT-PCR analysis. This study demonstrates the inhibitory effect of ACE on A549 cell proliferation in a dose-response manner with an [Formula: see text]. It was determined that ACE concentration at [Formula: see text] induced cell cycle arrest at S phase in A549 cells. The apoptosis-regulating protein p53 expression was enhanced and also associated with the downregulation of Bcl-2 in ACE treatment cells. The mRNA expression of p53 and Bcl-2 associated with Bxa was consistent with protein expression. The inhibition of migration of cancer cells treated with ACE was clearly evident. At the same time, suppression of expression of MMP-2 and MMP-9 at protein and mRNA levels was observed. The findings of this study highlight ACE as a potential agent of adjuvant therapy for lung cancer.

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http://hdl.handle.net/10453/156831