Tualang honey promotes apoptosis of the A549 lung adenocarcinoma cell line via modulation of PI3K/AKT signaling pathway-related proteins

The phosphatidylinositol 3-kinases (PI3Ks)/protein kinase B (AKT) signaling pathway is frequently overexpressed in lung adenocarcinoma and associated with carcinogenesis through cell proliferation, and apoptosis deactivation; and it also enhances chemotherapeutic drugs resistance. Tualang honey (...

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Main Authors: Nazirah A, Puteri Shafinaz Abdul-Rahman
Format: Article
Language:en
Published: Pusat Perubatan Universiti Kebangsaan Malaysia 2022
Online Access:http://journalarticle.ukm.my/19672/1/16_ms0561_pdf_50460.pdf
http://journalarticle.ukm.my/19672/
https://www.medicineandhealthukm.com/toc/17/1
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author Nazirah A,
Puteri Shafinaz Abdul-Rahman,
author_facet Nazirah A,
Puteri Shafinaz Abdul-Rahman,
author_sort Nazirah A,
building Tun Sri Lanang Library
collection Institutional Repository
content_provider Universiti Kebangsaan Malaysia
content_source UKM Journal Article Repository
continent Asia
country Malaysia
description The phosphatidylinositol 3-kinases (PI3Ks)/protein kinase B (AKT) signaling pathway is frequently overexpressed in lung adenocarcinoma and associated with carcinogenesis through cell proliferation, and apoptosis deactivation; and it also enhances chemotherapeutic drugs resistance. Tualang honey (TH) has proven anticancer property on lung adenocarcinoma. However, the underlying mechanisms remain unreported. Hence, this study investigates the apoptosisinducing effect of TH on A549 lung adenocarcinoma cell line using RayBio® Human Apoptosis Array and label-free quantitative liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis to elucidate the modulation of upstream and downstream proteins of PI3K/AKT signaling pathway. The apoptosis-promoting effects of TH were associated with (i) the upregulation of pro-apoptotic proteins (i.e. cytochrome c, histone H1.2, and histone H1.4) and tumor suppressor proteins (i.e. IGFBP-3 and IGFBP-5), and (ii) downregulation of XIAP, insulin-growth factor (IGF) system (i.e. IGF-1, IGF1R, IGFBP-1, IGFBP-2, and IGFBP-4), HSP90AB1, YWHAQ, endoplasmin, and ITGB1. The effects were also linked with the suppression of receptor tyrosine kinase, integrins, G proteins, CHUK, RAC1, and JAK. Thus, TH may promote apoptosis of A549 lung adenocarcinoma cell line through alteration of the PI3K/AKT signaling pathway-related proteins. However, further studies involving animal models to provide a better model of understanding would prove necessary.
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institution Universiti Kebangsaan Malaysia
language en
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publisher Pusat Perubatan Universiti Kebangsaan Malaysia
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spelling my-ukm.journal.196722022-09-12T02:05:01Z http://journalarticle.ukm.my/19672/ Tualang honey promotes apoptosis of the A549 lung adenocarcinoma cell line via modulation of PI3K/AKT signaling pathway-related proteins Nazirah A, Puteri Shafinaz Abdul-Rahman, The phosphatidylinositol 3-kinases (PI3Ks)/protein kinase B (AKT) signaling pathway is frequently overexpressed in lung adenocarcinoma and associated with carcinogenesis through cell proliferation, and apoptosis deactivation; and it also enhances chemotherapeutic drugs resistance. Tualang honey (TH) has proven anticancer property on lung adenocarcinoma. However, the underlying mechanisms remain unreported. Hence, this study investigates the apoptosisinducing effect of TH on A549 lung adenocarcinoma cell line using RayBio® Human Apoptosis Array and label-free quantitative liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis to elucidate the modulation of upstream and downstream proteins of PI3K/AKT signaling pathway. The apoptosis-promoting effects of TH were associated with (i) the upregulation of pro-apoptotic proteins (i.e. cytochrome c, histone H1.2, and histone H1.4) and tumor suppressor proteins (i.e. IGFBP-3 and IGFBP-5), and (ii) downregulation of XIAP, insulin-growth factor (IGF) system (i.e. IGF-1, IGF1R, IGFBP-1, IGFBP-2, and IGFBP-4), HSP90AB1, YWHAQ, endoplasmin, and ITGB1. The effects were also linked with the suppression of receptor tyrosine kinase, integrins, G proteins, CHUK, RAC1, and JAK. Thus, TH may promote apoptosis of A549 lung adenocarcinoma cell line through alteration of the PI3K/AKT signaling pathway-related proteins. However, further studies involving animal models to provide a better model of understanding would prove necessary. Pusat Perubatan Universiti Kebangsaan Malaysia 2022-06 Article PeerReviewed application/pdf en http://journalarticle.ukm.my/19672/1/16_ms0561_pdf_50460.pdf Nazirah A, and Puteri Shafinaz Abdul-Rahman, (2022) Tualang honey promotes apoptosis of the A549 lung adenocarcinoma cell line via modulation of PI3K/AKT signaling pathway-related proteins. Medicine & Health, 17 (1). pp. 211-225. ISSN 2289-5728 https://www.medicineandhealthukm.com/toc/17/1
spellingShingle Nazirah A,
Puteri Shafinaz Abdul-Rahman,
Tualang honey promotes apoptosis of the A549 lung adenocarcinoma cell line via modulation of PI3K/AKT signaling pathway-related proteins
title Tualang honey promotes apoptosis of the A549 lung adenocarcinoma cell line via modulation of PI3K/AKT signaling pathway-related proteins
title_full Tualang honey promotes apoptosis of the A549 lung adenocarcinoma cell line via modulation of PI3K/AKT signaling pathway-related proteins
title_fullStr Tualang honey promotes apoptosis of the A549 lung adenocarcinoma cell line via modulation of PI3K/AKT signaling pathway-related proteins
title_full_unstemmed Tualang honey promotes apoptosis of the A549 lung adenocarcinoma cell line via modulation of PI3K/AKT signaling pathway-related proteins
title_short Tualang honey promotes apoptosis of the A549 lung adenocarcinoma cell line via modulation of PI3K/AKT signaling pathway-related proteins
title_sort tualang honey promotes apoptosis of the a549 lung adenocarcinoma cell line via modulation of pi3k/akt signaling pathway-related proteins
url http://journalarticle.ukm.my/19672/1/16_ms0561_pdf_50460.pdf
http://journalarticle.ukm.my/19672/
https://www.medicineandhealthukm.com/toc/17/1
url_provider http://journalarticle.ukm.my/