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The apoptotic effect of 1’S-1’-Acetoxychavicol Acetate (ACA) enhanced by inhibition of non-canonical autophagy in human non-small cell lung cancer cells

Sok, Sophia P. M., Arshad, Norhafiza M., Azmi, Mohamad Nurul, Awang, Khalijah, Ozpolat, Bulent, Hasima Nagoor, Noor·2017·PLOS ONE
DOI 10.1371/journal.pone.0171329PMC PMC5291426
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Fig 1 ACA inhibited cell viability of A549 and SK-LU-1 cell lines. (A) Chemical structure of 1’S-1’-acetoxychavicol acetate (ACA). (B) The cell viability of MCF 10A, A549 and SK-LU-1 cells lines after exposure to ACA (0–30 μM) for 24 h was assessed using MTT assay. Data represented as mean percentage of cell viability ± SD for three independent experiments. (C) The cell viability of A549 and SK-LU-1 cells lines after exposure to IC50 of ACA (25 μM for SK-LU-1 and 30 μM for A549 cells) on respective cell lines for 0–24 h was assessed using MTT assay. Data represented as mean percentage of cell viability ± SD for three independent experiments. * p < 0.05 and ** p < 0.01 statistically different in comparison to 0 h (D) Representative photomicrograph (200 × magnification) of A549 and SK-LU-1 cell lines upon ACA treatment. Arrow indicates the cytoplasmic vacuole.
Fig 1 ACA inhibited cell viability of A549 and SK-LU-1 cell lines. (A) Chemical structure of 1’S-1’-acetoxychavicol acetate (ACA). (B) The cell viability of MCF 10A, A549 and SK-LU-1 cells lines after exposure to ACA (0–30 μM) for 24 h was assessed using MTT assay. Data represented as mean percentage of cell viability ± SD for three independent experiments. (C) The cell viability of A549 and SK-LU-1 cells lines after exposure to IC50 of ACA (25 μM for SK-LU-1 and 30 μM for A549 cells) on respective cell lines for 0–24 h was assessed using MTT assay. Data represented as mean percentage of cell viability ± SD for three independent experiments. * p < 0.05 and ** p < 0.01 statistically different in comparison to 0 h (D) Representative photomicrograph (200 × magnification) of A549 and SK-LU-1 cell lines upon ACA treatment. Arrow indicates the cytoplasmic vacuole.CC0 · PubMed Central
Fig 2 Autophagy effect of ACA on A549 and SK-LU-1 cell lines. (A) Representative fluorescence photomicrograph (400 × magnification) illustrating the acidic vesicular organelles in A549 and SK-LU-1 cell lines after treated with ACA for 0, 3, 6, 12, and 24 h. Data were presented as relative fluorescence intensity in comparison to untreated cells ± SD. * p < 0.05, ** p < 0.01, and *** p < 0.001 statistically different in comparison to untreated. (B) Representative fluorescence photomicrograph (400 × magnification) illustrating the GFP-LC3-II punctate formation in A549 and SK-LU-1 cell lines upon exposure to ACA. Data were represented as mean percentage of cells with GFP-LC3-II punctate ± SD of three independent experiments. * p < 0.05, ** p < 0.01, and *** p < 0.001 statistically different in comparison to untreated. (C) Protein expression of LC3-I/II and p62 after ACA treatment in A549 and SK-LU-1 cell lines. Data were represented as mean normalized intensity ± SD of three independent experiments. * p < 0.05, ** p < 0.01, and *** p < 0.001 statistically different in comparison to untreated.
Fig 2 Autophagy effect of ACA on A549 and SK-LU-1 cell lines. (A) Representative fluorescence photomicrograph (400 × magnification) illustrating the acidic vesicular organelles in A549 and SK-LU-1 cell lines after treated with ACA for 0, 3, 6, 12, and 24 h. Data were presented as relative fluorescence intensity in comparison to untreated cells ± SD. * p < 0.05, ** p < 0.01, and *** p < 0.001 statistically different in comparison to untreated. (B) Representative fluorescence photomicrograph (400 × magnification) illustrating the GFP-LC3-II punctate formation in A549 and SK-LU-1 cell lines upon exposure to ACA. Data were represented as mean percentage of cells with GFP-LC3-II punctate ± SD of three independent experiments. * p < 0.05, ** p < 0.01, and *** p < 0.001 statistically different in comparison to untreated. (C) Protein expression of LC3-I/II and p62 after ACA treatment in A549 and SK-LU-1 cell lines. Data were represented as mean normalized intensity ± SD of three independent experiments. * p < 0.05, ** p < 0.01, and *** p < 0.001 statistically different in comparison to untreated.CC0 · PubMed Central
Fig 3 ACA-induced autophagy is independent of Beclin-1/PI3K complex in A549 and SK-LU-1 cell lines. (A) Protein expression of Beclin-1 after ACA treatment in A549 and SK-LU-1 cell lines. Data were represented as mean normalized intensity against GAPDH ± SD. *** p < 0.001 statistically different in comparison to untreated. (B) Representative fluorescence photomicrograph (400 × magnification) illustrating the acidic vesicular organelles in A549 and SK-LU-1 cell lines after treatment with ACA in presence or absence of 3-MA. Data were presented as relative fluorescence intensity in comparison to untreated cells ± SD of three independent experiments * p < 0.05 and ** p < 0.01 statistically different in comparison to untreated. # p < 0.05 and ## p < 0.01 statistically different in comparison to 3-MA. (C) Representative fluorescence photomicrograph (400 × magnification) illustrating the GFP-LC3-II punctate formation in A549 and SK-LU-1 cell lines upon exposure to co-treatment of 3-MA and ACA. Data were represented as mean percentage of cells with GFP-LC3-II punctate ± SD of three independent experiments. *** p < 0.001 statistically different in comparison to untreated. ### p < 0.001 statistically different in comparison to 3-MA. (D) Effect of 3-MA on LC3-I/LC3-II protein expression after pre-treatment of 3-MA prior to ACA treatment in A549 and SK-LU-1 cell lines. Data were represented as normalized intensity ± SD of three independent experiments. * p < 0.05, ** p < 0.01 and *** p < 0.001 statistically different in comparison to untreated. ## p < 0.01 and ### p < 0.001 statistically different in comparison to 3-MA. (E) Effect of 3-MA on the cell viability of ACA-treated A549 and SK-LU-1 cell lines. Data represented as mean percentage of cell viability ± SD for three independent experiments. * p < 0.05 and *** p < 0.001 statistically different in comparison to untreated.
Fig 3 ACA-induced autophagy is independent of Beclin-1/PI3K complex in A549 and SK-LU-1 cell lines. (A) Protein expression of Beclin-1 after ACA treatment in A549 and SK-LU-1 cell lines. Data were represented as mean normalized intensity against GAPDH ± SD. *** p < 0.001 statistically different in comparison to untreated. (B) Representative fluorescence photomicrograph (400 × magnification) illustrating the acidic vesicular organelles in A549 and SK-LU-1 cell lines after treatment with ACA in presence or absence of 3-MA. Data were presented as relative fluorescence intensity in comparison to untreated cells ± SD of three independent experiments * p < 0.05 and ** p < 0.01 statistically different in comparison to untreated. # p < 0.05 and ## p < 0.01 statistically different in comparison to 3-MA. (C) Representative fluorescence photomicrograph (400 × magnification) illustrating the GFP-LC3-II punctate formation in A549 and SK-LU-1 cell lines upon exposure to co-treatment of 3-MA and ACA. Data were represented as mean percentage of cells with GFP-LC3-II punctate ± SD of three independent experiments. *** p < 0.001 statistically different in comparison to untreated. ### p < 0.001 statistically different in comparison to 3-MA. (D) Effect of 3-MA on LC3-I/LC3-II protein expression after pre-treatment of 3-MA prior to ACA treatment in A549 and SK-LU-1 cell lines. Data were represented as normalized intensity ± SD of three independent experiments. * p < 0.05, ** p < 0.01 and *** p < 0.001 statistically different in comparison to untreated. ## p < 0.01 and ### p < 0.001 statistically different in comparison to 3-MA. (E) Effect of 3-MA on the cell viability of ACA-treated A549 and SK-LU-1 cell lines. Data represented as mean percentage of cell viability ± SD for three independent experiments. * p < 0.05 and *** p < 0.001 statistically different in comparison to untreated.CC0 · PubMed Central
Fig 4 Knockdown of LC3 enhanced ACA-induced cytotoxicity through apoptosis. (A) Knockdown efficiency of the three unique 27 mer siRNA duplexes targeting LC3 in A549 and SK-LU-1. Data were represented as mean percentage of relative intensity ± SD of three independent experiments. * p < 0.05 and *** p < 0.001 statistically different in comparison to negative control (NC). (B) Effect of siLC3 on ACA-induced LC3-I/LC3-II protein expression in A549 and SK-LU-1 cell lines. Data were represented as normalized intensity ± SD of three independent experiments. *** p < 0.001 statistically different in comparison to negative control (NC). (C) Effect of siLC3 on the cell viability of ACA-treated A549 and SK-LU-1 cell lines. Data represented as mean percentage of cell viability ± SD for three independent experiments. ** p < 0.01 and *** p < 0.001 statistically different in comparison to negative control (NC). # p < 0.05 and ### p < 0.001 statistically different in comparison to NC + ACA. (D) Effect of siLC3 on ACA-induced apoptotic cells in A549 and SK-LU-1 cell lines. Representative annexin V-FITC/PI scatter plots of 1 × 104 cells after 24 h of treatment. Data represented as mean percentage of apoptotic cells ± SD for three independent experiments. * p < 0.05, ** p < 0.01 and *** p < 0.001 statistically different in comparison to negative control (NC). ### p < 0.001 statistically different in comparison to NC + ACA.
Fig 4 Knockdown of LC3 enhanced ACA-induced cytotoxicity through apoptosis. (A) Knockdown efficiency of the three unique 27 mer siRNA duplexes targeting LC3 in A549 and SK-LU-1. Data were represented as mean percentage of relative intensity ± SD of three independent experiments. * p < 0.05 and *** p < 0.001 statistically different in comparison to negative control (NC). (B) Effect of siLC3 on ACA-induced LC3-I/LC3-II protein expression in A549 and SK-LU-1 cell lines. Data were represented as normalized intensity ± SD of three independent experiments. *** p < 0.001 statistically different in comparison to negative control (NC). (C) Effect of siLC3 on the cell viability of ACA-treated A549 and SK-LU-1 cell lines. Data represented as mean percentage of cell viability ± SD for three independent experiments. ** p < 0.01 and *** p < 0.001 statistically different in comparison to negative control (NC). # p < 0.05 and ### p < 0.001 statistically different in comparison to NC + ACA. (D) Effect of siLC3 on ACA-induced apoptotic cells in A549 and SK-LU-1 cell lines. Representative annexin V-FITC/PI scatter plots of 1 × 104 cells after 24 h of treatment. Data represented as mean percentage of apoptotic cells ± SD for three independent experiments. * p < 0.05, ** p < 0.01 and *** p < 0.001 statistically different in comparison to negative control (NC). ### p < 0.001 statistically different in comparison to NC + ACA.CC0 · PubMed Central
Fig 5 Autophagy inhibitor chloroquine enhanced ACA-induced cytotoxicity through apoptosis. (A) Representative fluorescence photomicrograph (400 × magnification) illustrating the acidic vesicular organelles in A549 and SK-LU-1 cell lines after treatment with ACA in presence or absence of CQ. Data were presented as relative fluorescence intensity in comparison to untreated cells ± SD of three independent experiments. ** p < 0.01 and *** p < 0.001 statistically different in comparison to untreated. # p < 0.05 statistically different in comparison to CQ. (B) Representative fluorescence photomicrograph (400 × magnification) illustrating the GFP-LC3-II punctate formation in A549 and SK-LU-1 cell lines upon exposure to co-treatment of CQ and ACA. Data were represented as mean percentage of cells with GFP-LC3-II punctate ± SD of three independent experiments. *** p < 0.001 statistically different in comparison to untreated. # p < 0.05 and ### p < 0.001 statistically different in comparison to CQ. (C) Effect of CQ on LC3-I/LC3-II protein expression after pre-treated with CQ prior ACA treatment in A549 and SK-LU-1 cell lines. Data were represented as normalized intensity ± SD of three independent experiments. * p < 0.05, ** p < 0.01 and *** p < 0.001 statistically different in comparison to untreated. # p < 0.05 and ## p < 0.01 statistically different in comparison to CQ. (D) Effect of CQ on the cell viability of ACA-treated A549 and SK-LU-1 cell lines. Data represented as mean percentage of cell viability ± SD for three independent experiments. *** p < 0.001 statistically different in comparison to untreated. ### p < 0.001 statistically different in comparison to ACA. (E) Effect of CQ on ACA-induced apoptotic cells in A549 and SK-LU-1 cell lines. Representative annexin V-FITC/PI scatter plots of 1 × 104 cells after 24 h of treatment. Data represented as mean percentage of apoptotic cells ± SD for three independent experiments. *** p < 0.001 statistically different in comparison to untreated. # p < 0.05 and ### p < 0.001 statistically different in comparison to ACA.
Fig 5 Autophagy inhibitor chloroquine enhanced ACA-induced cytotoxicity through apoptosis. (A) Representative fluorescence photomicrograph (400 × magnification) illustrating the acidic vesicular organelles in A549 and SK-LU-1 cell lines after treatment with ACA in presence or absence of CQ. Data were presented as relative fluorescence intensity in comparison to untreated cells ± SD of three independent experiments. ** p < 0.01 and *** p < 0.001 statistically different in comparison to untreated. # p < 0.05 statistically different in comparison to CQ. (B) Representative fluorescence photomicrograph (400 × magnification) illustrating the GFP-LC3-II punctate formation in A549 and SK-LU-1 cell lines upon exposure to co-treatment of CQ and ACA. Data were represented as mean percentage of cells with GFP-LC3-II punctate ± SD of three independent experiments. *** p < 0.001 statistically different in comparison to untreated. # p < 0.05 and ### p < 0.001 statistically different in comparison to CQ. (C) Effect of CQ on LC3-I/LC3-II protein expression after pre-treated with CQ prior ACA treatment in A549 and SK-LU-1 cell lines. Data were represented as normalized intensity ± SD of three independent experiments. * p < 0.05, ** p < 0.01 and *** p < 0.001 statistically different in comparison to untreated. # p < 0.05 and ## p < 0.01 statistically different in comparison to CQ. (D) Effect of CQ on the cell viability of ACA-treated A549 and SK-LU-1 cell lines. Data represented as mean percentage of cell viability ± SD for three independent experiments. *** p < 0.001 statistically different in comparison to untreated. ### p < 0.001 statistically different in comparison to ACA. (E) Effect of CQ on ACA-induced apoptotic cells in A549 and SK-LU-1 cell lines. Representative annexin V-FITC/PI scatter plots of 1 × 104 cells after 24 h of treatment. Data represented as mean percentage of apoptotic cells ± SD for three independent experiments. *** p < 0.001 statistically different in comparison to untreated. # p < 0.05 and ### p < 0.001 statistically different in comparison to ACA.CC0 · PubMed Central

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Metadata

Authors
Sok, S. P. M., Arshad, N. M., Azmi, M. N., Awang, K., Ozpolat, B., & Hasima Nagoor, N.
ORCID
Hasima Nagoor, Noor
Venue
PLOS ONE
Publisher
Public Library of Science (PLoS)
Published
2017-02-03
Volume
12
Issue
2
Pages
e0171329
ISSN
1932-6203
DOI
10.1371/journal.pone.0171329
PMC
PMC5291426
Cited by
18
References
2
Language
en
Licence
creativecommons.org/publicdomain/zero/1.0/ (vor)
Funders
  • Science Technology and Innovation (MOSTI) and University of Malaya through Science Fund (SF014-2-13)
  • RU Operation Grant (RU005C-2014)

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CoChat. (2026). Citation check: The apoptotic effect of 1’S-1’-Acetoxychavicol Acetate (ACA) enhanced by inhibition of non-canonical autophagy in human non-small cell lung cancer cells. https://app.cochat.ai/papers/10.1371/journal.pone.0171329
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Sok, S. P. M., Arshad, N. M., Azmi, M. N., Awang, K., Ozpolat, B., & Hasima Nagoor, N. (2017). The apoptotic effect of 1’S-1’-Acetoxychavicol Acetate (ACA) enhanced by inhibition of non-canonical autophagy in human non-small cell lung cancer cells. PLOS ONE. https://doi.org/10.1371/journal.pone.0171329