Lucidone inhibits autophagy and MDR1 via HMGB1/RAGE/PI3K/Akt signaling pathway in pancreatic cancer cells

Gemcitabine (GEM) drug resistance remains a difficult challenge in pancreatic ductal adenocarcinoma (PDAC) treatment. Therefore, identifying a safe and effective treatment strategy for PDAC is urgent. Lucidone is a natural compound extracted from the fruits of Lindera erythrocarpa Makino. However, t...

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Published inPhytotherapy research Vol. 36; no. 4; pp. 1664 - 1677
Main Authors Chen, Sheng‐Yi, Hsu, Yi‐Hao, Wang, Sheng‐Yang, Chen, Ying‐Yin, Hong, Cheng‐Jie, Yen, Gow‐Chin
Format Journal Article
LanguageEnglish
Published Chichester, UK John Wiley & Sons, Ltd 01.04.2022
Wiley Subscription Services, Inc
Subjects
1-Phosphatidylinositol 3-kinase
Adenocarcinoma
Advanced glycosylation end products
AKT protein
Apoptosis
ATP Binding Cassette Transporter, Subfamily B, Member 1 - metabolism
Autophagy
Carcinoma, Pancreatic Ductal
Cell death
Cell Line, Tumor
Cell proliferation
Cyclopentanes
Cytotoxicity
Drug resistance
Gemcitabine
Glycosylation
HMGB1 Protein
Humans
Kinases
Lindera erythrocarpa
lucidone
MDR1
MDR1 protein
Multidrug resistance
nucleoproteins
P-Glycoprotein
P-glycoproteins
Pancreatic cancer
pancreatic ductal adenocarcinoma
Pancreatic Neoplasms
Pancreatic Neoplasms - pathology
Phosphatidylinositol 3-Kinases - metabolism
phytotherapy
Proteins
Proto-Oncogene Proteins c-akt - metabolism
Receptor for Advanced Glycation End Products
Signal Transduction
Signaling
siRNA
Toxicity
Transfection
Tumors
MDR1
gemcitabine
autophagy
lucidone
pancreatic ductal adenocarcinoma
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Abstract Gemcitabine (GEM) drug resistance remains a difficult challenge in pancreatic ductal adenocarcinoma (PDAC) treatment. Therefore, identifying a safe and effective treatment strategy for PDAC is urgent. Lucidone is a natural compound extracted from the fruits of Lindera erythrocarpa Makino. However, the role of lucidone in PDAC inhibition remains unclear. In addition, high‐mobility group box 1 (HMGB1) and receptor for advanced glycation end products (RAGE) are involved in multidrug resistance protein 1 (MDR1) regulation and GEM resistance. Thus, this study aimed to explore the function of lucidone in tumor cytotoxicity and chemosensitivity through the suppression of RAGE‐initiated signaling in PDAC cells. The data showed that lucidone significantly promoted apoptotic cell death and inhibited the expression of autophagic proteins (Atg5, Beclin‐1, LC3‐II, and Vps34) and MDR1 by inhibiting the HMGB1/RAGE/PI3K/Akt axis in both MIA Paca‐2 cells and MIA Paca‐2GEMR cells (GEM‐resistant cells). Notably, convincing data were also obtained in experiments involving RAGE‐specific siRNA transfection. In addition, remarkable cell proliferation was observed after treatment with lucidone combined with GEM, particularly in MIA Paca‐2GEMR cells, indicating that lucidone treatment enhanced chemosensitivity. Collectively, this study provided the underlying mechanism by which lucidone treatment inhibited HMGB1/RAGE‐initiated PI3K/Akt/MDR1 signaling and consequently enhanced chemosensitivity in PDAC.
AbstractList Gemcitabine (GEM) drug resistance remains a difficult challenge in pancreatic ductal adenocarcinoma (PDAC) treatment. Therefore, identifying a safe and effective treatment strategy for PDAC is urgent. Lucidone is a natural compound extracted from the fruits of Lindera erythrocarpa Makino. However, the role of lucidone in PDAC inhibition remains unclear. In addition, high‐mobility group box 1 (HMGB1) and receptor for advanced glycation end products (RAGE) are involved in multidrug resistance protein 1 (MDR1) regulation and GEM resistance. Thus, this study aimed to explore the function of lucidone in tumor cytotoxicity and chemosensitivity through the suppression of RAGE‐initiated signaling in PDAC cells. The data showed that lucidone significantly promoted apoptotic cell death and inhibited the expression of autophagic proteins (Atg5, Beclin‐1, LC3‐II, and Vps34) and MDR1 by inhibiting the HMGB1/RAGE/PI3K/Akt axis in both MIA Paca‐2 cells and MIA Paca‐2GEMR cells (GEM‐resistant cells). Notably, convincing data were also obtained in experiments involving RAGE‐specific siRNA transfection. In addition, remarkable cell proliferation was observed after treatment with lucidone combined with GEM, particularly in MIA Paca‐2GEMR cells, indicating that lucidone treatment enhanced chemosensitivity. Collectively, this study provided the underlying mechanism by which lucidone treatment inhibited HMGB1/RAGE‐initiated PI3K/Akt/MDR1 signaling and consequently enhanced chemosensitivity in PDAC.
Gemcitabine (GEM) drug resistance remains a difficult challenge in pancreatic ductal adenocarcinoma (PDAC) treatment. Therefore, identifying a safe and effective treatment strategy for PDAC is urgent. Lucidone is a natural compound extracted from the fruits of Lindera erythrocarpa Makino. However, the role of lucidone in PDAC inhibition remains unclear. In addition, high-mobility group box 1 (HMGB1) and receptor for advanced glycation end products (RAGE) are involved in multidrug resistance protein 1 (MDR1) regulation and GEM resistance. Thus, this study aimed to explore the function of lucidone in tumor cytotoxicity and chemosensitivity through the suppression of RAGE-initiated signaling in PDAC cells. The data showed that lucidone significantly promoted apoptotic cell death and inhibited the expression of autophagic proteins (Atg5, Beclin-1, LC3-II, and Vps34) and MDR1 by inhibiting the HMGB1/RAGE/PI3K/Akt axis in both MIA Paca-2 cells and MIA Paca-2GEMR cells (GEM-resistant cells). Notably, convincing data were also obtained in experiments involving RAGE-specific siRNA transfection. In addition, remarkable cell proliferation was observed after treatment with lucidone combined with GEM, particularly in MIA Paca-2GEMR cells, indicating that lucidone treatment enhanced chemosensitivity. Collectively, this study provided the underlying mechanism by which lucidone treatment inhibited HMGB1/RAGE-initiated PI3K/Akt/MDR1 signaling and consequently enhanced chemosensitivity in PDAC.Gemcitabine (GEM) drug resistance remains a difficult challenge in pancreatic ductal adenocarcinoma (PDAC) treatment. Therefore, identifying a safe and effective treatment strategy for PDAC is urgent. Lucidone is a natural compound extracted from the fruits of Lindera erythrocarpa Makino. However, the role of lucidone in PDAC inhibition remains unclear. In addition, high-mobility group box 1 (HMGB1) and receptor for advanced glycation end products (RAGE) are involved in multidrug resistance protein 1 (MDR1) regulation and GEM resistance. Thus, this study aimed to explore the function of lucidone in tumor cytotoxicity and chemosensitivity through the suppression of RAGE-initiated signaling in PDAC cells. The data showed that lucidone significantly promoted apoptotic cell death and inhibited the expression of autophagic proteins (Atg5, Beclin-1, LC3-II, and Vps34) and MDR1 by inhibiting the HMGB1/RAGE/PI3K/Akt axis in both MIA Paca-2 cells and MIA Paca-2GEMR cells (GEM-resistant cells). Notably, convincing data were also obtained in experiments involving RAGE-specific siRNA transfection. In addition, remarkable cell proliferation was observed after treatment with lucidone combined with GEM, particularly in MIA Paca-2GEMR cells, indicating that lucidone treatment enhanced chemosensitivity. Collectively, this study provided the underlying mechanism by which lucidone treatment inhibited HMGB1/RAGE-initiated PI3K/Akt/MDR1 signaling and consequently enhanced chemosensitivity in PDAC.
Gemcitabine (GEM) drug resistance remains a difficult challenge in pancreatic ductal adenocarcinoma (PDAC) treatment. Therefore, identifying a safe and effective treatment strategy for PDAC is urgent. Lucidone is a natural compound extracted from the fruits of Lindera erythrocarpa Makino. However, the role of lucidone in PDAC inhibition remains unclear. In addition, high-mobility group box 1 (HMGB1) and receptor for advanced glycation end products (RAGE) are involved in multidrug resistance protein 1 (MDR1) regulation and GEM resistance. Thus, this study aimed to explore the function of lucidone in tumor cytotoxicity and chemosensitivity through the suppression of RAGE-initiated signaling in PDAC cells. The data showed that lucidone significantly promoted apoptotic cell death and inhibited the expression of autophagic proteins (Atg5, Beclin-1, LC3-II, and Vps34) and MDR1 by inhibiting the HMGB1/RAGE/PI3K/Akt axis in both MIA Paca-2 cells and MIA Paca-2 cells (GEM-resistant cells). Notably, convincing data were also obtained in experiments involving RAGE-specific siRNA transfection. In addition, remarkable cell proliferation was observed after treatment with lucidone combined with GEM, particularly in MIA Paca-2 cells, indicating that lucidone treatment enhanced chemosensitivity. Collectively, this study provided the underlying mechanism by which lucidone treatment inhibited HMGB1/RAGE-initiated PI3K/Akt/MDR1 signaling and consequently enhanced chemosensitivity in PDAC.
Gemcitabine (GEM) drug resistance remains a difficult challenge in pancreatic ductal adenocarcinoma (PDAC) treatment. Therefore, identifying a safe and effective treatment strategy for PDAC is urgent. Lucidone is a natural compound extracted from the fruits of Lindera erythrocarpa Makino. However, the role of lucidone in PDAC inhibition remains unclear. In addition, high‐mobility group box 1 (HMGB1) and receptor for advanced glycation end products (RAGE) are involved in multidrug resistance protein 1 (MDR1) regulation and GEM resistance. Thus, this study aimed to explore the function of lucidone in tumor cytotoxicity and chemosensitivity through the suppression of RAGE‐initiated signaling in PDAC cells. The data showed that lucidone significantly promoted apoptotic cell death and inhibited the expression of autophagic proteins (Atg5, Beclin‐1, LC3‐II, and Vps34) and MDR1 by inhibiting the HMGB1/RAGE/PI3K/Akt axis in both MIA Paca‐2 cells and MIA Paca‐2ᴳᴱᴹᴿ cells (GEM‐resistant cells). Notably, convincing data were also obtained in experiments involving RAGE‐specific siRNA transfection. In addition, remarkable cell proliferation was observed after treatment with lucidone combined with GEM, particularly in MIA Paca‐2ᴳᴱᴹᴿ cells, indicating that lucidone treatment enhanced chemosensitivity. Collectively, this study provided the underlying mechanism by which lucidone treatment inhibited HMGB1/RAGE‐initiated PI3K/Akt/MDR1 signaling and consequently enhanced chemosensitivity in PDAC.
Gemcitabine (GEM) drug resistance remains a difficult challenge in pancreatic ductal adenocarcinoma (PDAC) treatment. Therefore, identifying a safe and effective treatment strategy for PDAC is urgent. Lucidone is a natural compound extracted from the fruits of Lindera erythrocarpa Makino. However, the role of lucidone in PDAC inhibition remains unclear. In addition, high‐mobility group box 1 (HMGB1) and receptor for advanced glycation end products (RAGE) are involved in multidrug resistance protein 1 (MDR1) regulation and GEM resistance. Thus, this study aimed to explore the function of lucidone in tumor cytotoxicity and chemosensitivity through the suppression of RAGE‐initiated signaling in PDAC cells. The data showed that lucidone significantly promoted apoptotic cell death and inhibited the expression of autophagic proteins (Atg5, Beclin‐1, LC3‐II, and Vps34) and MDR1 by inhibiting the HMGB1/RAGE/PI3K/Akt axis in both MIA Paca‐2 cells and MIA Paca‐2 GEMR cells (GEM‐resistant cells). Notably, convincing data were also obtained in experiments involving RAGE‐specific siRNA transfection. In addition, remarkable cell proliferation was observed after treatment with lucidone combined with GEM, particularly in MIA Paca‐2 GEMR cells, indicating that lucidone treatment enhanced chemosensitivity. Collectively, this study provided the underlying mechanism by which lucidone treatment inhibited HMGB1/RAGE‐initiated PI3K/Akt/MDR1 signaling and consequently enhanced chemosensitivity in PDAC.
Author Hsu, Yi‐Hao
Chen, Ying‐Yin
Hong, Cheng‐Jie
Chen, Sheng‐Yi
Yen, Gow‐Chin
Wang, Sheng‐Yang
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gemcitabine
autophagy
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Snippet Gemcitabine (GEM) drug resistance remains a difficult challenge in pancreatic ductal adenocarcinoma (PDAC) treatment. Therefore, identifying a safe and...
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SubjectTerms 1-Phosphatidylinositol 3-kinase
Adenocarcinoma
Advanced glycosylation end products
AKT protein
Apoptosis
ATP Binding Cassette Transporter, Subfamily B, Member 1 - metabolism
Autophagy
Carcinoma, Pancreatic Ductal
Cell death
Cell Line, Tumor
Cell proliferation
Cyclopentanes
Cytotoxicity
Drug resistance
Gemcitabine
Glycosylation
HMGB1 Protein
Humans
Kinases
Lindera erythrocarpa
lucidone
MDR1
MDR1 protein
Multidrug resistance
nucleoproteins
P-Glycoprotein
P-glycoproteins
Pancreatic cancer
pancreatic ductal adenocarcinoma
Pancreatic Neoplasms
Pancreatic Neoplasms - pathology
Phosphatidylinositol 3-Kinases - metabolism
phytotherapy
Proteins
Proto-Oncogene Proteins c-akt - metabolism
Receptor for Advanced Glycation End Products
Signal Transduction
Signaling
siRNA
Toxicity
Transfection
Tumors
Title Lucidone inhibits autophagy and MDR1 via HMGB1/RAGE/PI3K/Akt signaling pathway in pancreatic cancer cells
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fptr.7385
https://www.ncbi.nlm.nih.gov/pubmed/35224793
https://www.proquest.com/docview/2651388872
https://www.proquest.com/docview/2634535291
https://www.proquest.com/docview/2661009875
Volume 36
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