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Article

Picrasidine I Triggers Heme Oxygenase-1-Induced Apoptosis in Nasopharyngeal Carcinoma Cells via ERK and Akt Signaling Pathways

by
Hsin-Yu Ho
1,†,
Ping-Ju Chen
2,3,†,
Yi-Ching Chuang
1,
Yu-Sheng Lo
1,
Chia-Chieh Lin
1,
Ming-Ju Hsieh
1,3,4,5,* and
Mu-Kuan Chen
6,*
1
Oral Cancer Research Center, Changhua Christian Hospital, Changhua 500, Taiwan
2
Department of Dentistry, Changhua Christian Hospital, Changhua 500, Taiwan
3
Institute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan
4
Department of Post-Baccalaureate Medicine, College of Medicine, National Chung Hsing University, Taichung 402, Taiwan
5
Graduate Institute of Biomedical Sciences, China Medical University, Taichung 404, Taiwan
6
Department of Otorhinolaryngology, Head and Neck Surgery, Changhua Christian Hospital, Changhua 500, Taiwan
*
Authors to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Int. J. Mol. Sci. 2022, 23(11), 6103; https://doi.org/10.3390/ijms23116103
Submission received: 25 April 2022 / Revised: 26 May 2022 / Accepted: 27 May 2022 / Published: 29 May 2022
(This article belongs to the Special Issue Molecular Mechanisms of Cancer Progression and Targeted Therapy Attempts)
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Abstract

Nasopharyngeal carcinoma (NPC) has a higher incidence in Taiwan than worldwide. Although it is a radiosensitive malignancy, cancer recurrence is still high in the advanced stages because of its ability to induce lymph node metastasis. Picrasidine I from Picrasma quassioides has been reported as a potential drug for targeting multiple signaling pathways. The present study aimed to explore the role of picrasidine I in the apoptosis of NPC cells. Our results show that picrasidine I induced cytotoxic effects in NPC cells and caused cell cycle arrest in the sub-G1, S, and G2/M phases. Western blot analysis further demonstrated that the modulation of apoptosis through the extrinsic and intrinsic pathways was involved in picrasidine I-induced cell death. Downregulation of the ERK1/2 and Akt signaling pathways was also found in picrasidine I-induced apoptosis. Additionally, the apoptosis array showed that picrasidine I significantly increased heme oxygenase-1 (HO-1) expression, which could act as a critical molecule in picrasidine I-induced apoptosis in NPC cells. The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets also revealed that the HMOX1 mRNA level (HO-1) is lower in patients with head and neck squamous carcinoma (HNSCC) and NPC than in patients without cancer. Our study indicated that picrasidine I exerts anticancer effects in NPC by modulating HO-1 via the ERK and Akt signaling pathways.
Keywords: picrasidine I; apoptosis; mitogen-activated protein kinase (MAPK) pathway; heme oxygenase-1 picrasidine I; apoptosis; mitogen-activated protein kinase (MAPK) pathway; heme oxygenase-1

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MDPI and ACS Style

Ho, H.-Y.; Chen, P.-J.; Chuang, Y.-C.; Lo, Y.-S.; Lin, C.-C.; Hsieh, M.-J.; Chen, M.-K. Picrasidine I Triggers Heme Oxygenase-1-Induced Apoptosis in Nasopharyngeal Carcinoma Cells via ERK and Akt Signaling Pathways. Int. J. Mol. Sci. 2022, 23, 6103. https://doi.org/10.3390/ijms23116103

AMA Style

Ho H-Y, Chen P-J, Chuang Y-C, Lo Y-S, Lin C-C, Hsieh M-J, Chen M-K. Picrasidine I Triggers Heme Oxygenase-1-Induced Apoptosis in Nasopharyngeal Carcinoma Cells via ERK and Akt Signaling Pathways. International Journal of Molecular Sciences. 2022; 23(11):6103. https://doi.org/10.3390/ijms23116103

Chicago/Turabian Style

Ho, Hsin-Yu, Ping-Ju Chen, Yi-Ching Chuang, Yu-Sheng Lo, Chia-Chieh Lin, Ming-Ju Hsieh, and Mu-Kuan Chen. 2022. "Picrasidine I Triggers Heme Oxygenase-1-Induced Apoptosis in Nasopharyngeal Carcinoma Cells via ERK and Akt Signaling Pathways" International Journal of Molecular Sciences 23, no. 11: 6103. https://doi.org/10.3390/ijms23116103

APA Style

Ho, H.-Y., Chen, P.-J., Chuang, Y.-C., Lo, Y.-S., Lin, C.-C., Hsieh, M.-J., & Chen, M.-K. (2022). Picrasidine I Triggers Heme Oxygenase-1-Induced Apoptosis in Nasopharyngeal Carcinoma Cells via ERK and Akt Signaling Pathways. International Journal of Molecular Sciences, 23(11), 6103. https://doi.org/10.3390/ijms23116103

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