Molecular mechanisms of apoptosis and autophagy elicited by combined treatment with oridonin and cetuximab in laryngeal squamous cell carcinoma.


Journal

Apoptosis : an international journal on programmed cell death
ISSN: 1573-675X
Titre abrégé: Apoptosis
Pays: Netherlands
ID NLM: 9712129

Informations de publication

Date de publication:
02 2019
Historique:
pubmed: 16 11 2018
medline: 21 4 2020
entrez: 16 11 2018
Statut: ppublish

Résumé

Combined oridonin (ORI), a natural and safe kaurene diterpenoid isolated from Rabdosia rubescens, and cetuximab (Cet), an anti-EGFR monoclonal antibody, have been reported to exert synergistic anti-tumor effects against laryngeal squamous cell carcinoma (LSCC) both in vitro and in vivo by our group. In the present study, we further found that ORI/Cet treatment not only resulted in apoptosis but also induced autophagy. AMPK/mTOR signaling pathway was found to be involved in the activation of autophagy in ORI/Cet-treated LSCC cells, which is independent of p53 status. Additionally, chromatin immunoprecipitation (ChIP) assay showed that ORI/Cet significantly increased the binding NF-κB family member p65 with the promotor of BECN 1, and p65-mediated up-regulation of BECN 1 caused by ORI/Cet is coupled to increased autophagy. On the other hand, we demonstrated that either Beclin 1 SiRNA or autophagy inhibitors could increase ORI/Cet induced-apoptosis, indicating that autophagy induced by combination of the two agents plays a cytoprotective role. Interestingly, 48 h after the combined treatment, autophagy began to decrease but apoptosis was significantly elevated. Our findings suggest that autophagy might be strongly associated with the antitumor efficacy of ORI/Cet, which may be beneficial to the clinical application of ORI/Cet in LSCC treatment.

Identifiants

pubmed: 30430397
doi: 10.1007/s10495-018-1497-0
pii: 10.1007/s10495-018-1497-0
doi:

Substances chimiques

Diterpenes, Kaurane 0
Reactive Oxygen Species 0
oridonin 0APJ98UCLQ
Cetuximab PQX0D8J21J

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

33-45

Subventions

Organisme : National Natural Science Foundation of China
ID : 81373797
Pays : International
Organisme : National Natural Science Foundation of China
ID : 81102855
Pays : International
Organisme : China postdoctoral Science Special Foundation
ID : 2014T70224
Pays : International
Organisme : China Postdoctoral Science Foundation
ID : 2013M541192
Pays : International

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Auteurs

Shijie Cao (S)

Tianjin State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, 300193, People's Republic of China.

Yiyuan Huang (Y)

School of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, 312 Anshanxi Road, Tianjin, 300193, People's Republic of China.
Tianjin State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, 300193, People's Republic of China.

Qiang Zhang (Q)

School of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, 312 Anshanxi Road, Tianjin, 300193, People's Republic of China.

Fangjin Lu (F)

School of Chinese Materia Medica, Tianjin University of Traditional Chinese Medicine, Tianjin, 300193, People's Republic of China.

Paul Owusu Donkor (PO)

School of Pharmacy, University of Health and Allied Sciences, Ho, PMB 31, Ghana.

Yan Zhu (Y)

Tianjin State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, 300193, People's Republic of China.

Feng Qiu (F)

School of Chinese Materia Medica, Tianjin University of Traditional Chinese Medicine, Tianjin, 300193, People's Republic of China.

Ning Kang (N)

School of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, 312 Anshanxi Road, Tianjin, 300193, People's Republic of China. kangndd@163.com.

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