Min Hye Noh
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Min Hye Noh has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Dae Young Hur
Department of Anatomy, Inje University College of Medicine, Busan 47392, Republic of Korea
1 shared publication - Hyun-Kyung Lee
Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Internal Medicine, Inje University Busan Paik Hospital, Busan, Republic of Korea
1 shared publication Seung-Mi Kim
Department of Anatomy and Tumor Immunology, Inje University College of Medicine, Busan, Republic of Korea
1 shared publicationSeung-Woo Hong
Department of Anatomy and Tumor Immunology, Inje University College of Medicine, Busan, Republic of Korea
1 shared publication- Sung Hyun Kim
Division of Hepatobiliary and Pancreatic Surgery, Department of Surgery, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea
1 shared publication - V. Courtney Broaddus
Division of Pulmonary, Critical Care, Allergy and Sleep Medicine, Department of Medicine, Zuckerberg San Francisco General Hospital and Trauma Center, University of California San Francisco, San Francisco, CA, U.S.A.
1 shared publication
Latest Publications
- Open Access
- 3 March 2021
- Published by International Institute of Anticancer Research in Anticancer Research
- Vol. 41 (3) , 1261-1269
Erlotinib Activates Different Cell Death Pathways in EGFR-mutant Lung Cancer Cells Grown in 3DVersus2D Culture Systems
Background/Aim: Non-small cell lung cancer patients with epidermal growth factor receptor (EGFR) mutation have been shown to have a good response to erlotinib, a receptor tyrosine kinase inhibitor of EGFR. In this study, we found that the cell death pathways activated by erlotinib in 2D and 3D culture systems are different. Materials and Methods: The cell death pathways induced by erlotinib were evaluated by flow cytometry and immunoblotting in both 2D and 3D culture systems of EGFR mutant lung cancer cells. Results: Treatment with erlotinib induced caspase 8 activation and up-regulation of TNF-related apoptosis-inducing ligand (TRAIL) expression only in 3D cultures. Knockdown of TRAIL attenuated both erlotinib-induced activation of caspase-8 and apoptosis in 3D cultures. Erlotinib also increased LC3, an autophagy marker, expression and c-Jun N terminal kinase (JNK) activation. Both 3-MA as an autophagy inhibitor and SP600125 as a JNK inhibitor, significantly inhibited erlotinib-induced cell death. Conclusion: Erlotinib induces apoptotic cell death in 3D cultures through an autophagy-TRAIL-JNK pathway.
- 3 March 2021
- Published by International Institute of Anticancer Research in Anticancer Research
- Vol. 41 (3) , 1261-1269
Open AccessErlotinib Activates Different Cell Death Pathways in EGFR-mutant Lung Cancer Cells Grown in 3DVersus2D Culture Systems
Background/Aim: Non-small cell lung cancer patients with epidermal growth factor receptor (EGFR) mutation have been shown to have a good response to erlotinib, a receptor tyrosine kinase inhibitor of EGFR. In this study, we found that the cell death pathways activated by erlotinib in 2D and 3D culture systems are different. Materials and Methods: The cell death pathways induced by erlotinib were evaluated by flow cytometry and immunoblotting in both 2D and 3D culture systems of EGFR mutant lung cancer cells. Results: Treatment with erlotinib induced caspase 8 activation and up-regulation of TNF-related apoptosis-inducing ligand (TRAIL) expression only in 3D cultures. Knockdown of TRAIL attenuated both erlotinib-induced activation of caspase-8 and apoptosis in 3D cultures. Erlotinib also increased LC3, an autophagy marker, expression and c-Jun N terminal kinase (JNK) activation. Both 3-MA as an autophagy inhibitor and SP600125 as a JNK inhibitor, significantly inhibited erlotinib-induced cell death. Conclusion: Erlotinib induces apoptotic cell death in 3D cultures through an autophagy-TRAIL-JNK pathway.