Downregulation of AP1S1 causes the lysosomal degradation of EGFR in non-small cell lung cancer
- Authors
- Jeong, Jangho; Hwang, Ye Eun; Lee, Minwoo; Keum, Seula; Song, Seongeun; Kim, Jung-Woong; Choi, Jee-Hye; Rhee, Sangmyung
- Issue Date
- Oct-2023
- Publisher
- WILEY
- Keywords
- adaptor-related protein complex 1 subunit sigma 1; epidermal growth factor receptor; lung adenocarcinoma; matrix stiffness; tyrosine kinase inhibitor resistance
- Citation
- JOURNAL OF CELLULAR PHYSIOLOGY, v.238, no.10, pp 2335 - 2347
- Pages
- 13
- Journal Title
- JOURNAL OF CELLULAR PHYSIOLOGY
- Volume
- 238
- Number
- 10
- Start Page
- 2335
- End Page
- 2347
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/68210
- DOI
- 10.1002/jcp.31112
- ISSN
- 0021-9541
1097-4652
- Abstract
- Matrix stiffness has been shown to play a critical role in cancer progression by influencing various cellular processes, including epidermal growth factor (EGF) signaling. However, the underlying molecular mechanisms are not fully understood. Here, we investigated the role of adaptor-related protein complex 1 subunit sigma 1 (AP1S1), a component of adaptor protein complex-1, in the regulation of EGF receptor (EGFR) intracellular trafficking during cancer cell progression. We found that AP1S1 expression was upregulated under stiff matrix conditions, resulting in the regulation of EGFR trafficking in non-small cell lung adenocarcinoma cells. Knockout of AP1S1 caused the lysosomal degradation of EGFR, leading to suppressed EGF-induced anaplastic lymphoma receptor tyrosine kinase phosphorylation. In addition, the downregulation of AP1S1 increased the sensitivity of H1975 cancer cells, which are resistant to tyrosine kinase inhibitors, to erlotinib. Collectively, our results suggest that AP1S1 could regulate EGFR recycling under stiff matrix conditions, and AP1S1 inhibition could be a novel strategy for treating cancer cells resistant to EGFR-targeted anticancer drugs.
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Collections - College of Natural Sciences > Department of Life Science > 1. Journal Articles
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