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. 2022 Dec 8;11(12):12279. doi: 10.1002/jev2.12279

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© 2022 The Authors. Journal of Extracellular Vesicles published by Wiley Periodicals, LLC on behalf of the International Society for Extracellular Vesicles.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

PMC Copyright notice

A schematic diagram for the proposed role of ORAI1 calcium channel in regulating the sEV PD‐L1 release of lung cancer cells and suppressing tumor growth through upregulation of anti‐tumor immunity. Upon influx through ORAI1 channels, intracellular calcium is critical for calpain proteolytic enzyme activities, which sustain the MLPH functions to cooperate with Rab27 transporting the sEV‐contained MVB to the plasma membrane. When MVB fuse with the PM, the intraluminal PD‐L1 vesicles will be released. During the Rab27‐dependent vesicle trafficking, SLP2‐a also plays a key role in correct MVB transport and intracellular calcium dynamics. Thus, the ORAI1 calcium channel is essential for sEV PD‐L1 release and tumor growth. Interruption of the intracellular calcium signal by inhibition of ORAI1 channel can suppress the sEV PD‐L1 release and tumor growth.