Research
Extracellular vesicle-mediated CD47 transfer rewires integrin-IGF1R signaling and tumor immune remodeling to propagate cetuximab resistance
Cell Reports · By Tatsuya Sakaguchi, Juntaro Yamasaki, Yukie Hata, Momoko Yoshikawa, Tomoya Soma, Kaho Hiasa, Shunichi Yoshida, Kazuhiro Fukumura, Taiju Ando, Eiji Sugihara, Hiroyuki Nobusue, Seiji Asoda, Satoru Morikawa, Hideyuki Saya, Taneaki Nakagawa & Osamu Nagano ·
The Brief
- ALIX-dependent sorting of CD47 into extracellular vesicles is reported to propagate cetuximab resistance by promoting integrin-IGF1R signaling.
- Disrupting EV release is reported to remodel the tumor immune microenvironment and restore cetuximab sensitivity.
Why it matters
The study suggests cetuximab resistance may spread between tumor cells via extracellular vesicles, pointing to EV release as a possible target for overcoming therapy resistance.
Who’s affected
- cancer researchers
- oncologists studying cetuximab therapy
- #extracellular vesicles
- #cd47
- #cetuximab
- #cancer drug resistance
- #tumor microenvironment
Sakaguchi et al. demonstrate that ALIX-dependent sorting of CD47 into extracellular vesicles propagates cetuximab resistance by promoting integrin-IGF1R signaling. Disrupting EV release remodels the tumor immune microenvironment and restores cetuximab sensitivity.