Documentdetail
ID kaart

doi:10.1007/s13577-023-00895-6...

Auteur
Mito, Remi Iriki, Toyohisa Fujiwara, Yukio Pan, Cheng Ikeda, Tsuyoshi Nohara, Toshihiro Suzuki, Makoto Sakagami, Takuro Komohara, Yoshihiro
Langue
en
Editor

Springer

Categorie

Life Sciences

Jaar

2023

vermelding datum

29-03-2023

Trefwoorden
small-cell lung cancer interleukin-6 signal transducer and activator of... tumor-associated macrophage cell–cell interaction cancer il-6 proliferation compounds natural sclc cell–cell ona
Metriek

Beschrijving

Tumor-associated macrophage (TAM)-derived IL-6 is involved in small-cell lung cancer (SCLC) progression and chemoresistance via the activation of signal transducer and activator of transcription 3 (STAT3) in the tumor microenvironment.

This study aimed to identify natural compounds that suppress cell–cell interactions between TAMs and SCLC cells by inhibiting STAT3 activation.

We used a library of natural compounds to identify candidate agents possessing anti-SCLC effects by inhibiting macrophage-induced tumor proliferation.

SBC-3 and SBC-5, human SCLC cell lines, were used for in vitro experiments.

Furthermore, we assessed the efficacy of these candidate agents in a murine xenograft model of human SCLC.

Among the natural compounds examined, onionin A (ONA) inhibited IL-6-induced STAT3 activation and SCLC cell proliferation.

ONA also reduced the secretion of IL-6 from macrophages and interfered with the direct effect of cell–cell interactions between macrophages and SCLC cells.

Furthermore, ONA administration suppressed tumor progression in a tumor-bearing mouse model.

ONA was identified as the most useful candidate for targeting cell–cell interactions between cancer cells and TAMs for anti-SCLC therapy.

Mito, Remi,Iriki, Toyohisa,Fujiwara, Yukio,Pan, Cheng,Ikeda, Tsuyoshi,Nohara, Toshihiro,Suzuki, Makoto,Sakagami, Takuro,Komohara, Yoshihiro, 2023, Onionin A inhibits small-cell lung cancer proliferation through suppressing STAT3 activation induced by macrophages-derived IL-6 and cell–cell interaction with tumor-associated macrophage, Springer

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