RBMS1 Coordinates with the m6A Reader YTHDF1 to Promote NSCLC Metastasis through Stimulating S100P Translation
© 2024 The Authors. Advanced Science published by Wiley‐VCH GmbH..
Metastasis is the leading cause for the high mortality of lung cancer, however, effective anti-metastatic drugs are still limited. Here it is reported that the RNA-binding protein RBMS1 is positively associated with increased lymph node metastasis in non-small cell lung cancer (NSCLC). Depletion of RBMS1 suppresses cancer cell migration and invasion in vitro and inhibits cancer cell metastasis in vivo. Mechanistically, RBMS1 interacts with YTHDF1 to promote the translation of S100P, thereby accelerating NSCLC cell metastasis. The RRM2 motif of RBMS1 and the YTH domain of YTHDF1 are required for the binding of RBMS1 and YTHDF1. RBMS1 ablation inhibits the translation of S100P and suppresses tumor metastasis. Targeting RBMS1 with NTP, a small molecular chemical inhibitor of RBMS1, attenuates tumor metastasis in a mouse lung metastasis model. Correlation studies in lung cancer patients further validate the clinical relevance of the findings. Collectively, the study provides insight into the molecular mechanism by which RBMS1 promotes NSCLC metastasis and offers a therapeutic strategy for metastatic NSCLC.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2024 |
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Erschienen: |
2024 |
Enthalten in: |
Zur Gesamtaufnahme - volume:11 |
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Enthalten in: |
Advanced science (Weinheim, Baden-Wurttemberg, Germany) - 11(2024), 15 vom: 09. Apr., Seite e2307122 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Sun, Yu [VerfasserIn] |
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Links: |
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Anmerkungen: |
Date Completed 18.04.2024 Date Revised 25.04.2024 published: Print-Electronic Citation Status MEDLINE |
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doi: |
10.1002/advs.202307122 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM368321681 |
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520 | |a Metastasis is the leading cause for the high mortality of lung cancer, however, effective anti-metastatic drugs are still limited. Here it is reported that the RNA-binding protein RBMS1 is positively associated with increased lymph node metastasis in non-small cell lung cancer (NSCLC). Depletion of RBMS1 suppresses cancer cell migration and invasion in vitro and inhibits cancer cell metastasis in vivo. Mechanistically, RBMS1 interacts with YTHDF1 to promote the translation of S100P, thereby accelerating NSCLC cell metastasis. The RRM2 motif of RBMS1 and the YTH domain of YTHDF1 are required for the binding of RBMS1 and YTHDF1. RBMS1 ablation inhibits the translation of S100P and suppresses tumor metastasis. Targeting RBMS1 with NTP, a small molecular chemical inhibitor of RBMS1, attenuates tumor metastasis in a mouse lung metastasis model. Correlation studies in lung cancer patients further validate the clinical relevance of the findings. Collectively, the study provides insight into the molecular mechanism by which RBMS1 promotes NSCLC metastasis and offers a therapeutic strategy for metastatic NSCLC | ||
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650 | 7 | |a DNA-Binding Proteins |2 NLM | |
650 | 7 | |a S100P protein, human |2 NLM | |
650 | 7 | |a Calcium-Binding Proteins |2 NLM | |
650 | 7 | |a Neoplasm Proteins |2 NLM | |
650 | 7 | |a YTHDF1 protein, human |2 NLM | |
700 | 1 | |a Chen, Dan |e verfasserin |4 aut | |
700 | 1 | |a Sun, Siwen |e verfasserin |4 aut | |
700 | 1 | |a Ren, Menglin |e verfasserin |4 aut | |
700 | 1 | |a Zhou, Liang |e verfasserin |4 aut | |
700 | 1 | |a Chen, Chaoqun |e verfasserin |4 aut | |
700 | 1 | |a Zhao, Jinyao |e verfasserin |4 aut | |
700 | 1 | |a Wei, Huanhuan |e verfasserin |4 aut | |
700 | 1 | |a Zhao, Qingzhi |e verfasserin |4 aut | |
700 | 1 | |a Qi, Yangfan |e verfasserin |4 aut | |
700 | 1 | |a Zhang, Jinrui |e verfasserin |4 aut | |
700 | 1 | |a Zhang, Ge |e verfasserin |4 aut | |
700 | 1 | |a Liu, Han |e verfasserin |4 aut | |
700 | 1 | |a Yang, Qingkai |e verfasserin |4 aut | |
700 | 1 | |a Liu, Quentin |e verfasserin |4 aut | |
700 | 1 | |a Wang, Yang |e verfasserin |4 aut | |
700 | 1 | |a Zhang, Wenjing |e verfasserin |4 aut | |
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