Stress granules promote DNA damage repair through the G3BP1/NAT10/ATF3 axis to facilitate nasopharyngeal carcinoma progression.
Blocking a stress-response mechanism in nasopharyngeal cancer cells reduced treatment resistance in preclinical studies, identifying a new therapeutic target.
This study reveals that stress granules in NPC cells exploit NAT10-mediated N4-acetylcytosine (ac4C) RNA modification to selectively protect DNA repair gene mRNAs during stress, enhancing therapy resistance and metastasis. The G3BP1/NAT10/ATF3 axis represents a novel therapeutic vulnerability in NPC, with remodelin (NAT10 inhibitor) demonstrating preclinical antitumor activity.
What the study was
- Study design
- Mechanistic study: NPC patient tissue cohort + in vitro/in vivo functional studies
- Population
- NPC patient tissue samples (n=111) + cell lines + mouse models
- Sample size
- 111
- Category
- Drug Development
- Maturity
- Exploratory
- Journal
- Oncogene
Why it surfaced
ac4C-SG-DNA repair axis is genuinely novel; n=111 tissue cohort adds clinical correlate; score capped at 5 per non-human primary mechanism rule; NAT10 inhibitor is a testable therapeutic angle.
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