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Regnase-1 Promotes Tumour-Initiating Activity in Non-Small Cell Lung Cancer.
Keito Okazaki1,2, Madoka Kawaguchi2, Shohei Murakami2
1Department of Gene Expression Regulation, Institute of Development, Aging and Cancer, Tohoku University, 4-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan.
Journal of Biochemistry
|October 23, 2025
Summary
Regnase-1 (ZC3H12A) promotes non-small cell lung cancer (NSCLC) by activating the SOX2 pathway. Inhibiting Regnase-1 may offer a novel therapeutic strategy for treating NSCLC, even in resistant cases.
Area of Science:
- Molecular Biology
- Oncology
Background:
- Regnase-1 (ZC3H12A) is an RNase known to suppress inflammation.
- Its role in cancer, particularly non-small cell lung cancer (NSCLC), is not well understood.
Purpose of the Study:
- To investigate the function of Regnase-1 in NSCLC pathogenesis.
- To evaluate Regnase-1 as a potential therapeutic target for NSCLC.
Main Methods:
- Analysis of public NSCLC patient databases.
- Gene knockout of ZC3H12A in NSCLC cell lines.
- Transcriptome analysis to identify affected pathways.
- In vitro assays for oncosphere growth and tumor formation.
- Assessment of efficacy in NRF2-activated and post-tumorigenic models.
Main Results:
- Higher ZC3H12A expression correlated with worse prognosis in NSCLC patients.
- Regnase-1 deficiency suppressed the SOX2 pathway, impacting cancer stemness.
- Regnase-1 inhibition impaired tumor growth and formation in various NSCLC subtypes.
- Regnase-1 targeting was effective against NRF2-activated, therapy-resistant NSCLC cells.
- Post-tumorigenic suppression of Regnase-1 significantly inhibited tumor growth.
Conclusions:
- Regnase-1 plays a crucial role in NSCLC progression, particularly through the SOX2 pathway.
- Targeting Regnase-1 presents a promising therapeutic strategy for NSCLC, including resistant and post-tumorigenic stages.
- Combined cancer cell suppression and anti-cancer immunity activation by Regnase-1 inhibition offer a potential approach for intractable cancers.
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