Evaluating the efficacy and mechanisms of action of seriniquinone against pediatric neuroblastoma.

P Peter E. Zage (University of California San Diego, School of Medicine, La Jolla, CA) S Sriprada Kattamuri (University of California San Diego, La Jolla, CA) E Erin Yamaoka (University of California San Diego, La Jolla, CA) D Disha Surana (University of California San Diego, La Jolla, CA) C Carla Sofia Sampaio (University of California San Diego, La Jolla, CA) W William Fenical (University of California San Diego, La Jolla, CA)

Abstract

e15125 Background: Children diagnosed with neuroblastoma face poor prognosis despite aggressive multimodal therapies, highlighting the urgent need for effective and targeted treatments. Natural products derived from microbial sources like marine actinomycetes are promising novel anticancer agents. Seriniquinone, a quinone-based compound originally isolated from a Serinicoccus species, has demonstrated potent anticancer activity across a variety of tumor types via targeting dermcidin, a peptide associated with cancer cell survival and proliferation, inducing autophagocytosis followed by apoptosis. Given its unique mechanism of action and prior efficacy, we hypothesize that seriniquinone may represent a novel and selective therapeutic option for pediatric neuroblastoma. Methods: Techniques used included neuroblastoma cell culture and quantification, CCK-8 viability assays, and Western Blot analysis. Synthetic seriniquinone was tested by preparing MYCN-amplified and non-amplified neuroblastoma cell lines for treatment with increasing concentrations of seriniquinone. Treated cells were analyzed vy CCK-8 viaiblity assays and Western blots analysis of whole cell lysates to evaluate protein expression changes due to the effect of seriniquinone on intraceullar markers and markers of apoptosis such as PARP and Caspase-3. Results: Treatment of various MYCN-amplified and non-amplified neuroblastoma cell lines shows that Seriniquinone inhibits cell growth and viability in a concentration-dependent manner, with observed cell rounding, detachment and death compared to the healthy monolayers in the control cells. Seriniquinone treatment also resulted in decreased expression of dermcidin and MYCN and induction of apoptosis compared to control cells. Conclusions: Our results support the efficacy of seriniquinone as a potent therapeutic agent with efficacy against pediatric neuroblastoma cells, with further studies planned to confirm the efficacy and mechanisms of action. Ultimately, we hope these findings lay the groundwork for further preclinical validation and support future clinical investigation, including the potential for translation into early phase clinical trials.

Article Details

Volume / Issue Vol. 44, Issue 16_suppl
Published June 01, 2026
ISSN 0732-183X
Publisher Lippincott Williams & Wilkins

Journal Info

Journal of Clinical Oncology

Lippincott Williams & Wilkins

ISSN: 0732-183X Health Sciences

Authors (6)

P

Peter E. Zage

University of California San Diego, School of Medicine, La Jolla, CA

S

Sriprada Kattamuri

University of California San Diego, La Jolla, CA

E

Erin Yamaoka

University of California San Diego, La Jolla, CA

D

Disha Surana

University of California San Diego, La Jolla, CA

C

Carla Sofia Sampaio

University of California San Diego, La Jolla, CA

W

William Fenical

University of California San Diego, La Jolla, CA