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Parimifasor elicits broad-spectrum antitumor effects by suppressing the expression of oncogenic genes
Kai Li1,2, Minshan Sun3, Ruijuan Du1,2
1Zhang Zhongjing College of Chinese Medicine, Nanyang Institute of Technology, Nanyang, China.
Background:
Cancer remains a leading cause of death worldwide, constrained by limitations of current therapies, such as systemic toxicity, narrow therapeutic windows, and acquired drug resistance, highlighting the urgent need for novel agents. This study aimed to evaluate the antitumor efficacy of parimifasor and elucidate its molecular mechanism through transcriptomic profiling.
Methods:
This study evaluated the efficacy of parimifasor in vitro and in vivo. Transcriptomic profiling [RNA sequencing (RNA-seq)] of treated cells was performed to identify differentially expressed genes (DEGs), followed by functional enrichment, validation in The Cancer Genome Atlas (TCGA) database, and quantitative polymerase chain reaction (qPCR) confirmation.
Results:
This study presents the first mechanistic exploration of the small-molecule immunomodulator parimifasor (CAS: 1796641-10-5) as a broad-spectrum antitumor agent. In vitro cytotoxicity assays demonstrated potent suppression of 12 human tumor cell lines, with 50% inhibitory concentration (IC50) values <1 μM for nine cell lines. In Bagg Albino mouse (BALB)/c nude xenograft models, intraperitoneal administration of parimifasor (2 and 4 mg/kg) significantly inhibited tumor growth in esophageal squamous carcinoma (KYSE140) and glioblastoma (LN229) in a dose-dependent manner (P<0.05). RNA sequencing of parimifasor-treated cells revealed 81 common DEGs enriched in the RIG-I-like, nucleotide-binding oligomerization domain (NOD)-like, and Toll-like receptor signaling pathways. Integration with TCGA data identified 10 oncogenic genes (PARP10, OAS1, OAS3, PRR4, ZNFX1, HELZ2, SP110, CSRNP1, DDX3L, and PARP14) dysregulated across 20+ cancer types; qPCR confirmed their consistent downregulation posttreatment in both cell lines (P<0.05).
Conclusions:
This study establishes parimifasor's antitumor efficacy via the suppression of immune pathway-associated oncogenes, supporting its repurposing as a cancer therapeutic agent and providing biomarker candidates for clinical development.
Insights
Parimifasor demonstrates broad-spectrum antitumor efficacy by downregulating immune pathway-associated oncogenes. This small molecule shows promise as a novel cancer therapeutic agent with potential biomarker candidates for clinical development.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Cancer is a leading global cause of death, with current therapies facing limitations like toxicity and drug resistance.
- There is an urgent need for novel anticancer agents with improved efficacy and safety profiles.
Purpose of the Study:
- To evaluate the antitumor efficacy of the small-molecule immunomodulator parimifasor.
- To elucidate the molecular mechanisms underlying parimifasor's anticancer activity through transcriptomic profiling.
Main Methods:
- In vitro cytotoxicity assays and in vivo xenograft models were used to assess parimifasor's efficacy.
- RNA sequencing (RNA-seq) identified differentially expressed genes (DEGs) in treated cells.
- Functional enrichment, TCGA database validation, and qPCR confirmed gene expression changes.
Main Results:
- Parimifasor exhibited potent in vitro cytotoxicity against 12 human tumor cell lines (IC50 < 1 μM for nine lines).
- In vivo, parimifasor significantly inhibited tumor growth in esophageal squamous carcinoma and glioblastoma models.
- RNA-seq revealed enrichment of immune signaling pathways (RIG-I-like, NOD-like, Toll-like receptors) and identified 10 key oncogenes consistently downregulated by parimifasor.
Conclusions:
- Parimifasor demonstrates broad-spectrum antitumor efficacy by suppressing immune pathway-associated oncogenes.
- The findings support parimifasor's repurposing as a cancer therapeutic agent.
- Identified dysregulated oncogenes serve as potential biomarker candidates for parimifasor's clinical development.
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