ArticlebioRxiv : the preprint server for biology2025
Targeted suppression of SPP1 inhibits tumor invasion and metastasis in NRF2 hyperactivated cisplatin resistant HNSCC.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Purpose: Cisplatin is the gold standard systemic agent for definitive treatment of HNSCC. The purpose of this study was to investigate the role of SPP1 in the progression and metastasis of cisplatin-resistant HNSCC, particularly in the context of NRF2 hyperactivation. Experimental Design: CDDP resistant HNSCC cell lines stably expressing various shRNA SPP1 constructs were generated. Clonogenic survival assays and a mouse model of oral cancer were used to examine the impact of silenced SPP1 Results: Targeted suppression of SPP1 improved cisplatin sensitivity, inhibited tumor invasion and metastasis Conclusions: Targeting dysregulated SPP1 improved cisplatin sensitivity, inhibited tumor invasion and metastasis in NRF2-hyperactivated HNSCC. These findings highlight the therapeutic potential of targeting SPP1 and the need for developing specific SPP1 inhibitors to improve outcomes for patients with HNSCC. Translational Relevance: Cisplatin-based chemotherapy remains the standard of care for patients with locally advanced head and neck squamous cell carcinoma. Cisplatin resistance often leads to treatment failure and metastasis which accounts for the majority of mortality associated with this disease. Unfortunately, there are no effective therapeutic agents to overcome cisplatin resistance in HNSCC. Here, we present compelling evidence that targeting SPP1 (also known as osteopontin) inhibits cisplatin resistance, tumor progression and metastasis in NRF2-hyperactivated HNSCC, positioning it as a potential therapeutic target to improve treatment outcomes in HNSCC.
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