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Updated: Sep 8, 2025

Identification of OTX1 and OTX2 As Two Possible Molecular Markers for Sinonasal Carcinomas and Olfactory Neuroblastomas
Published on: February 28, 2019
PRDX3 promotes nasopharyngeal carcinoma tumor growth by regulating PINK1/Parkin pathway-dependent lipid peroxidation
Hualong Qiang1, Wei Wang2, Xiaodong Zhan2
1The First Clinical College, Jinan University, Guangzhou, 510632, Guangdong Province, China; Otolaryngology Head and Neck Surgery, The First Affiliated Hospital of Bengbu Medical University, Bengbu, 233004, Anhui Province, China.
Background:
Nasopharyngeal carcinoma (NPC) is a challenging malignancy characterized by aggressive progression and limited therapeutic efficacy. Emerging evidence implicates peroxiredoxin 3 (PRDX3), a mitochondrial peroxidase, as a critical regulator of redox homeostasis and mitochondrial integrity. Given its role in modulating cell death through mitochondrial quality control, we investigated the therapeutic potential of targeting PRDX3 in NPC.
Methods:
PRDX3 expression patterns were assessed in clinical NPC specimens using immunohistochemical and immunoblotting. Functional studies employed siRNA-mediated PRDX3 knockdown followed by cellular assays: CCK-8 proliferation, clonogenic survival, and mitochondrial parameter quantification (reactive oxygen species flux using DCFH-DA/C11-BODIPY, ATP biosynthesis, membrane polarization, and mtDNA integrity). Molecular interplay between PRDX3 and PTEN-induced kinase 1 (PINK1) was elucidated through co-immunoprecipitation and immunofluorescence analysis. In vivo therapeutic efficacy was validated using a xenograft model to evaluate tumor growth modulation.
Results:
Clinical specimens revealed significant PRDX3 overexpression in NPC compared to non-malignant controls. PRDX3 knockdown substantially attenuated malignant behavior and induced mitochondrial dysfunction in NPC cells. Mechanistically, PRDX3 interacted with PINK1 to stabilize Parkin-mediated mitophagic flux. PRDX3 safeguarded against apoptosis by sustaining PINK1/Parkin-dependent mitophagy clearance of damaged mitochondria. In vivo validation confirmed that PRDX3 knockdown suppressed tumor growth.
Conclusion:
PRDX3 acts as an upstream activator of the PINK1/Parkin signaling cascade, regulating lipid peroxidation-mediated mitochondrial dysfunction, mitophagy, survival and apoptosis of NPC cell.
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