ArticleRedox biology2022
Cationic antimicrobial peptide NRC-03 induces oral squamous cell carcinoma cell apoptosis via CypD-mPTP axis-mediated mitochondrial oxidative stress.
Article in Redox biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 42 citations in OpenAlex.
- Therapeutic Potential of Allomyrinasin in Oral Squamous Cell Carcinoma via Decreased NBC Activity.Pharmaceutics · 2026Article
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- Circulating miRNAs Correlate With rIPC-Induced Cardioprotection and Its Impairment in Diabetic Myocardial Infarction via AMPK Signalling.Journal of cellular and molecular medicine · 2026Article
- Mitochondrial dysfunction in Alzheimer's disease: targeting the powerhouse with nanomedicine.Frontiers in pharmacology · 2026Review
- Coptisine suppresses oral squamous cell carcinoma via regulating the JAK2/STAT3 to induce mitochondrial dysfunction in cancer cells and promote macrophage polarization to M1.American journal of cancer research · 2026Article
- Natural product-induced apoptosis in oral squamous cell carcinoma via targeting mitochondrial multifunctionality.Frontiers in oncology · 2026Review
- Next-Generation Anticancer Peptides: Engineering, Nanotheranostics and Clinical Translation.Nanotheranostics · 2026Review
- Mitochondrial-targeted therapeutics in oral squamous cell carcinoma: molecular and therapeutic implications.Frontiers in medicine · 2026Review
- Cyclophilin D suppresses colorectal cancer progression through the activation of an autophagy-mediated apoptotic pathway.Scientific reports · 2025Article
- Black phosphorus nanosheets boost mitochondrial oxidative phosphorylation improving immunotherapy outcomes.Nature nanotechnology · 2025Article
- TSH upregulates CYP4B1 through the PI3K/AKT/CREB pathway to promote cardiac hypertrophy.Journal of endocrinological investigation · 2025Article
- N-Acety-L-Cysteine Alleviates Isoflurane-Triggered Neuronal Cell Parthanatos by Suppressing Reactive Oxygen Species Accumulation Through the Induction of c-Jun N-Terminal Kinase Signaling Pathway Inhibition.Journal of biochemical and molecular toxicology · 2025Article
- The Mechanism of a Novel Mitochondrial-Targeted Icaritin Derivative in Regulating Apoptosis of BEL-7402 Cells Based on the SIRT3 and CypD-Mediated ROS/p38 MAPK Signaling Pathway.Molecules (Basel, Switzerland) · 2025Article
- Exploring the potential of anticancer peptides as therapeutic agents for cancer treatment.Research in pharmaceutical sciences · 2025Review
- D-M159 Synergistically Induces Apoptosis in HeLa Cells Through Endoplasmic Reticulum Stress and Mitochondrial Dysfunction.International journal of molecular sciences · 2025Article
- Oral administration of antimicrobial peptide MPX can effectively regulate LPS-mediated testicular oxidative stress and blood‒testis barrier damage.Scientific reports · 2025Article
- The Role of P53 in Myocardial Ischemia-Reperfusion Injury.Cardiovascular drugs and therapy · 2025Review
- Synaptotagmin-1 attenuates myocardial programmed necrosis and ischemia/reperfusion injury through the mitochondrial pathway.Cell death & disease · 2025Article
- Neutrophil extracellular traps in tumor metabolism and microenvironment.Biomarker research · 2025Review
- Green Synthesis of Silver Nanoparticles with Roasted Green Tea: Applications in Alginate-Gelatin Hydrogels for Bone Regeneration.Gels (Basel, Switzerland) · 2024Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pleurocidin-family cationic antimicrobial peptide NRC-03 exhibits potent and selective cytotoxicity towards cancer cells. However, the anticancer effect of NRC-03 in oral squamous cell carcinoma (OSCC) and the molecular mechanism of NRC-03 induced cancer cell death is still unclear. This study focused to investigate mitochondrial oxidative stress-mediated altered mitochondrial function involved in NRC-03-induced apoptosis of OSCC cells. NRC-03 entered the OSCC cells more easily than that of normal cells and bound to mitochondria as well as the nucleus, causing cell membrane blebbing, mitochondria swelling, and DNA fragmentation. NRC-03 induced high oxygen consumption, reactive oxygen species (ROS) release, mitochondrial dysfunction, and apoptosis in OSCC cells. Non-specific antioxidant N-acetyl-l-cysteine (NAC), or mitochondria-specific antioxidant mitoquinone (MitoQ) alleviated NRC-03-induced apoptosis and mitochondrial dysfunction indicated that NRC-03 exerts a cytotoxic effect in cancer cells via inducing cellular and mitochondrial oxidative stress. Moreover, the expression of cyclophilin D (CypD), the key component of mitochondrial permeability transition pore (mPTP), was upregulated in NRC-03-treated cancer cells. Blockade of CypD by siRNA-mediated depletion or pharmacological inhibitor cyclosporine A (CsA) significantly suppressed NRC-03-induced mitochondrial oxidative stress, mitochondrial dysfunction, and apoptosis. NRC-03 also activated MAPK/ERK and NF-κB pathways. Importantly, intratumoral administration of NRC-03 inhibited the growth of CAL-27 cells-derived tumors on xenografted animal models. Taken together, our study indicates that NRC-03 induces apoptosis in OSCC cells via the CypD-mPTP axis mediated mitochondrial oxidative stress.
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