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Photodynamic Therapy with Blended Conducting Polymer/Fullerene Nanoparticle Photosensitizers
Published on: October 28, 2015
Effect and underlying mechanism of a photochemotherapy dual-function nanodrug delivery system for head and neck
Qian Lin1, Hui-Min Liu2, Li-Zhi Wu1
1Department of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, 238 Jie-Fang Road, Wuhan, Hubei, 430060, P. R. China.
Background:
The novel nanomaterials PNA-TN (PN) and PNA-TN-Dox (PND) have been shown to have strong inhibitory effects on breast cancer; however, it is unclear whether PN and PND have anti-head and neck squamous cell carcinoma (HNSCC) activity, and their potential mechanisms of activity are unknown. So, our study aims to explore the therapeutic effects of PN and PND on HNSCC and their possible mechanisms.
Methods:
We used a series of phenotypic research to evaluate the effects of PN + Laser (L) and PND + L on the biological function of HNSCC cells in vitro and in vivo. We subsequently used mechanism research to examine changes in mRNA and protein expression related to apoptosis, epithelial‒mesenchymal transition (EMT), and the JNK signalling pathway.
Results:
Our study revealed that PN and PND have strong inhibitory effects on HNSCC cells both in vitro and in vivo. In vitro, PN and PND significantly inhibited the proliferation, migration, invasion and EMT ability of HNSCC cells and promoted apoptosis; the inhibitory effect in the PND + L group was significantly greater than that in the PN + L group. In vivo, both treatments led to significant reductions in tumour volume and weight. Notably, the tumour volume and weight in the PND + L group were significantly lower than those in the PN + L group. Mechanism research confirmed that PN + L activated the expression of apoptosis-related proteins and inhibited the expression of EMT-related proteins via the JNK pathway. Furthermore, the anti-HNSCC effect of PN + L was blocked after the use of a JNK pathway inhibitor.
Conclusion:
Treatment with PN + L or PND + L significantly inhibited the malignant progress of HNSCC cells, and the therapeutic effect of PND + L was significantly stronger than that of PN + L. The JNK signalling pathway is a key mechanism by which PN exerts its anti-HNSCC activity.
Insights
Novel nanomaterials PNA-TN (PN) and PNA-TN-Dox (PND) show significant anti-cancer effects against head and neck squamous cell carcinoma (HNSCC). The PND treatment demonstrated superior efficacy, mediated through the JNK signaling pathway.
Area of Science:
- Nanomedicine
- Oncology
- Biochemistry
Background:
- The efficacy of PNA-TN (PN) and PNA-TN-Dox (PND) against breast cancer is established, but their activity against head and neck squamous cell carcinoma (HNSCC) remains uninvestigated.
- The underlying mechanisms of action for PN and PND in HNSCC are currently unknown.
Purpose of the Study:
- To investigate the therapeutic potential of PN and PND, in combination with laser therapy, against HNSCC.
- To elucidate the molecular mechanisms responsible for the anti-HNSCC effects of PN and PND.
Main Methods:
- Phenotypic evaluation of PN+Laser (L) and PND+L on HNSCC cell function in vitro and in vivo.
- Mechanism-based studies analyzing mRNA and protein expression related to apoptosis, epithelial-mesenchymal transition (EMT), and the JNK signaling pathway.
Main Results:
- Both PN+L and PND+L significantly inhibited HNSCC cell proliferation, migration, invasion, and EMT, while promoting apoptosis in vitro.
- PND+L exhibited a significantly greater inhibitory effect on HNSCC cells compared to PN+L, both in vitro and in vivo, evidenced by reduced tumor volume and weight.
- Mechanism studies revealed that PN+L activates apoptosis-related proteins and inhibits EMT-related proteins via the JNK pathway, with JNK inhibition blocking the anti-HNSCC effect.
Conclusions:
- PN+L and PND+L treatments effectively suppress the malignant progression of HNSCC.
- PND+L demonstrates superior therapeutic efficacy over PN+L in HNSCC treatment.
- The JNK signaling pathway is identified as a critical mediator of the anti-HNSCC activity of PN.
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