Characteristics of an Impaired PDT Response.
David KesselWon Jin ChoJoseph RakowskiHarold E KimHyeong-Reh C KimPublished in: Photochemistry and photobiology (2021)
A concurrent human papilloma virus (HPV) infection potentiates the efficacy of ionizing radiation for treatment of head and neck cancer by promoting apoptosis. Studies in cell culture indicated an opposite effect for photodynamic therapy (PDT) when this leads to mitochondrial and ER photodamage. The explanation for this difference in PDT efficacy remains to be established. While apoptosis was impaired in HPV(-) cells, such cells can be killed via photodamage directed at the ER: this leads to a nonapoptotic death pathway termed paraptosis. No differences in photosensitizer uptake or reactive oxygen species (ROS) production were observed in HPV(+) vs. HPV(-) tumors. We now provide evidence that death pathways initiated by ER/mitochondrial photodamage leading to either paraptosis or apoptosis are impaired in an HPV(+) head and neck cell line. These results illustrate the complex determinants of PDT efficacy, a topic that has yet to be fully explored.
Keyphrases
- photodynamic therapy
- cell cycle arrest
- cell death
- oxidative stress
- induced apoptosis
- high grade
- endoplasmic reticulum stress
- pi k akt
- reactive oxygen species
- fluorescence imaging
- cervical cancer screening
- estrogen receptor
- endothelial cells
- breast cancer cells
- endoplasmic reticulum
- squamous cell carcinoma
- cell proliferation
- locally advanced
- radiation therapy