Published online Mar 15, 2024. doi: 10.4251/wjgo.v16.i3.968
Peer-review started: October 8, 2023
First decision: December 2, 2023
Revised: December 23, 2023
Accepted: January 19, 2024
Article in press: January 19, 2024
Published online: March 15, 2024
Processing time: 156 Days and 8.3 Hours
Traditional treatments for pancreatic cancer (PC) are inadequate. Photodynamic therapy (PDT) is non-invasive, and proven safe to kill cancer cells, including PC. However, the mitochondrial concentration of the photosensitizer, such as verteporfin, is key.
To investigate the distribution of fluorescence of verteporfin in PC cells treated with antitumor drugs, post-PDT.
Workable survival rates of PC cells (AsPC-1, BxPC-3) were determined with chemotherapy [doxorubicin (DOX) and gemcitabine (GEM)] and non-chemotherapy [sirolimus (SRL) and cetuximab (CTX)] drugs in vitro, with or without verteporfin, as measured via MTT, flow cytometry, and laser confocal microscopy. Reduced cell proliferation was associated with GEM that was more enduring compared with DOX. Confocal laser microscopy allowed observation of GEM- and verteporfin-treated PC cells co-stained with 4’,6-diamidino-2-phenylindole and MitoTracker Green to differentiate living and dead cells and subcellular localization of verteporfin, respectively.
Cell survival significantly dropped upon exposure to either chemotherapy drug, but not to SRL or CTX. Both cell lines responded similarly to GEM. The intensity of fluorescence was associated with the concentration of verteporfin. Additional experiments using GEM showed that survival rates of the PC cells treated with 10 μmol/L verteporfin (but not less) were significantly lower relative to nil verte
Verteporfin was observed in living cells. In GEM -treated human PC cells, verteporfin was particularly prevalent in the mitochondria. This study supports further study of PDT for the treatment of PC after neoadjuvant chemotherapy.
Core Tip: Photodynamic therapy (PDT) for pancreatic cancer (PC) is more effective when the photosensitizer is concentrated in the mitochondria. This study showed that 10 μmol/L verteporfin treatment at various times significantly reduced the survival of human PC cells, but lower concentrations had no discernible results. After gemcitabine treatment, verteporfin was located primarily in the mitochondria. Verteporfin was more prevalent in living than dead cells, and in the latter was found mainly in the mitochondria. This study provides a significant theoretical foundation for using PDT in the comprehensive treatment of PC after neoadjuvant chemotherapy.