New era of photodynamic therapy for lung cancers

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  • 肺癌に対するＰＤＴの適応拡大と将来

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It is very important to elucidate the mechanism of action and identify molecular determinants, in order to increase the number of clinical applications and develope new photosensitizer. We have previously reported that photodynamic therapy (PDT) using some photosensitizers, such as phthalocyanine (Pc) 4 damages anti-apoptotic protein Bcl-2, and that Bcl-2 is a molecular target of PDT. We examined molecular target of Photofin-PDT and Laserphyrin-PDT, by evaluating the photodamage of Bcl-2. We found that Bcl-2 was a molecular determinant of Photofrin-PDT but not Laserphyrin-PDT. Our results show that Laserphyrin-PDT does not damage Bcl-2 and Bcl-2 overexpressing cells are resistant to the sensitivity against PDT. Photofrin-PDT damages Bcl-2 and induces apoptosis earlier than Laserphyrin-PDT. We conclude that Photofrin-PDT damages different molecular target from Laserphyrin-PDT. Many advanced cancer cells have elevated amounts of Bcl-2 protein and we hypothesize that in most situations, Bcl-2 photodamage eliminates the normal protection against cell death. In this paper, we evaluated the role of photodamage to Bcl-2 in regulating the fate of cancer cells after PDT using Photofrin and Laserphyrin, and we will discuss the target molecules and new clinical applications.

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