title: ALA-PDT inhibits proliferation and promotes apoptosis of SCC cells through STAT3 signal pathway.
abstract: Previous studies suggest that apoptosis of carcinoma cells led by photodynamics is mainly intrinsic apoptosis, but whether the extrinsic pathway is involved in the treatment of carcinoma by photodynamic therapy is not confirmed. This research investigated the effect of ALA-PDT on the proliferation and apoptosis of SCC cell A431 and COLO-16, and discussed the role played by JAK/STAT3 signal pathway in this process. Our data showed that the expression levels STAT3 and p-STAT3 protein in the cancer tissue are higher than the corresponding adjacent tissue to carcinoma. The expression level of p-STAT3 in cancerous tissue has a correlation with the tumor size and tissue histopathological differentiation. ALA-PDT could inhibit proliferation of A431 and COLO-16 cells, STAT3 knock down could enhance ALA-PDT's inhibition of cell proliferation, and promote apoptosis induced by ALA-PDT. On the other hand, overexpression of STAT3 has the opposite effect. In addition, ALA-PDT can weaken the protein expression of STAT3 and its target gene Bcl-2 mRNA, and ALA-PDT can strengthen the protein expression of STAT3's target gene Bax mRNA. Overexpression of STAT3 can offset the effect on Bcl-2 and Bax by ALA-PDT; on the other hand, STAT3 knocking down can strengthen ALA-PDT's effect on Bcl-2 and Bax.
authors.affiliation: Department of Dermatology, The Air Force General Hospital of PLA, Beijing 100142, China. Electronic address: Winhp2006@163.com.
authors.forename: Li
authors.initials: L
authors.lastname: Qiao
authors.affiliation: Aviation Medicine Research Laboratory, Air Force General Hospital, PLA, Beijing 100142, China. Electronic address: mzsa@163.com.
authors.forename: Zhusong
authors.initials: Z
authors.lastname: Mei
authors.affiliation: Department of Dermatology, The Air Force General Hospital of PLA, Beijing 100142, China. Electronic address: yzywxl@163.com.
authors.forename: Zhiyong
authors.initials: Z
authors.lastname: Yang
authors.affiliation: Department of Radiation Oncology, Air Force General Hospital, PLA, Beijing 100142, China. Electronic address: leexinji@126.com.
authors.forename: Xinji
authors.initials: X
authors.lastname: Li
authors.affiliation: Department of Dermatology, The Air Force General Hospital of PLA, Beijing 100142, China. Electronic address: ch1031@163.com.
authors.forename: Hong
authors.initials: H
authors.lastname: Cai
authors.affiliation: Department of Dermatology, The Air Force General Hospital of PLA, Beijing 100142, China. Electronic address: liuwei5811@126.com.
authors.forename: Wei
authors.initials: W
authors.lastname: Liu
mesh_terms: D000622:Aminolevulinic Acid / Q000494:pharmacology / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D006258:Head and Neck Neoplasms / Q000628:therapy*; D006801:Humans; D010778:Photochemotherapy; D060888:Real-Time Polymerase Chain Reaction; D050796:STAT3 Transcription Factor / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; D000622:Aminolevulinic Acid
keywords: 5-Aminolevulinic acid (ALA); Cell apoptosis; Human skins squamous cell carcinoma; JAK/STAT3; Photodynamic therapy (PDT)