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已发表论文
内质网应激介导的自噬通过 PERK-eIF2α 通路为由 5-乙氨基-9-二乙氨基苯并 [a] phenoselenazinium 介导的光动力疗法助力
Authors Chen J, Huang JH, Wang Z, Song X, Chen Z, Zeng Q, Zhou X, Zuo Z, Zhao S, Chen X, Kang J
Received 22 January 2018
Accepted for publication 23 May 2018
Published 24 July 2018 Volume 2018:11 Pages 4315—4325
DOI https://doi.org/10.2147/OTT.S163366
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Justinn Cochran
Peer reviewer comments 3
Editor who approved publication: Prof. Dr. Geoffrey Pietersz
Introduction: 5-ethylamino-9-diethylaminobenzo[a]phenoselenazinium
(EtNBSe) is a novel synthetic bipolar photosensitizer with many promising
applications. This study investigated the impact of EtNBSe-mediated
photodynamic therapy (EtNBSe-PDT) on the autophagy and endoplasmic reticulum
(ER) stress of squamous carcinoma cells (A-431 cells), as well as the related
molecular mechanisms.
Methods: The potency of EtNBSe-PDT against squamous cell carcinoma was evaluated in BALB/c nude mice. Cell viability was evaluated using MTT. Western blotting and immunofluorescence were used to determine the expression levels of ER stress- and autophagy-related proteins.
Results: Both morphological and microscopic findings showed that the tumor on the xenograft mice exhibited an apparent reduction in volume and was replaced with fibrosis 20 days after EtNBSe-PDT. Additionally, in an in vitro study using A-431 cells, EtNBSe-PDT was found to inhibit A-431 cell survival in an EtNBSe concentration- and light dose- dependent manner, and to induce ER stress via the PERK-eIF2α signaling pathway. Additionally, EtNBSe-PDT could also induce autophagy of A-431 cells. Furthermore, the ER stress inhibitor 4-PBA and the eIF2α inhibitor salubrinal were found to inhibit the autophagy induced by EtNBSe-PDT.
Conclusion: This study demonstrated that the PERK-eIF2α signaling pathway was involved in the ER stress induced by EtNBSe-PDT. Meanwhile, the ER stress via the PERK-eIF2α pathway promoted the occurrence of autophagy in A-431 cells.
Keywords: photodynamic therapy, endoplasmic reticulum stress, squamous cell carcinoma, autophagy
Methods: The potency of EtNBSe-PDT against squamous cell carcinoma was evaluated in BALB/c nude mice. Cell viability was evaluated using MTT. Western blotting and immunofluorescence were used to determine the expression levels of ER stress- and autophagy-related proteins.
Results: Both morphological and microscopic findings showed that the tumor on the xenograft mice exhibited an apparent reduction in volume and was replaced with fibrosis 20 days after EtNBSe-PDT. Additionally, in an in vitro study using A-431 cells, EtNBSe-PDT was found to inhibit A-431 cell survival in an EtNBSe concentration- and light dose- dependent manner, and to induce ER stress via the PERK-eIF2α signaling pathway. Additionally, EtNBSe-PDT could also induce autophagy of A-431 cells. Furthermore, the ER stress inhibitor 4-PBA and the eIF2α inhibitor salubrinal were found to inhibit the autophagy induced by EtNBSe-PDT.
Conclusion: This study demonstrated that the PERK-eIF2α signaling pathway was involved in the ER stress induced by EtNBSe-PDT. Meanwhile, the ER stress via the PERK-eIF2α pathway promoted the occurrence of autophagy in A-431 cells.
Keywords: photodynamic therapy, endoplasmic reticulum stress, squamous cell carcinoma, autophagy
