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Please use this identifier to cite or link to this item: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/38431

Title: Pre-existing fas ligand (FasL) in cancer cells elicits tumor-specific protective immunity, but delayed induction of FasL expression after inoculation facilitates tumor formation
Authors: Hsiao-Ying Chiu;Guang-Huan Sun;Shiow-Yi Chen;Hsiao-Hsien Wang;Ming-Yi Ho;Chia-Yi Chu;Wan-Lin Wu;Ren-Shiang Jhou;Yi-Lin Tsai;Rui-Ting Huang;Kuang-Hui Sun;Shye-Jye Tang
Contributors: 國立臺灣海洋大學:生命科學暨生物科技學系
Date: 2013
Issue Date: 2016-09-01T06:03:17Z
Publisher: Molecular Carcinogenesis
Abstract: Abstract: Overexpression of Fas ligand (FasL) in cancer cells elicits potential antitumor effects via recruitment of neutrophils. Conversely, FasL-expressing tumors may counterattack tumor-infiltrating lymphocytes by delivering apoptotic death signals via Fas/FasL interactions, which may lead to tumor escape. In order to distinguish the role of FasL in antitumor activity and tumor progression, Lewis lung carcinoma cells (LLC-1) were used to establish the cell line LLC-FasL, in which FasL expression was repressed by doxycycline (Dox) treatment and induced in the absence of Dox. LLC-FasL cells promote tumor regression when expressing FasL, whereas tumor outgrowth is observed by depletion of FasL expression. To investigate whether initial expression of FasL during tumor formation is critical for FasL-mediated tumor regression, Dox-treated LLC-FasL cells were inoculated into Dox-treated mice, but Dox treatment was stopped 5 days after inoculation. When low cell numbers were inoculated, we observed 80% survival and no tumor formation, whereas no mice survived inoculation with high cell numbers, despite the delayed induction of FasL by Dox withdrawal. The inoculation of a high density of cells may establish a favorable tumor microenvironment before the expression of FasL. Our findings demonstrate that FasL may elicit antitumor activity when it is initially present on injected cancer cells and thus can act prior to tumor microenvironment formation. Furthermore, a well-established tumor microenvironment abrogates FasL-mediated antitumor activity. © 2012 Wiley Periodicals, Inc.
Relation: 52(9)
URI: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/38431
Appears in Collections:[生命科學系] 期刊論文

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