title: Granzyme M expressed by tumor cells promotes chemoresistance and EMT in vitro and metastasis in vivo associated with STAT3 activation.
abstract: Granzyme M is a serine protease known to be often expressed by natural killer cells and induce target cells apoptosis in combination with perforin. However, we detected granzyme M expression in murine and human cancer cell lines and human tumor samples in our study. Granzyme M increased chemoresistance, colony-formation, cytokine secretion and invasiveness in vitro. Most importantly, granzyme M facilitated tumor growth and metastasis in vivo. Granzyme M induced the epithelial-mesenchymal transition (EMT) in cancer cells associated with STAT3 activation. Our study revealed the role of granzyme M expressed by tumor in chemoresistance, invasion, metastasis and EMT.
authors: Department of Immunology, Cancer Hospital & Cancer Institute, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, China.
authors: Huiru
authors: H
authors: Wang
authors: Department of Parasitology, Capital Medical University, Beijing, China.
authors: Qing
authors: Q
authors: Sun
authors: Department of Immunology, Cancer Hospital & Cancer Institute, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, China.
authors: Yanhong
authors: Y
authors: Wu
authors: Department of Pathology, Cancer Hospital & Cancer Institute, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, China.
authors: Lin
authors: L
authors: Wang
authors: Department of Immunology, Cancer Hospital & Cancer Institute, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, China.
authors: Chunxia
authors: C
authors: Zhou
authors: Department of Immunology, Cancer Hospital & Cancer Institute, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, China.
authors: Wenbo
authors: W
authors: Ma
authors: Department of Immunology, Cancer Hospital & Cancer Institute, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, China.
authors: Youhui
authors: Y
authors: Zhang
authors: Center of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
authors: Shengdian
authors: S
authors: Wang
authors: Department of Immunology, Cancer Hospital & Cancer Institute, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, China.
authors: Shuren
authors: S
authors: Zhang
mesh_terms: D000818:Animals; D045744:Cell Line, Tumor; D058750:Epithelial-Mesenchymal Transition; D053804:Granzymes / Q000096:biosynthesis / Q000378:metabolism*; D019073:HT29 Cells; D056945:Hep G2 Cells; D006801:Humans; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016688:Mice, Inbred NOD; D016513:Mice, SCID; D009362:Neoplasm Metastasis; D050796:STAT3 Transcription Factor / Q000096:biosynthesis / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; C494087:Stat3 protein, mouse; C509218:GZMM protein, human; D053804:Granzymes; C509219:Gzmm protein, mouse
keywords: cancer; chemoresistance; epithelial-mesenchymal transition; granzyme M; metastasis