Haruka Kuriyama1, Satoshi Fukushima2, Toshihiro Kimura1, Etsuko Okada1, Takayuki Ishibashi1, Satoru Mizuhashi1, Hisashi Kanemaru1, Ikko Kajihara1, Katsunari Makino1, Azusa Miyashita1, Jun Aoi1, Seiji Okada3, Hironobu Ihn1, Kanako Kita4. 1. Department of Dermatology and Plastic Surgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan. 2. Department of Dermatology and Plastic Surgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan. Electronic address: s_fukushima@kumamoto-u.ac.jp. 3. Division of Hematopoiesis, Center for AIDS Research, Kumamoto University, Kumamoto, Japan. 4. Department of Comprehensive Molecular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan. Electronic address: kitakana@kumamoto-u.ac.jp.
Abstract
BACKGROUND: A previous study revealed that matrin-3 is an essential component in maintaining fibroblast growth factor 2 (FGF2)-mediated undifferentiation of neural stem cells (NSCs) using a proteomics approach. Malignant melanoma (MM) arises from melanocytes that originate from neural crest stem cells during development. Additionally, it has been reported that the expression of FGF2 is positively correlated with the progression of MM. OBJECTIVE: We expected that matrin-3, as a downstream component of FGF2, might be associated with the aggressiveness or differentiation of MM. METHODS: Matrin-3 expression was measured in human melanoma patient tissues and human MM cell lines. We analyzed the effect of matrin-3 siRNA on the proliferation of human MM cell lines and focused on cell cycle progression and apoptosis. We carried out in vivo xenograft tumor experiments by implanting A375 cells transfected with matrin-3 shRNA. RESULTS: Matrin-3 was highly expressed in MM, and matrin-3 knockdown inhibited the proliferation of melanoma cellsin vivo and in vitro. Furthermore, we found that matrin-3 knockdown led to an accumulation of cells in the G1 phase and an increase in apoptotic cell number. CONCLUSION: Our results suggest that matrin-3 could be a new therapeutic target for the treatment of MM.
BACKGROUND: A previous study revealed that matrin-3 is an essential component in maintaining fibroblast growth factor 2 (FGF2)-mediated undifferentiation of neural stem cells (NSCs) using a proteomics approach. Malignant melanoma (MM) arises from melanocytes that originate from neural crest stem cells during development. Additionally, it has been reported that the expression of FGF2 is positively correlated with the progression of MM. OBJECTIVE: We expected that matrin-3, as a downstream component of FGF2, might be associated with the aggressiveness or differentiation of MM. METHODS:Matrin-3 expression was measured in humanmelanomapatient tissues and human MM cell lines. We analyzed the effect of matrin-3 siRNA on the proliferation of human MM cell lines and focused on cell cycle progression and apoptosis. We carried out in vivo xenograft tumor experiments by implanting A375 cells transfected with matrin-3 shRNA. RESULTS:Matrin-3 was highly expressed in MM, and matrin-3 knockdown inhibited the proliferation of melanoma cellsin vivo and in vitro. Furthermore, we found that matrin-3 knockdown led to an accumulation of cells in the G1 phase and an increase in apoptotic cell number. CONCLUSION: Our results suggest that matrin-3 could be a new therapeutic target for the treatment of MM.
Authors: Edward P Retzbach; Stephanie A Sheehan; Harini Krishnan; Haiyan Zheng; Caifeng Zhao; Gary S Goldberg Journal: Mol Carcinog Date: 2022-04-26 Impact factor: 5.139