Bongkun Choi1, Eun-Jin Lee1, Young Soo Park2, Sang-Min Kim1, Eun-Young Kim1, Youngsup Song1, Sang-Wook Kang1, Min-Hee Rhu3, Eun-Ju Chang4. 1. Department of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea Cell Dysfunction Research Center, University of Ulsan College of Medicine, Seoul, Republic of Korea. 2. Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea. 3. Department of Oncology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea. 4. Department of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea Cell Dysfunction Research Center, University of Ulsan College of Medicine, Seoul, Republic of Korea ejchang@amc.seoul.kr.
Abstract
BACKGROUND: Chronic inflammation characterized by the recruitment and activation of macrophages has been implicated in the development of gastric cancer. MATERIALS AND METHODS: Expression of the long form of pentraxin-3 (PTX3) in gastric cancer cells was examined by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. The migratory capacity of gastric cancer cells and chemotaxis of macrophages by PTX3 were assessed by wound-healing and transwell assays. PTX3 silencing using small interfering RNA (siRNA) was performed to confirm PTX3-mediated effects. RESULTS: We demonstrated that PTX3 expression was elevated in human advanced gastric cancer tissues with increased infiltration of CD11b+ macrophages. Tumor necrosis factor-alpha increased PTX3 expression via nuclear factor-kappa B activation in human gastric cancer cells. PTX3 promoted the tumor cell migratory potential, the recruitment of macrophages and their subsequent binding to gastric cancer cells. These effects were suppressed by PTX3 knockdown using siRNA. CONCLUSION: Our findings suggest that gastric cancer-derived PTX3 promotes macrophage recruitment, which may contribute to gastric cancer-related inflammation. Copyright
BACKGROUND:Chronic inflammation characterized by the recruitment and activation of macrophages has been implicated in the development of gastric cancer. MATERIALS AND METHODS: Expression of the long form of pentraxin-3 (PTX3) in gastric cancer cells was examined by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. The migratory capacity of gastric cancer cells and chemotaxis of macrophages by PTX3 were assessed by wound-healing and transwell assays. PTX3 silencing using small interfering RNA (siRNA) was performed to confirm PTX3-mediated effects. RESULTS: We demonstrated that PTX3 expression was elevated in human advanced gastric cancer tissues with increased infiltration of CD11b+ macrophages. Tumor necrosis factor-alpha increased PTX3 expression via nuclear factor-kappa B activation in humangastric cancer cells. PTX3 promoted the tumor cell migratory potential, the recruitment of macrophages and their subsequent binding to gastric cancer cells. These effects were suppressed by PTX3 knockdown using siRNA. CONCLUSION: Our findings suggest that gastric cancer-derived PTX3 promotes macrophage recruitment, which may contribute to gastric cancer-related inflammation. Copyright
Authors: Cecilia Garlanda; Barbara Bottazzi; Elena Magrini; Antonio Inforzato; Alberto Mantovani Journal: Physiol Rev Date: 2018-04-01 Impact factor: 37.312
Authors: S Tartare-Deckert; M Deckert; M Rathore; C Girard; M Ohanna; M Tichet; R Ben Jouira; E Garcia; F Larbret; M Gesson; S Audebert; J-P Lacour; H Montaudié; V Prod'Homme Journal: Oncogene Date: 2019-06-28 Impact factor: 9.867