Reduction of intersectin1-s induced apoptosis of human glioblastoma cells.
Malignant gliomas have a high proliferation ability and high tendency to invade diffusely into surrounding healthy brain tissues, thereby precluding their successful surgical removal. Intersectin1 (also called ITSN1) as a molecular linker in the central nervous system is well known as an important regulator of endocytosis and exocytosis. ITSN1 has two isoforms: ITSN1-l and ITSN1-s. In this study, we show that siRNA-mediated down regulation of ITSN1-s induced glioma cells apoptosis. In addition, we demonstrate the possible mechanisms by which ITSN1-s functions in glioma cells apoptosis. Our data demonstrate that several key proteins, including FAK, Akt, Bcl-2, BAD which are critical for cells apoptosis were probably involved in ITSN1-s signaling pathways. Our results indicate that ITSN1-s is an effecter in regulation of gliomas cells apoptosis, and identify that ITSN1-s may be a new potentially anti-apoptosis target for therapeutic of gliomas.
Ma
Yongjie
Y
Central Laboratory of Oncology Department, Tianjin Medical University Cancer Institute and Hospital, Key Laboratory of Breast Cancer Prevention and Therapy of the Ministry of Education; Key Laboratory of Cancer Prevention and Therapy of Tianjin, China.
Wang
Bingbing
B
Central Laboratory of Oncology Department, Tianjin Medical University Cancer Institute and Hospital, Key Laboratory of Breast Cancer Prevention and Therapy of the Ministry of Education; Key Laboratory of Cancer Prevention and Therapy of Tianjin, China.
Li
Wenliang
W
Department of Neurosurgery, Tianjin Medical University Cancer Institute and Hospital, Key Laboratory of Breast Cancer Prevention and Therapy of the Ministry of Education; Key Laboratory of Cancer Prevention and Therapy of Tianjin, China.
Ying
Guoguang
G
Central Laboratory of Oncology Department, Tianjin Medical University Cancer Institute and Hospital, Key Laboratory of Breast Cancer Prevention and Therapy of the Ministry of Education; Key Laboratory of Cancer Prevention and Therapy of Tianjin, China.
Fu
Li
L
Department of Breast Pathology, Tianjin Medical University Cancer Institute and Hospital, Key Laboratory of Breast Cancer Prevention and Therapy of the Ministry of Education; Key Laboratory of Cancer Prevention and Therapy of Tianjin, China.
Niu
Ruifang
R
Department of Public Laboratory, Tianjin Medical University Cancer Institute and Hospital, Key Laboratory of Breast Cancer Prevention and Therapy of the Ministry of Education; Key Laboratory of Cancer Prevention and Therapy of Tianjin, China.
Gu
Feng
F
Department of Breast Pathology, Tianjin Medical University Cancer Institute and Hospital, Key Laboratory of Breast Cancer Prevention and Therapy of the Ministry of Education; Key Laboratory of Cancer Prevention and Therapy of Tianjin, China. Electronic address: fenggumayo@yahoo.com.cn.
D033942:Adaptor Proteins, Vesicular Transport / Q000235:genetics / Q000502:physiology*; D000818:Animals; D017209:Apoptosis / Q000235:genetics / Q000502:physiology*; D001932:Brain Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D045744:Cell Line, Tumor; D015536:Down-Regulation / Q000235:genetics / Q000502:physiology*; D005909:Glioblastoma / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D008297:Male; D051379:Mice; D008819:Mice, Nude; D034741:RNA, Small Interfering / Q000235:genetics; D023041:Xenograft Model Antitumor Assays / Q000379:methods
D033942:Adaptor Proteins, Vesicular Transport; C485568:ITSN1 protein, human; D034741:RNA, Small Interfering