Sam68 affects cell proliferation and apoptosis of human adult T-acute lymphoblastic leukemia cells via AKT/mTOR signal pathway.
Sam68 (Src associated in mitosis, 68kDa) belongs to the signal，transduction and activation of RNA (STAR) family and its function has been linked to the onset and progression of many tumors. However, the role of Sam68 in T-acute lymphoblastic leukemia (T-ALL) remains unclear. This present study aimed to investigate whether and how Sam68 involved in T-ALL. Our results showed high expression of Sam68 in adult T-ALL cases, Jurkat and CCRF-CEM cell lines. Knockdown of Sam68 repressed cell proliferation, increased apoptosis, induced S arrest along with upregulation of p21, Bad, cleaved caspase-9, caspase-3, PARP and downregulation of CDK2 and Bcl-xl. Furthermore, the data indicated that the expression change of Sam68 went with the changes of AKT/mTOR signaling pathway in T-ALL cell lines. Our findings demonstrated that Sam68 possibly participated in the progresses of T-ALL at least partially via AKT/mTOR signaling pathway.
State Key Laboratory of Experimental Hematology, Institute of Hematology and Hospital of Blood Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing Road 288, Tianjin 300020, China.
Qi
Q
Wang
State Key Laboratory of Experimental Hematology, Institute of Hematology and Hospital of Blood Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing Road 288, Tianjin 300020, China.
Yuanye
Y
Li
State Key Laboratory of Experimental Hematology, Institute of Hematology and Hospital of Blood Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing Road 288, Tianjin 300020, China.
Jingying
J
Cheng
State Key Laboratory of Experimental Hematology, Institute of Hematology and Hospital of Blood Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing Road 288, Tianjin 300020, China.
Long
L
Chen
State Key Laboratory of Experimental Hematology, Institute of Hematology and Hospital of Blood Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing Road 288, Tianjin 300020, China.
Hua
H
Xu
State Key Laboratory of Experimental Hematology, Institute of Hematology and Hospital of Blood Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing Road 288, Tianjin 300020, China.
Qinghua
Q
Li
State Key Laboratory of Experimental Hematology, Institute of Hematology and Hospital of Blood Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing Road 288, Tianjin 300020, China. Electronic address: pang@ihcams.ac.cn.
Tianxiang
T
Pang
D048868:Adaptor Proteins, Signal Transducing / Q000235:genetics / Q000502:physiology*; D000328:Adult; D017209:Apoptosis; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D004268:DNA-Binding Proteins / Q000235:genetics / Q000502:physiology*; D005260:Female; D015973:Gene Expression Regulation, Leukemic; D055785:Gene Knockdown Techniques; D006801:Humans; D008297:Male; D008875:Middle Aged; D054218:Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / Q000473:pathology*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D016601:RNA-Binding Proteins / Q000235:genetics / Q000502:physiology*; D015398:Signal Transduction; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism; D014407:Tumor Cells, Cultured
D048868:Adaptor Proteins, Signal Transducing; D004268:DNA-Binding Proteins; C489559:KHDRBS1 protein, human; D016601:RNA-Binding Proteins; C546842:MTOR protein, human; D051057:Proto-Oncogene Proteins c-akt; D058570:TOR Serine-Threonine Kinases
AKT/mTOR signaling pathway; Apoptosis; Proliferation; Sam68; T-cell acute lymphoblastic leukemia