Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8453482 | Leukemia Research | 2016 | 9 Pages |
Abstract
Sam68 (Src associated in mitosis, 68Â kDa) belongs to the signalï¼transduction 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.
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Authors
Qi Wang, Yuanye Li, Jingying Cheng, Long Chen, Hua Xu, Qinghua Li, Tianxiang Pang,