PMID- 26478515
OWN - NLM
STAT- MEDLINE
DCOM- 20160426
LR  - 20200315
IS  - 1365-2184 (Electronic)
IS  - 0960-7722 (Print)
IS  - 0960-7722 (Linking)
VI  - 48
IP  - 6
DP  - 2015 Dec
TI  - Sam68 regulates cell proliferation and cell adhesion-mediated drug resistance 
      (CAM-DR) via the AKT pathway in non-Hodgkin's lymphoma.
PG  - 682-90
LID - 10.1111/cpr.12220 [doi]
AB  - OBJECTIVES: Sam68 (Src-associated in mitosis 68 kDa), a substrate for tyrosine 
      kinase c-Src during mitosis, is up-regulated in a variety of human cancers and 
      acts oncogenically promoting tumour progression. This study has explored 
      biological function and clinical significance of Sam68 in non-Hodgkin's lymphoma 
      (NHL). MATERIALS AND METHODS: To examine Sam68 expression in NHL, clinically, 
      eight diffuse large B-cell lymphomas and four reactive lymphoid hyperplasia 
      fresh-frozen tissues were obtained for western blot and quantitative real-time 
      PCR analyses. Using immunohistochemical staining, paraffin wax embedded sections 
      from 164 cases of NHL patients were used to evaluate prognostic value of Sam68. 
      Cell Counting Kit-8 (CCK-8) and soft agar colony assays were conducted to 
      investigate the role of Sam68 in cell viability and cell proliferation 
      respectively. Furthermore, effects of Sam68 on cell adhesion-mediated drug 
      resistance (CAM-DR) was determined by CCK-8 assay and flow cytometric analysis. 
      RESULTS: Expression status of Sam68 inversely correlated with clinical outcomes 
      of patients with NHL, and it was also an independent prognostic factor for the 
      outcomes. In addition, Sam68 was associated with proliferation of NHL cells. 
      Knock-down of its gene inhibited cell proliferation and colony formation by 
      delaying cell cycle progression. Furthermore, OCI-Ly8 and Jeko-1 cells adhering 
      to FN and HS-5 expressed higher Sam68 protein, compared to their suspension 
      counterparts. Sam68 promoted cell adhesion-mediated drug resistance (CAM-DR) via 
      the AKT pathway. CONCLUSIONS: Increased Sam68 expression in NHL resulted in poor 
      prognosis, and it promoted CAM-DR in NHL via AKT.
CI  - (c) 2015 John Wiley & Sons Ltd.
FAU - Wu, Yaxun
AU  - Wu Y
AD  - Department of Pathology, Affiliated Cancer Hospital of Nantong University, 
      Nantong, 226361, Jiangsu, China.
FAU - Xu, Xiaohong
AU  - Xu X
AD  - Department of Oncology, Affiliated Cancer Hospital of Nantong University, 
      Nantong, 226361, Jiangsu, China.
FAU - Miao, Xiaobing
AU  - Miao X
AD  - Department of Pathology, Affiliated Cancer Hospital of Nantong University, 
      Nantong, 226361, Jiangsu, China.
FAU - Zhu, Xinghua
AU  - Zhu X
AD  - Department of Pathology, Affiliated Cancer Hospital of Nantong University, 
      Nantong, 226361, Jiangsu, China.
FAU - Yin, Haibing
AU  - Yin H
AD  - Department of Pathology, Affiliated Cancer Hospital of Nantong University, 
      Nantong, 226361, Jiangsu, China.
FAU - He, Yunhua
AU  - He Y
AD  - Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, 
      Nantong University, Nantong, 226001, Jiangsu, China.
FAU - Li, Chunsun
AU  - Li C
AD  - Department of Pathology, Affiliated Cancer Hospital of Nantong University, 
      Nantong, 226361, Jiangsu, China.
FAU - Liu, Yushan
AU  - Liu Y
AD  - Department of Pathology, Affiliated Cancer Hospital of Nantong University, 
      Nantong, 226361, Jiangsu, China.
FAU - Chen, Yali
AU  - Chen Y
AD  - Department of Pathology, Affiliated Cancer Hospital of Nantong University, 
      Nantong, 226361, Jiangsu, China.
FAU - Lu, Xiaoyun
AU  - Lu X
AD  - Department of Pathology, Affiliated Cancer Hospital of Nantong University, 
      Nantong, 226361, Jiangsu, China.
FAU - Wang, Yuchan
AU  - Wang Y
AD  - Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, 
      Nantong University, Nantong, 226001, Jiangsu, China.
FAU - He, Song
AU  - He S
AD  - Department of Pathology, Affiliated Cancer Hospital of Nantong University, 
      Nantong, 226361, Jiangsu, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20151019
PL  - England
TA  - Cell Prolif
JT  - Cell proliferation
JID - 9105195
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (KHDRBS1 protein, human)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA-Binding Proteins)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - Adaptor Proteins, Signal Transducing/*genetics/metabolism
MH  - Apoptosis/genetics
MH  - Biomarkers, Tumor/genetics
MH  - Cell Adhesion/*genetics
MH  - Cell Line, Tumor
MH  - Cell Proliferation/*genetics
MH  - Coculture Techniques
MH  - DNA-Binding Proteins/*genetics/metabolism
MH  - Drug Resistance/*genetics
MH  - Female
MH  - Humans
MH  - Lymphoma, Non-Hodgkin/*genetics/mortality/pathology
MH  - Male
MH  - Middle Aged
MH  - Prognosis
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - RNA, Messenger/biosynthesis
MH  - RNA-Binding Proteins/*genetics/metabolism
PMC - PMC6495998
COIS- There are no potential conflicts of interest to disclose.
EDAT- 2015/10/20 06:00
MHDA- 2016/04/27 06:00
PMCR- 2015/10/19
CRDT- 2015/10/20 06:00
PHST- 2015/07/24 00:00 [received]
PHST- 2015/07/31 00:00 [accepted]
PHST- 2015/10/20 06:00 [entrez]
PHST- 2015/10/20 06:00 [pubmed]
PHST- 2016/04/27 06:00 [medline]
PHST- 2015/10/19 00:00 [pmc-release]
AID - CPR12220 [pii]
AID - 10.1111/cpr.12220 [doi]
PST - ppublish
SO  - Cell Prolif. 2015 Dec;48(6):682-90. doi: 10.1111/cpr.12220. Epub 2015 Oct 19.