PMID- 30180469
OWN - NLM
STAT- MEDLINE
DCOM- 20190219
LR  - 20201209
IS  - 0253-2727 (Print)
IS  - 2707-9740 (Electronic)
IS  - 0253-2727 (Linking)
VI  - 39
IP  - 8
DP  - 2018 Aug 14
TI  - [MicroRNA-138 regulates cell adhesion-mediated drug resistance phenotype by 
      targeting SGTA in non-Hodgkin's lymphoma].
PG  - 668-673
LID - 10.3760/cma.j.issn.0253-2727.2018.08.011 [doi]
AB  - Objective: To analyze the effects of miR-138 on the expression of small 
      glutamine-rich TPR-containing protein A (SGTA) and cell adhesion-mediated drug 
      resistance (CAM-DR) phenotype in non-Hodgkin's lymphoma (NHL). Methods: The 
      adhesion model was constructed using fibronectin (FN) or bone marrow stromal 
      cells HS-5. The effect of miR-138 on the expression of SGTA was analyzed by 
      Western blotting and RQ-PCR. Dual-luciferase assays were performed to probe the 
      effects of miR-138 on SGTA 3' UTR activities. Subsequently, we investigated the 
      effect of miR-138 on cell cycle, adhesion ability and CAM-DR. Moreover, the 
      correlation between miR-138 expression and therapeutic response was analyzed in 
      35 paraffin-embedded diffuse large B cell lymphoma samples. Results: Our data 
      showed that adhesion of NHL cells to FN or HS-5 cells significantly increased 
      miR-138 expression (P<0.05). Knockdown of miR-138 markedly increased the protein 
      (all P<0.05) but not for mRNA (all P>0.05) levels of SGTA in NHL cell. The 
      luciferase activity of SGTA 3' UTR was significantly suppressed by miR-138 
      transfected cells (0.73+/-0.03 vs 1.00+/-0.02, t=0.914, P=0.002). No change in terms 
      of reporter activity was observed in SGTA 3'UTR mutant transfected cells 
      (0.93+/-0.04 vs 1.00+/-0.02, t=1.375, P=0.241). Also we found that ectopic expression 
      of miR-138 significantly induced cell cycle arrest at G(1) phase in both 
      suspension and adherent cells (all P<0.05). Knockdown of miR-138 had no effect on 
      cell adhesion ability (all P>0.05). More importantly, in suspension cells, 
      knockdown of miR-138 significantly decreased the percentage of 
      doxorubicin-induced cell death. However, knockdown of miR-138 dramatically 
      increased the percentage of doxorubicin-induced cell death in FN/HS-5-adherent 
      cells. Furthermore, the miR-138 expression was significantly higher in patients 
      with progression of disease/stable disease than those experiencing complete 
      response/partial response (9.72+/-1.11 vs 3.06+/-0.22, t=9.144, P<0.001). Conclusion: 
      MiR-138 promoted CAM-DR phenotype through cell adhesion-mediated SGTA 
      down-regulation and cell cycle arrest.
FAU - Wu, Y X
AU  - Wu YX
FAU - He, S
AU  - He S
FAU - Xu, X H
AU  - Xu XH
AD  - Department of Oncology, Nantong Cancer Hospital, Nantong 226361, China.
LA  - chi
GR  - 81670196/National Natural Science Foundation of China/
GR  - HS2014076, HS2015003/Nantong Science and Technology Project/
PT  - Journal Article
PL  - China
TA  - Zhonghua Xue Ye Xue Za Zhi
JT  - Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
JID - 8212398
RN  - 0 (Carrier Proteins)
RN  - 0 (MIRN138 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (Molecular Chaperones)
RN  - 0 (SGTA protein, human)
SB  - IM
MH  - Carrier Proteins
MH  - *Cell Adhesion
MH  - Cell Line, Tumor
MH  - Cell Proliferation
MH  - Drug Resistance, Neoplasm
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - *Lymphoma, Non-Hodgkin
MH  - MicroRNAs
MH  - Molecular Chaperones
MH  - Phenotype
PMC - PMC7342837
OTO - NOTNLM
OT  - Cell adhesion-mediated drug resistance
OT  - Micro RNAs
OT  - Non-Hodgkin's lymphoma
OT  - SGTA
EDAT- 2018/09/06 06:00
MHDA- 2019/03/21 06:00
PMCR- 2018/08/01
CRDT- 2018/09/06 06:00
PHST- 2018/09/06 06:00 [entrez]
PHST- 2018/09/06 06:00 [pubmed]
PHST- 2019/03/21 06:00 [medline]
PHST- 2018/08/01 00:00 [pmc-release]
AID - cjh-39-08-668 [pii]
AID - 10.3760/cma.j.issn.0253-2727.2018.08.011 [doi]
PST - ppublish
SO  - Zhonghua Xue Ye Xue Za Zhi. 2018 Aug 14;39(8):668-673. doi: 
      10.3760/cma.j.issn.0253-2727.2018.08.011.