PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

Effects of DTX3L on the cell proliferation, adhesion, and drug resistance of multiple myeloma cells.

Abstract Cell adhesion-mediated drug resistance is an important factor that influences the effects of chemotherapy in multiple myeloma. DTX3L, a ubiquitin ligase, plays a key role in cell-cycle-related process. Here, we found that the expression of DTX3L gradually increased during the proliferation of myeloma cells, which resulted in arrest of the cell cycle in the G1 phase and promoted the adherence of myeloma cells to fibronectin or bone marrow stromal cells. In addition, silencing of DTX3L improved sensitivity to chemotherapy drugs in multiple myeloma cell lines adherent to bone marrow stromal cells and increased the expression of caspase-3 and poly-adenosine diphosphate-ribose polymerase, two markers of apoptosis. Finally, we also found that DTX3L expression was regulated by focal adhesion kinase. Taken together, the results of this study show that DTX3L plays an important role in the proliferation and cell adhesion-mediated drug resistance of multiple myeloma cells and as such may play a key role in the development of multiple myeloma.
PMID
Related Publications

EphA4 promotes cell proliferation and cell adhesion-mediated drug resistance via the AKT pathway in multiple myeloma.

Etodolac induces apoptosis and inhibits cell adhesion to bone marrow stromal cells in human myeloma cells.

Proteasomal degradation of topoisomerase I is preceded by c-Jun NH2-terminal kinase activation, Fas up-regulation, and poly(ADP-ribose) polymerase cleavage in SN38-mediated cytotoxicity against multiple myeloma.

Bone marrow stromal-derived soluble factors and direct cell contact contribute to de novo drug resistance of myeloma cells by distinct mechanisms.

RBQ3 participates in multiple myeloma cell proliferation, adhesion and chemoresistance.

Authors

Mayor MeshTerms
Keywords

DTX3L

adhesion

drug resistance

multiple myeloma

proliferation

Journal Title tumour biology : the journal of the international society for oncodevelopmental biology and medicine
Publication Year Start




PMID- 28653881
OWN - NLM
STAT- MEDLINE
DA  - 20170627
DCOM- 20170711
LR  - 20170713
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 6
DP  - 2017 Jun
TI  - Effects of DTX3L on the cell proliferation, adhesion, and drug resistance of
      multiple myeloma cells.
PG  - 1010428317703941
LID - 10.1177/1010428317703941 [doi]
AB  - Cell adhesion-mediated drug resistance is an important factor that influences the
      effects of chemotherapy in multiple myeloma. DTX3L, a ubiquitin ligase, plays a
      key role in cell-cycle-related process. Here, we found that the expression of
      DTX3L gradually increased during the proliferation of myeloma cells, which
      resulted in arrest of the cell cycle in the G1 phase and promoted the adherence
      of myeloma cells to fibronectin or bone marrow stromal cells. In addition,
      silencing of DTX3L improved sensitivity to chemotherapy drugs in multiple myeloma
      cell lines adherent to bone marrow stromal cells and increased the expression of 
      caspase-3 and poly-adenosine diphosphate-ribose polymerase, two markers of
      apoptosis. Finally, we also found that DTX3L expression was regulated by focal
      adhesion kinase. Taken together, the results of this study show that DTX3L plays 
      an important role in the proliferation and cell adhesion-mediated drug resistance
      of multiple myeloma cells and as such may play a key role in the development of
      multiple myeloma.
FAU - Shen, Yaodong
AU  - Shen Y
AD  - 1 Department of Hematology, Affiliated Hospital of Nantong University, Nantong,
      People's Republic of China.
FAU - Sun, Yuxiang
AU  - Sun Y
AD  - 2 Jiangsu Province Key Laboratory of Neuroregeneration, Nantong University,
      Nantong, People's Republic of China.
FAU - Zhang, Linlin
AU  - Zhang L
AD  - 1 Department of Hematology, Affiliated Hospital of Nantong University, Nantong,
      People's Republic of China.
AD  - 2 Jiangsu Province Key Laboratory of Neuroregeneration, Nantong University,
      Nantong, People's Republic of China.
FAU - Liu, Hong
AU  - Liu H
AD  - 1 Department of Hematology, Affiliated Hospital of Nantong University, Nantong,
      People's Republic of China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Tumour Biol
JT  - Tumour biology : the journal of the International Society for Oncodevelopmental
      Biology and Medicine
JID - 8409922
RN  - 0 (Fibronectins)
RN  - EC 2.3.2.27 (DTX3L protein, human)
RN  - EC 2.3.2.27 (Ubiquitin-Protein Ligases)
RN  - EC 2.7.10.2 (Focal Adhesion Protein-Tyrosine Kinases)
RN  - EC 3.4.22.- (Caspase 3)
SB  - IM
MH  - Apoptosis/drug effects
MH  - Bone Marrow Cells/drug effects/pathology
MH  - Caspase 3/genetics
MH  - Cell Adhesion/drug effects
MH  - Cell Cycle/drug effects
MH  - Cell Division/drug effects
MH  - Cell Line, Tumor
MH  - Cell Proliferation/*drug effects
MH  - Drug Resistance, Neoplasm/genetics
MH  - Drug Therapy
MH  - Fibronectins/genetics
MH  - Focal Adhesion Protein-Tyrosine Kinases/*genetics
MH  - Gene Expression Regulation, Neoplastic/drug effects
MH  - Gene Silencing
MH  - Humans
MH  - Multiple Myeloma/*drug therapy/genetics/pathology
MH  - Stromal Cells/drug effects/pathology
MH  - Ubiquitin-Protein Ligases/antagonists & inhibitors/*biosynthesis/genetics
OTO - NOTNLM
OT  - DTX3L
OT  - adhesion
OT  - drug resistance
OT  - multiple myeloma
OT  - proliferation
EDAT- 2017/06/28 06:00
MHDA- 2017/07/14 06:00
CRDT- 2017/06/28 06:00
AID - 10.1177/1010428317703941 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Jun;39(6):1010428317703941. doi: 10.1177/1010428317703941.