PMID- 33577050
OWN - NLM
STAT- MEDLINE
DCOM- 20210630
LR  - 20210630
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 25
IP  - 2
DP  - 2021 Jan
TI  - Dexmedetomidine represses proliferation and promotes apoptosis of esophageal 
      cancer cells by regulating C-Myc gene expression via the ERK signaling pathway.
PG  - 950-956
LID - 24664 [pii]
LID - 10.26355/eurrev_202101_24664 [doi]
AB  - OBJECTIVE: The aim of this study was to investigate the effects of 
      dexmedetomidine (DEX) on proliferation and apoptosis of esophageal cancer (EC) 
      cells, and to explore the possible underlying mechanism. MATERIALS AND METHODS: 
      EC cells (Eca109) were randomly divided into two groups, namely, Control group 
      and DEX group. The viability, proliferation, and apoptosis of Eca109 cells were 
      detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) 
      assay, 5-Ethynyl-2'-deoxyuridine (EdU) staining and terminal deoxynucleotidyl 
      transferase-mediated dUTP nick end labeling (TUNEL) staining, respectively. 
      Meanwhile, the messenger ribonucleic acid (mRNA) and protein expression levels of 
      extracellular signal-regulated kinase (ERK) 1/2 and c-Myc in Eca109 cells were 
      measured by quantitative Reverse Transcription-Polymerase Chain Reaction 
      (qRT-PCR) and Western blotting, respectively. RESULTS: The viability of Eca109 
      cells was remarkably weakened in DEX group when compared with Control group 
      (p<0.05). DEX could significantly inhibit the proliferation and promote the 
      apoptosis of Eca109 cells (p<0.05). Moreover, the mRNA and protein levels of 
      ERK1/2 and c-Myc in Eca109 cells declined notably (p<0.05). CONCLUSIONS: DEX 
      represses the proliferation and facilitates the apoptosis of Eca109 cells 
      prominently. The possible underlying mechanism may be associated with the 
      inhibition of c-Myc gene expression through the ERK signaling pathway.
FAU - Hu, Y
AU  - Hu Y
AD  - Department of Anesthesiology, The First Affiliated Hospital of Wenzhou Medical 
      University, Wenzhou, China. 158026072@qq.com.
FAU - Qiu, L-L
AU  - Qiu LL
FAU - Zhao, Z-F
AU  - Zhao ZF
FAU - Long, Y-X
AU  - Long YX
FAU - Yang, T
AU  - Yang T
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Proto-Oncogene Proteins c-myc)
RN  - 67VB76HONO (Dexmedetomidine)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
SB  - IM
MH  - Antineoplastic Agents/*pharmacology
MH  - Apoptosis/*drug effects
MH  - Cell Proliferation/drug effects
MH  - Dexmedetomidine/*pharmacology
MH  - Dose-Response Relationship, Drug
MH  - Drug Screening Assays, Antitumor
MH  - Esophageal Neoplasms/*drug therapy/metabolism/pathology
MH  - Extracellular Signal-Regulated MAP Kinases/*metabolism
MH  - Humans
MH  - Proto-Oncogene Proteins c-myc/genetics/*metabolism
MH  - Signal Transduction/drug effects
MH  - Tumor Cells, Cultured
EDAT- 2021/02/13 06:00
MHDA- 2021/07/01 06:00
CRDT- 2021/02/12 12:13
PHST- 2021/02/12 12:13 [entrez]
PHST- 2021/02/13 06:00 [pubmed]
PHST- 2021/07/01 06:00 [medline]
AID - 24664 [pii]
AID - 10.26355/eurrev_202101_24664 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2021 Jan;25(2):950-956. doi: 
      10.26355/eurrev_202101_24664.