PMID- 34018348
OWN - NLM
STAT- MEDLINE
DCOM- 20210706
LR  - 20210805
IS  - 1899-5276 (Print)
IS  - 1899-5276 (Linking)
VI  - 30
IP  - 6
DP  - 2021 Jun
TI  - Ginsenoside Rg1 induces senescence of leukemic stem cells by upregulating 
      p16INK4a and downregulating hTERT expression.
PG  - 599-605
LID - 10.17219/acem/133485 [doi]
AB  - BACKGROUND: Leukemic stem cells (LSCs) play an important role in the pathogenesis 
      of leukemia. This research attempted to clarify effects of the telomere system on 
      ginsenoside Rg1-induced senescence of LSCs. OBJECTIVES: This research attempted 
      to clarify effects of the telomere system on ginsenoside Rg1-induced senescence 
      of LSCs. MATERIAL AND METHODS: CD34+CD38- LSCs were isolated, sorted, and divided 
      into a control group and a Rg1 group (treated with 40 mumol/L Rg1). Cell Counting 
      Kit-8 (CCK-8) was used to evaluate cell proliferation, and flow cytometry was 
      used to assess the cell cycle of CD34+CD38- LSCs. The senescence-associated 
      beta-galactosidase (SA-beta-Gal) staining and CFU-Mix assay were conducted to measure 
      senescence of CD34+CD38- LSCs. The mRNA transcription and protein expression of 
      p16INK4a and human telomerase reverse transcriptase (hTERT) were determined using 
      a real-time polymerase chain reaction (RT-PCR) and western blot assay, 
      respectively. RESULTS: The Rg1 treatment significantly attenuated proliferative 
      activity and decreased the proliferative index (PI) of CD34+CD38- LSCs compared 
      to those of the control group (p < 0.05). It remarkably increased positive 
      SA-beta-Gal staining rate, and suppressed formation of the CFU-Mix of CD34+CD38- 
      LSCs compared with those of the control group (p < 0.05). The Rg1 treatment 
      markedly boosted telomere effector, p16INK4a, in CD34+CD38- LSCs compared with 
      that of control group (p < 0.05). Such treatment obviously reduced telomere 
      regulator, hTERT, in CD34+CD38- LSCs compared with the control group (p < 0.05). 
      CONCLUSIONS: Ginsenoside Rg1-induced senescence of CD34+CD38- LSCs through 
      upregulating p16INK4a and downregulating hTERT expression, both of which are 
      associated with telomere systems. The present study would be beneficial for the 
      treatment of leukemia by providing a promising strategy to induce senescence of 
      CD34+CD38- LSCs.
FAU - Tang, Yan-Long
AU  - Tang YL
AD  - Department of Radiology, Affiliated Hospital of Dali University, China.
FAU - Wang, Xiao-Bo
AU  - Wang XB
AD  - Department of Histology and Embryology, Dali University, China.
FAU - Zhou, Yue
AU  - Zhou Y
AD  - Department of Histology and Embryology, Dali University, China.
FAU - Wang, Ya-Ping
AU  - Wang YP
AD  - Department of Histology and Embryology, Chongqing Medical University, China.
FAU - Ding, Ji-Chao
AU  - Ding JC
AD  - Department of Histology and Embryology, Dali University, China.
LA  - eng
PT  - Journal Article
PL  - Poland
TA  - Adv Clin Exp Med
JT  - Advances in clinical and experimental medicine : official organ Wroclaw Medical 
      University
JID - 101138582
RN  - 0 (Ginsenosides)
RN  - PJ788634QY (ginsenoside Rg1)
SB  - IM
MH  - Cell Cycle
MH  - *Cellular Senescence
MH  - *Ginsenosides
MH  - Humans
MH  - Stem Cells
OTO - NOTNLM
OT  - ginsenoside Rg1
OT  - leukemic stem cells
OT  - senescence
OT  - telomere
EDAT- 2021/05/22 06:00
MHDA- 2021/07/07 06:00
CRDT- 2021/05/21 06:56
PHST- 2021/05/22 06:00 [pubmed]
PHST- 2021/07/07 06:00 [medline]
PHST- 2021/05/21 06:56 [entrez]
AID - 10.17219/acem/133485 [doi]
PST - ppublish
SO  - Adv Clin Exp Med. 2021 Jun;30(6):599-605. doi: 10.17219/acem/133485.