PMID- 31424667
OWN - NLM
STAT- MEDLINE
DCOM- 20200317
LR  - 20210908
IS  - 2241-6293 (Electronic)
IS  - 1107-0625 (Linking)
VI  - 24
IP  - 3
DP  - 2019 May-Jun
TI  - In vitro and in vivo human gastric cancer inhibition by Trifolirhizin is 
      facilitated via autophagy, mitochondrial mediated programmed cell death, G2/M 
      phase cell cycle arrest and inhibition of m-TOR/PI3K/AKT signalling pathway.
PG  - 1100-1105
AB  - PURPOSE: To investigate the anticancer effects of Trifolirhizin in SNU-5 human 
      gastric cancer cells along with evaluation of its effects on autophagy, 
      apoptosis, cell cycle phase distribution and m-TOR/PI3K signalling pathway. 
      METHODS: The antiproliferative effect on gastric cancer cells was assessed by MTT 
      assay. Autophagy was detected by electron microscopy and western blot. Apoptotic 
      cell death was revealed by acridine orange (AO)/ethidium bromide (EB) and annexin 
      V/propidium iodide (PI) staining using flow cytometry. Cell cycle analysis was 
      carried out by flow cytometry. Protein expression was determined by 
      immunoblotting. Xenografted mice models were used to evaluate in vivo the 
      anticancer effects of Trifolirhizin. RESULTS: Trifolirhizin could significantly 
      inhibit the proliferation of the gastric cancer cells. The anticancer activity of 
      Trifolirhizin against the gastric cancer cells was found to be due to induction 
      of autophagy and mitochondrial-mediated apoptosis. It was further observed that 
      both apoptosis and autophagy-related protein expressions sere significantly 
      altered. Further, it was found that Trifolirhizin could inhibit the 
      m-TOR/PI3K/AKT signalling pathway. In vivo evaluation in xenografted mice 
      indicated that Trifolirhizin inhibited significantly both tumor weight and tumor 
      volume. CONCLUSIONS: In conclusion, it can be safely stated that Trifolirhizin 
      has the potential to be developed as a potent anticancer agent against gastric 
      carcinoma provided further in depth evaluation of this compound is performed.
FAU - Zhang, Ke
AU  - Zhang K
AD  - Department of General Surgery, Xiangya Hospital Central South University, 
      Changsha, Hunan, China, 410008.
FAU - Liu, Weidong
AU  - Liu W
FAU - Qu, Zhan
AU  - Qu Z
FAU - Liu, Qin
AU  - Liu Q
FAU - Chen, Jie
AU  - Chen J
FAU - Tao, Ran
AU  - Tao R
FAU - Deng, Youming
AU  - Deng Y
FAU - Zhang, Yu
AU  - Zhang Y
LA  - eng
PT  - Journal Article
PT  - Retracted Publication
PL  - Cyprus
TA  - J BUON
JT  - Journal of B.U.ON. : official journal of the Balkan Union of Oncology
JID - 100883428
RN  - 0 (Glucosides)
RN  - 0 (Heterocyclic Compounds, 4 or More Rings)
RN  - 0 (trifolirhizin)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
RIN - J BUON. 2021 Mar-Apr;26(2):639. PMID: 34077023
MH  - Animals
MH  - Apoptosis
MH  - Autophagy
MH  - Disease Models, Animal
MH  - G2 Phase Cell Cycle Checkpoints/*drug effects
MH  - Glucosides/pharmacology/*therapeutic use
MH  - Heterocyclic Compounds, 4 or More Rings/pharmacology/*therapeutic use
MH  - Humans
MH  - M Phase Cell Cycle Checkpoints/*drug effects
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Nude
MH  - Mitochondria
MH  - Phosphatidylinositol 3-Kinases/*metabolism
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - Signal Transduction
MH  - Stomach Neoplasms/*drug therapy
EDAT- 2019/08/20 06:00
MHDA- 2020/03/18 06:00
CRDT- 2019/08/20 06:00
PHST- 2021/04/30 00:00 [retracted]
PHST- 2019/08/20 06:00 [entrez]
PHST- 2019/08/20 06:00 [pubmed]
PHST- 2020/03/18 06:00 [medline]
PST - ppublish
SO  - J BUON. 2019 May-Jun;24(3):1100-1105.