PMID- 30358228
OWN - NLM
STAT- MEDLINE
DCOM- 20190919
LR  - 20211204
IS  - 1107-0625 (Print)
IS  - 1107-0625 (Linking)
VI  - 23
IP  - 4
DP  - 2018 Jul-Aug
TI  - Methyl eugenol induces potent anticancer effects in RB355 human retinoblastoma 
      cells by inducing autophagy, cell cycle arrest and inhibition of PI3K/mTOR/Akt 
      signalling pathway.
PG  - 1174-1178
AB  - PURPOSE: Retinoblastoma is one of the lethal malignancies in children. 
      Approximately half of the children that are diagnosed with retinoblastoma die of 
      this disease. Enucleation is commonly used for the treatment of retinoblastoma 
      but this leads to loss of vision. Therefore there is an urgent need to look for 
      viable chemotherapeutic agents for the treatment of retinoblastoma. Consistent 
      with this, natural products can produce efficient anticancer agents and in the 
      present study a plant-derived phenylpropene methyl eugenol (ME) was evaluated 
      against retinoblastoma RB355 cells. METHODS: The cytotoxic activity of this 
      molecule was evaluated by MTT cell viability assay, while autophagic effects were 
      evaluated by flow cytometry using acridine orange (AO)/monodansylcadaverine 
      (AO/MDC) staining dyes. The effects on the cell cycle progression were analyzed 
      by flow cytometry while the effects on mTOR/PI3K/Akt signalling pathway were 
      assessed by western blot method. RESULTS: The results indicated that ME exhibited 
      an IC50 value of 50 muM and exerted its cytotoxic effects in a dosedependent 
      manner in RB355 cells. Moreover, it was observed that the ME lessens the cell 
      viability and triggers G2/M cell cycle arrest. It was also observed that ME 
      induced autophagy dose-dependently in retinoblastoma RB355 cells. Western blot 
      analysis revealed that ME could modulate the mTOR/ PI3K/Akt signalling pathway in 
      RB355 cells at the IC50 concentration. CONCLUSIONS: The above results clearly 
      indicate that ME is a potent anticancer agent and may be developed further as a 
      possible anticancer lead molecule against retinoblastoma provided further in 
      depth in vivo studies are carried out.
FAU - Yin, Li
AU  - Yin L
AD  - Department of Ophthalmology, the First Hospital of Shijiazhung, Shijiazhuang 
      050000, China.
FAU - Sun, Zhaohui
AU  - Sun Z
FAU - Ren, Qian
AU  - Ren Q
FAU - Su, Xian
AU  - Su X
FAU - Zhang, Delong
AU  - Zhang D
LA  - eng
PT  - Journal Article
PL  - Cyprus
TA  - J BUON
JT  - Journal of B.U.ON. : official journal of the Balkan Union of Oncology
JID - 100883428
RN  - 0 (Anticarcinogenic Agents)
RN  - 0 (Phosphoinositide-3 Kinase Inhibitors)
RN  - 29T9VA6R7M (methyleugenol)
RN  - 3T8H1794QW (Eugenol)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Anticarcinogenic Agents/pharmacology/*therapeutic use
MH  - Autophagy/drug effects
MH  - Cell Cycle Checkpoints/drug effects
MH  - Eugenol/*analogs & derivatives/pharmacology
MH  - Flow Cytometry
MH  - Humans
MH  - Microbial Sensitivity Tests
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - *Phosphoinositide-3 Kinase Inhibitors
MH  - Proto-Oncogene Proteins c-akt/*antagonists & inhibitors/metabolism
MH  - Retinoblastoma/*drug therapy/metabolism/pathology
MH  - Signal Transduction/drug effects
MH  - TOR Serine-Threonine Kinases/*antagonists & inhibitors/metabolism
EDAT- 2018/10/26 06:00
MHDA- 2019/09/20 06:00
CRDT- 2018/10/26 06:00
PHST- 2018/10/26 06:00 [entrez]
PHST- 2018/10/26 06:00 [pubmed]
PHST- 2019/09/20 06:00 [medline]
PST - ppublish
SO  - J BUON. 2018 Jul-Aug;23(4):1174-1178.