PMID- 29328424
OWN - NLM
STAT- MEDLINE
DCOM- 20180814
LR  - 20211204
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Linking)
VI  - 17
IP  - 3
DP  - 2018 Mar
TI  - Vitexin induces G2/M‑phase arrest and apoptosis via Akt/mTOR signaling pathway in 
      human glioblastoma cells.
PG  - 4599-4604
LID - 10.3892/mmr.2018.8394 [doi]
AB  - Glioblastoma is a common primary brain tumor with aggressive malignancy, which 
      results in poor outcomes, short survival time and high mortality. Vitexin, an 
      active ingredient from natural products, has been reported to inhibit cell growth 
      and induce cell apoptosis in various cancer cell lines including hepatocellular 
      carcinoma, oral and esophageal cancer. To the best of the authors knowledge, the 
      present study was the first to investigate anticancer effects of vitexin on human 
      glioblastoma cells and potential underlying mechanisms. The present study 
      demonstrated that vitexin inhibited cell viability in a dose‑ and time‑dependent 
      manner. In the present study, vitexin induced G2/M cell cycle arrest, as 
      demonstrated by flow cytometry. Induction of cell apoptosis following vitexin 
      treatment, was further indicated by observation of morphological alterations, 
      flow cytometry analysis and detection of cleaved‑poly (ADP‑ribose) polymerase. 
      The present study also demonstrated that vitexin inhibited RAC‑alpha 
      serine/threonine‑protein kinase (Akt)/mechanistic target of rapamycin kinase 
      (mTOR) signaling in human glioblastoma cells. Collectively, the results of the 
      present study demonstrated that vitexin induced G2/M cell cycle arrest and 
      apoptosis by inhibiting Akt/mTOR signaling in human glioblastoma cells. Vitexin 
      may in the future be used as a therapeutic agent for treatment of malignant 
      glioblastoma.
FAU - Zhang, Guangning
AU  - Zhang G
AD  - Department of Neurosurgery, Affiliated Hospital of Jining Medical University, 
      Jining, Shandong 272000, P.R. China.
FAU - Li, Dongyuan
AU  - Li D
AD  - Department of Neurosurgery, China‑Japan Union Hospital of Jilin University, 
      Changchun, Jilin 130033, P.R. China.
FAU - Chen, Hao
AU  - Chen H
AD  - Department of Neurosurgery, Affiliated Hospital of Jining Medical University, 
      Jining, Shandong 272000, P.R. China.
FAU - Zhang, Junchen
AU  - Zhang J
AD  - Department of Neurosurgery, Affiliated Hospital of Jining Medical University, 
      Jining, Shandong 272000, P.R. China.
FAU - Jin, Xingyi
AU  - Jin X
AD  - Department of Neurosurgery, China‑Japan Union Hospital of Jilin University, 
      Changchun, Jilin 130033, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20180108
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 7V515PI7F6 (Apigenin)
RN  - 9VP70K75OK (vitexin)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Apigenin/*pharmacology
MH  - Apoptosis/*drug effects
MH  - Brain Neoplasms/metabolism/pathology
MH  - Cell Line, Tumor
MH  - Cell Survival/drug effects
MH  - G2 Phase Cell Cycle Checkpoints/*drug effects
MH  - Glioblastoma/metabolism/pathology
MH  - Humans
MH  - M Phase Cell Cycle Checkpoints/drug effects
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Signal Transduction/*drug effects
MH  - TOR Serine-Threonine Kinases/metabolism
OTO - NOTNLM
OT  - vitexin
OT  - G2/M-phase arrest
OT  - apoptosis
OT  - signaling pathway
OT  - glioblastoma
EDAT- 2018/01/13 06:00
MHDA- 2018/08/15 06:00
CRDT- 2018/01/13 06:00
PHST- 2017/07/26 00:00 [received]
PHST- 2017/10/24 00:00 [accepted]
PHST- 2018/01/13 06:00 [pubmed]
PHST- 2018/08/15 06:00 [medline]
PHST- 2018/01/13 06:00 [entrez]
AID - 10.3892/mmr.2018.8394 [doi]
PST - ppublish
SO  - Mol Med Rep. 2018 Mar;17(3):4599-4604. doi: 10.3892/mmr.2018.8394. Epub 2018 Jan 
      8.