PMID- 30066879
OWN - NLM
STAT- MEDLINE
DCOM- 20181108
LR  - 20211204
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Linking)
VI  - 18
IP  - 3
DP  - 2018 Sep
TI  - Isoliquiritigenin inhibits proliferation and metastasis of MKN28 gastric cancer 
      cells by suppressing the PI3K/AKT/mTOR signaling pathway.
PG  - 3429-3436
LID - 10.3892/mmr.2018.9318 [doi]
AB  - Isoliquiritigenin (ISL) is a  fl avonoid extracted from licorice root, which is 
      known to serve important antitumor roles in numerous types of cancers; however, 
      its effect on gastric cancer remains to be elucidated. The present study aimed to 
      explore the roles and underlying mechanisms of ISL in MKN28 gastric cancer cells. 
      MKN28 cell proliferation was measured using the Cell Counting Kit‑8 (CCK8) assay. 
      A Transwell assay was used to determine the effects of ISL on the migration and 
      invasion of MKN28 cells. Apoptosis was assessed by flow cytometry, and the 
      expression levels of apoptosis‑, autophagy‑ and signaling pathway‑related 
      proteins were detected by western blot analysis. The results of the CCK8 assay 
      demonstrated that ISL significantly inhibited the proliferation of MKN28 cells 
      (P<0.05). Transwell assays demonstrated that the migration and invasion of MKN28 
      cells were significantly inhibited following treatment with ISL (P<0.05). Flow 
      cytometric analysis indicated that ISL induced apoptosis of MKN28 cells. In 
      addition, western blot analysis revealed that the ratio of microtubule‑associated 
      proteins 1A/1B light chain 3B (LC3)II/LC3I was upregulated, as was Beclin 1 
      expression; however, p62 was downregulated following ISL pretreatment, thus 
      suggesting that ISL triggered autophagy in MKN28 cells. In addition, the 
      phosphorylation levels of protein kinase B (AKT) and mammalian target of 
      rapamycin (mTOR) were significantly reduced following ISL treatment. These 
      results indicated that ISL may influence apoptosis and autophagy in MKN28 cells 
      by suppressing the phosphoinositide 3‑kinase/AKT/mTOR signaling pathway. In 
      conclusion, the findings of the present study suggested that ISL may inhibit 
      MKN28 cell proliferation, migration and invasion by inducing apoptosis and 
      autophagy, implying potential as a therapeutic agent for gastric cancer.
FAU - Zhang, Xiu-Rong
AU  - Zhang XR
AD  - Department of Traditional Chinese Medicine, Maternal and Child Health Care of 
      Shandong Province, Jinan, Shandong 250014, P.R. China.
FAU - Wang, Shi-Yao
AU  - Wang SY
AD  - Department of Chinese Medicine, The Second Clinical Medical College of Guangzhou 
      University of Traditional Chinese Medicine, Guangzhou, Guangdong 510000, P.R. 
      China.
FAU - Sun, Wen
AU  - Sun W
AD  - Department of Research, Beijing Splinger Medical Research Institute, Jinan, 
      Shandong 250021, P.R. China.
FAU - Wei, Chao
AU  - Wei C
AD  - Department of Ophthalmology, The Second Hospital of Shandong University, Jinan, 
      Shandong 250033, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20180725
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (Antineoplastic Agents, Phytogenic)
RN  - 0 (Chalcones)
RN  - B9CTI9GB8F (isoliquiritigenin)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Animals
MH  - Antineoplastic Agents, Phytogenic/*pharmacology
MH  - Apoptosis/drug effects
MH  - Autophagy/drug effects
MH  - Cell Line, Tumor
MH  - Cell Movement/drug effects
MH  - Cell Proliferation/drug effects
MH  - Chalcones/*pharmacology
MH  - Humans
MH  - Mice
MH  - Phosphatidylinositol 3-Kinases/*metabolism
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - Signal Transduction/*drug effects
MH  - Stomach Neoplasms/metabolism/pathology
MH  - TOR Serine-Threonine Kinases/*metabolism
EDAT- 2018/08/02 06:00
MHDA- 2018/11/09 06:00
CRDT- 2018/08/02 06:00
PHST- 2017/11/03 00:00 [received]
PHST- 2018/06/19 00:00 [accepted]
PHST- 2018/08/02 06:00 [pubmed]
PHST- 2018/11/09 06:00 [medline]
PHST- 2018/08/02 06:00 [entrez]
AID - 10.3892/mmr.2018.9318 [doi]
PST - ppublish
SO  - Mol Med Rep. 2018 Sep;18(3):3429-3436. doi: 10.3892/mmr.2018.9318. Epub 2018 Jul 
      25.