Isoliquiritigenin inhibits proliferation and metastasis of MKN28 gastric cancer cells by suppressing the PI3K/AKT/mTOR signaling pathway
Authors: Shi-Yao Wang
Xiu-Rong Zhang
Wen Sun
Chao Wei
Journal: Molecular Medicine Reports (2018)
Discipline: CLINICAL MEDICINE
Keywords: Isoliquiritigenin; gastric cancer; apoptosis; autophagy; proliferation
Affiliations: Department of Traditional Chinese Medicine, Maternal and Child Health Care of Shandong Province, Jinan, Shandong 250014, P.R. China, Department of Chinese Medicine, The Second Clinical Medical College of Guangzhou University of Traditional Chinese Medicine, Guangzhou, Guangdong 510000, P.R. China, Department of Research, Beijing Splinger Medical Research Institute, Jinan, Shandong 250021, P.R. China, Department of Ophthalmology, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China

Abstract:  Isoliquiritigenin (ISL) is a ﬂavonoid 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&lt;0.05). Transwell assays demonstrated that the migration and invasion of MKN28 cells were significantly inhibited following treatment with ISL (P&lt;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. 

Retracted: No

PubPeer comments:
 *[right]* Figure 4A from [Zhang et al (2018)] .  ISL triggers autophagy in MKN28 cells. (A) LC3II, LC3I, Beclin 1 and p62 protein expression levels were determined by western blotting. *[left]* Fig 6A from [Liu et al (2018)] .  Prucalopride promotes autophagy of ovarian cancer cell SKOV3. (A) Expression levels of LC3-II, Beclin1, and p62 were measured in the SKOV3 cells treated with prucalopride using Western blot analysis . ![file] A band seems to recur between papers. ,