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[Quinalizarin Induces Apoptosis in Gastric Cancer AGS Cells via MAPK and Akt Signaling Pathway]

[Quinalizarin Induces Apoptosis in Gastric Cancer AGS Cells via MAPK and Akt Signaling Pathway]

Chang Liu, Ying-Hua Luo, Xian-Ji Piao, Yue Wang, Ling-Qi Meng, Hao Wang, Jia-Ru Wang, Yi Zhang, Jin-Qian Li, Cheng-Hao Jin

Nan Fang Yi Ke Da Xue Xue Bao. 2017 Aug 20;37(8):1085-1091.

PMID: 28801290

Abstract:

Objective:
To investigate quinalizarin-induced apoptosis in gastric cancer cells in vitro and explore the molecular mechanisms.
Methods:
MTT assay was used to determine the cytotoxic effects of quinalizarin on human gastric cancer AGS, MKN-28 and MKN-45 cells. Annexin V-FITC/PI staining and flow cytometry were used to assess quinalizarin-induced apoptosis in AGS cells and its effect on intracellular ROS levels; the expression levels of apoptotic proteins in the cells were determined with Western blotting.
Results:
Quinalizarin dose-dependently reduced the cell viabilities of the 3 gastric cancer cells (P<0.05). The IC50 values of quinalizarin in AGS, MKN-28 and MKN-45 cells were 7.07 µmol/L, 22.55 µmol/L and 14.18 µmol/L, respectively. Quinalizarin time-dependently induced apoptosis of AGS cells and potentiated the generation of intracellular reactive oxygen species (ROS) levels. Pretreatment with NAC, a scavenger of ROS, inhibited quinalizarin-induced apoptosis (P<0.001). Western blotting results showed that quinalizarin also up-regulated the expression levels of the apoptotic proteins including p-p38, p-JNK, Bad, cleaved caspase-3, and cleaved PARP-1 (P<0.05), and down-regulated the expression of the anti-apoptotic proteins p-Akt, p-ERK, and Bcl-2 (P<0.05).
Conclusion:
Quinalizarin inhibits the proliferation and induces apoptosis in gastric cancer cells in vitro through regulating intracellular ROS levels via the MAPK and Akt signaling pathways.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP81618	Quinalizarin		81-61-8	Price

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