scholarly journals Antitumor Effects of Paeoniflorin on Hippo Signaling Pathway in Gastric Cancer Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Kai Niu ◽  
Yanling Liu ◽  
Zijun Zhou ◽  
Xuefeng Wu ◽  
Huaiwu Wang ◽  
...  

Background. Paeoniflorin has been reported to exert antitumor effects on human cancers. However, the role of paeoniflorin in gastric cancer and the underlying molecular mechanism are unelucidated. Therefore, we determined whether paeoniflorin could exhibit anticancer activity in gastric cancer cells. Methods. MTT was used to measure the viability of cells after paeoniflorin treatment. FACS was performed to examine cell apoptosis. Wound healing and transwell invasion assays were conducted to examine cell migratory and invasive activities. Western blotting was used to explore the mechanism by which paeoniflorin exerted tumor suppressive effects. Results. We found that paeoniflorin suppressed cell growth, enhanced apoptosis, and reduced cell invasion. Notably, we showed that paeoniflorin inhibited the expression of TAZ in gastric cancer cells. The overexpression of TAZ abrogated the antitumor activity of paeoniflorin in gastric cancer cells. In contrast, the downregulation of TAZ promoted the tumor suppressive effects of paeoniflorin treatment. Conclusion. Hence, targeting TAZ with paeoniflorin could be a novel approach for the treatment of human gastric cancer.

2015 ◽  
Author(s):  
Tetsushi Kubota ◽  
Shinji Kuroda ◽  
Katsuyuki Aoyama ◽  
Hiroshi Tazawa ◽  
Shunsuke Kagawa ◽  
...  

2021 ◽  
Author(s):  
Hou Binfen ◽  
Li Zhao ◽  
Min Deng

Abstract AimGastric cancer is one of the most common malignant tumors.Chrysophanol has been reported to have antitumor effects on a variety of cancers, but the role of chrysophanol in gastric cancer remains unclear. The aim of this study was to investigate the effects of chrysophanol on proliferation, pyroptosis, migration and invasion of gastric cancer cells.MethodsMKN 28 and AGS cells were treatde with different concentrations of chrysophanol, then cell proliferation, migration,invasion and pyroptosis were decteed by CCK-8, Colony-forming assay, Wound Healing assay, Transwell and flow cytometry, respectively.Subsequently, NLRP3 siRNA was transfected into MKN 28 cells, cell proliferation pyroptosis, migration and invasion were reassessed in these transfected cells. The expression of caspase-1 and IL-1β in the downstream of NLRP3 was detected by qRT PCR and Western blot.ResultsChrysophanol significantly inhibited the proliferation of GC cells, promoted pyroptosis, inhibited cell migration and invasion, and up-regulated the expression level of NLRP3 inflammasome in GC cells. Silencing NLRP3 inhibited the effects of chrysophanol on proliferation, pyroptosis, migration and invasion of MKN 28 cells. Chrysophanol plays an anti-cancer role through high expression of NLRP3.CoclusionsChrysophanol can inhibit the proliferation, migration and invasion of gastric cancer cells by regulating NLRP3, promote the death of gastric cancer cells, and play an anti-tumor role,which is a clinical strategy with great potential for the treatment of gastric cancer.


2019 ◽  
Author(s):  
Liang-Yu Bie ◽  
Dan Li ◽  
Yan Wei ◽  
Ning Li ◽  
Xiao-Bing Chen ◽  
...  

Abstract PAX8 is identified as a regulator in the pathogenesis of human tumors and an indicator of the prognosis for patients. However, the role of PAX8 on proliferation in gastric cancer have not been studied. This study was aimed to explore the expression pattern of PAX8 in gastric cancer, and investigate the effect of PAX8 on the proliferation of gastric cancer cells. PAX8 and SOX13 were identified to be synchronously upregulated in primary gastric cancer in human gastric cancer tissues and the gastric cancer datasets of TCGA, and gastric cancer patients of combined high PAX8 and SOX13 expression showed poor prognosis. Furthermore, SOX13 can mediate PAX8 and its targeted genes, Aurora B and Cyclin B1, expression in AGS and MGC803 cell lines. Flow cytometry and EdU incorporation assays showed that silencing PAX8 can block the cell cycle of gastric cancer cell in G1 phase and SOX13 expression can rescue the arrested proliferative process induced by PAX8 silenced in CCK8 and colony formation assays. Thus, combined SOX13 and PAX8 expression regulate the proliferation of gastric cancer cells, and both SOX13 and PAX8 play an oncogene function in gastric cancer.


2018 ◽  
Vol 9 (23) ◽  
pp. 4527-4535 ◽  
Author(s):  
Yan Liu ◽  
Lei Qin ◽  
Tingting Bi ◽  
Wei Dai ◽  
Wei Liu ◽  
...  

2001 ◽  
Author(s):  
Takashi Oshima ◽  
Toshio Imada ◽  
Yoji Nagashima ◽  
Haruhiko Cho ◽  
Manabu Shiozawa ◽  
...  

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1596 ◽  
Author(s):  
Ho Jeong Lee ◽  
Venu Venkatarame Gowda Saralamma ◽  
Seong Min Kim ◽  
Sang Eun Ha ◽  
Preethi Vetrivel ◽  
...  

Pectolinarigenin (PEC), a natural flavonoid that is present in citrus fruits, has been reported to exhibit antitumor effects in several cancers. Though the mechanism of PEC-induced cytotoxicity effects has been documented, the proteomic changes that are associated with the cellular response to this flavonoid are poorly understood in gastric cancer cells. In this study, a comparative proteomic analysis was performed to identify proteins associated with PEC-induced cell death in two human gastric cancer cell lines: AGS and MKN-28. Two-dimensional gel electrophoresis (2-DE) revealed a total of 29 and 56 protein spots with significant alteration were screened in AGS and MKN-28 cells respectively. In total, 13 (AGS) and 39 (MKN28) proteins were successfully identified by mass spectrometry from the differential spots and they are known to be involved in signal transduction, apoptosis, transcription and translation, cell structural organization, and metabolism, as is consistent with multiple effects of PEC on tumor cells. Notably, novel target proteins like Probable ATP-dependent RNA helicase DDX4 (DDX4) and E3 ubiquitin-protein ligase LRSAM1 (LRSAM1) along with the commonly differential expressed proteins on both the cell lines that are treated with PEC were confirmed by immunoblotting. The DDX4 accelerates cell cycle progression by abrogating the G2 checkpoint when overexpressed in cancer cells, while the aberrant expression of LRSAM1 may be involved in the cancer pathology. Thus, proteomic analysis provides vital information about target proteins that are important for PEC-induced cell death in gastric cancer cells.


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