scholarly journals Traditional Uyghur medicine Quercus infectoria galls water extract triggers apoptosis and autophagic cell death in colorectal cancer cells

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Hui Zhang ◽  
Yongbing Wang ◽  
Jiayang Liu ◽  
Kudelaidi Kuerban ◽  
Jian Li ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Flow Cytometry ◽  
Cell Death ◽  
Alternative Medicine ◽  
Signaling Pathway ◽  
Water Extract ◽  
Underlying Mechanism ◽  
Autophagic Cell Death ◽  
Therapeutic Effects ◽  
Traditional Uyghur Medicine

Abstract Background The water extract of Quercuse infectoria galls (QIG) is the active ingredient of Uyghur medicine Xipayi Kui Jie’an (KJA) which has promising therapeutic effects on Ulcerative Colitis (UC) as an alternative medicine. Considering the relationship between UC and the development of colorectal cancer (CRC), the present work aims to explore the direct anti-CRC activity of QIG extract. Methods CCK8 assay and flow cytometry were used to detect cytotoxicity and apoptosis. Transmission electron microscopy (TEM), flow cytometry, laser confocal and western blotting were performed to examine autophagy. We also adopted Reactive Oxygen Assay kit, as well as transwell and wound healing tests to study the underlying mechanism of QIG against CRC cells. Results First, we found that QIG extract could suppress the viability of CRC cells and trigger caspases-dependent apoptosis. Subsequently, we proved for the first time that QIG extract also triggered autophagic cell death in CRC cells, which together with apoptosis contributed to the cytotoxic effect on CRC cells. Further investigation revealed that QIG-induced cytotoxicity associated with intracellular ROS accumulation which could suppress the AKT/mTOR signaling pathway, and then induce autophagy and inhibit cell growth. Besides, Erk signaling pathway was also involved in the process of autophagic cell death. Moreover, QIG extract also influenced EMT process and inhibited CRC cell migration. Conclusion Altogether, this study provides a basis for the utilization of QIG as an alternative medicine for CRC prevention and treatment.

scholarly journals MiR-9-5p promotes MSC migration by activating β-catenin signaling pathway

2017 ◽  
Vol 313 (1) ◽  
pp. C80-C93 ◽  
Author(s):  
Xianyang Li ◽  
Lihong He ◽  
Qing Yue ◽  
Junhou Lu ◽  
Naixin Kang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Target Genes ◽  
Focal Adhesions ◽  
Underlying Mechanism ◽  
Therapeutic Effects ◽  
Migration Ability ◽  
Tissue Damages ◽  
First Time ◽  
Hepatocyte Growth ◽  
High Migration

Mesenchymal stem cells (MSCs) have the potential to treat various tissue damages, but the very limited number of cells that migrate to the damaged region strongly restricts their therapeutic applications. Full understanding of mechanisms regulating MSC migration will help to improve their migration ability and therapeutic effects. Increasing evidence shows that microRNAs play important roles in the regulation of MSC migration. In the present study, we reported that miR-9-5p was upregulated in hepatocyte growth factor -treated MSCs and in MSCs with high migration ability. Overexpression of miR-9-5p promoted MSC migration, whereas inhibition of endogenous miR-9-5p decreased MSC migration. To elucidate the underlying mechanism, we screened the target genes of miR-9-5p and report for the first time that CK1α and GSK3β, two inhibitors of β-catenin signaling pathway, were direct targets of miR-9-5p in MSCs and that overexpression of miR-9-5p upregulated β-catenin signaling pathway. In line with these data, inhibition of β-catenin signaling pathway by FH535 decreased the miR-9-5p-promoted migration of MSCs, while activation of β-catenin signaling pathway by LiCl rescued the impaired migration of MSCs triggered by miR-9-5p inhibitor. Furthermore, the formation and distribution of focal adhesions as well as the reorganization of F-actin were affected by the expression of miR-9-5p. Collectively, these results demonstrate that miR-9-5p promotes MSC migration by upregulating β-catenin signaling pathway, shedding light on the optimization of MSCs for cell replacement therapy through manipulating the expression level of miR-9-5p.

scholarly journals SPAG6 silencing induces autophagic cell death in SKM‑1 cells via the AMPK/mTOR/ULK1 signaling pathway

2020 ◽  
Vol 20 (1) ◽  
pp. 551-560
Author(s):  
Meng Zhang ◽  
Jie Luo ◽  
Xiaohua Luo ◽  
Lin Liu
Keyword(s):  
Cell Death ◽  
Signaling Pathway ◽  
Autophagic Cell Death

scholarly journals Roles of the pyroptosis signaling pathway in a sepsis-associated encephalopathy cell model

2020 ◽  
Vol 48 (8) ◽  
pp. 030006052094976
Author(s):  
Yan Wang ◽  
Xueyan Liu ◽  
Qiang Wang ◽  
Xin Yang
Keyword(s):  
Flow Cytometry ◽  
Protective Effect ◽  
Signaling Pathway ◽  
Cell Model ◽  
Cell Damage ◽  
Combined Treatment ◽  
Therapeutic Effects ◽  
Inhibitory Effects ◽  
Caspase Cleavage ◽  
Associated Proteins

Objectives The inhibition of pyroptosis has a protective effect in sepsis-associated encephalopathy (SAE). However, the mechanisms underlying pyroptosis in SAE remain to be elucidated. Methods Here, we investigated the effects of the caspase inhibitors, Belnacasan (Beln) and Wedelolactone (Wede), on an induced model of SAE in P12 cells, using immunofluorescence, ELISA, western blotting, and flow cytometry. Results The cell viability decreased, IL-1β and IL-18 secretion increased, and the levels of the caspase cleavage products, N-terminal gasdermin D, cleaved caspase-1, and cleaved caspase-11, increased in P12 cells following combined treatment with lipopolysaccharides (LPS) and adenosine triphosphate (ATP). However, treatment with Beln or Wede ameliorated the effects induced by LPS and ATP. Neither Beln nor Wede notably affected the levels of cell apoptosis-associated proteins but these inhibitors regulated the levels of cell pyroptosis-associated proteins. Further, the combination of Beln and Wede exerted greater inhibitory effects on cell pyroptosis than either Beln or Wede alone. Conclusions The results demonstrated that both the canonical and non-canonical signaling pathways of cell pyroptosis are involved in LPS-induced cell damage and that the non-canonical signaling pathway may be involved to a greater extent. This suggests that the inhibition of pyroptosis may exert potential therapeutic effects on SAE.

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