Targeting of high mobility group A2 by small interfering RNA‐loaded nanoliposome‐induced apoptosis and migration inhibition in gastrointestinal cancer cells

2018 ◽  
Vol 120 (6) ◽  
pp. 9203-9212 ◽  
Author(s):  
Ali Mohammadi ◽  
Behzad Mansoori ◽  
Pouria Savadi ◽  
Vahid khaze ◽  
Mahsa Minouei ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Gastrointestinal Cancer ◽  
Small Interfering Rna ◽  
High Mobility ◽  
High Mobility Group ◽  
Migration Inhibition ◽  
And Migration ◽  
Induced Apoptosis ◽  
Interfering Rna

scholarly journals Interferon-αEnhances 5′-Deoxy-5-Fluorouridine-Induced Apoptosis by ERK-Dependant Upregulation of Thymidine Phosphorylase

2013 ◽  
Vol 2013 ◽  
pp. 1-8
Author(s):  
Yike Zhu ◽  
Ling Xu ◽  
Yibo Fan ◽  
Ce Li ◽  
Ye Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Small Interfering Rna ◽  
Thymidine Phosphorylase ◽  
Antitumor Efficacy ◽  
Erk Signaling ◽  
Gastric Cancer Cells ◽  
High Concentrations ◽  
Induced Apoptosis ◽  
Interfering Rna

5-Florouracil (5-FU) is the basic agent used in the treatment of gastric cancer. Capecitabine, a prodrug of 5-FU, displays increased antitumor efficacy compared with 5-FU in the clinic.5′-Deoxy-5-fluorouracil (5′-DFUR), the metabolite of capecitabine, is converted to 5-FU by the enzyme thymidine phosphorylase (TP), which is present at high concentrations in human tumors. In this study, we investigated the effect of interferon-α(IFN-α) on the sensitivity of gastric cancer cells to treatment with5′-DFUR and its relationship with TP expression. Preincubation of gastric cancer cells with IFN-αenhanced5′-DFUR-induced apoptosis via IFN-α-mediated upregulation of TP. The depletion of TP with small interfering RNA (siRNA) obviously inhibited IFN-α-induced upregulation of TP expression and thus prevented apoptosis induced by IFN-αand5′-DFUR. Treatment with IFN-αand combined IFN-αand5′-DFUR treatment were also associated with concomitant activation of ERK signaling. Treatment with the ERK inhibitor PD98059 or depletion of ERK with siRNA partially reversed IFN-α-induced upregulation of TP expression, thus partially preventing apoptosis induced by IFN-αand5′-DFUR. Taken together, our study shows that IFN-αenhanced5′-DFUR-induced apoptosis in gastric cancer cells by upregulation of TP expression, which is partially regulated by activation of ERK signaling.

scholarly journals HMGA1 Attenuates Doxorubicin-Induced Cardiomyocyte Pyroptosis By Inhibiting SOX9

2021 ◽  
Author(s):  
Yaxiu Liu ◽  
Yao Tang ◽  
Hui Fu ◽  
Shuang Fu ◽  
Xinbin Zheng ◽  
...  
Keyword(s):  
Small Interfering Rna ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
High Mobility ◽  
Underlying Mechanism ◽  
High Mobility Group ◽  
Hmg Box ◽  
Interfering Rna

Abstract Doxorubicin (DOX) is widely used as an anti-tumor drug with severe cardiotoxicity, encephalotoxicity, nephrotoxicity and so on, especially cardiotoxicity, which severely limit its application. Researchers have extensively studied the mechanisms of DOX-induced cardiotoxicity. However, the underlying mechanism of DOX-induced cardiotoxicity needs to be further evaluated. Studies reveal that High-mobility group AT-hook1 (HMGA1) and Sex-determining-region-Y (SRY)-related HMG box-containing protein 9 (SOX9) contribute to caspase-3-mediated apoptosis, but whether HMGA1 and SOX9 participate in caspase-3/gasdermin E (GSDME)-mediated pyroptosis remains unknown. This study was performed to investigate whether HMGA1 and SOX9 participate in DOX-induced cardiomyocyte pyroptosis induced by DOX in vitro, and to reveal the molecular mechanisms of HMGA1 and SOX9 in regulating DOX-induced cardiomyocyte pyroptosis via caspase/GSDME pathway. Results showed that the expression of HMGA1 is significantly up-regulated while SOX9 is down-regulated in HL-1 cells after DOX treatment. We found that both inhibition of HMGA1 by small interfering RNA (siRNA) and overexpression of SOX9 by transfection of SOX9 plasmid significantly promote cardiomyocyte pyroptosis induced by DOX. In addition, HMGA1 interacts with SOX9. Finally, our results show that silencing SOX9 reverses cardiomyocyte pyroptosis induced by silencing HMGA1 after DOX treatment.

scholarly journals Small interfering RNA-mediated downregulation of beta-catenin inhibits invasion and migration of colon cancer cells in vitro

2012 ◽  
Vol 18 (7) ◽  
pp. BR273-BR280 ◽  
Author(s):  
Jianjun Han ◽  
Binbin Gao ◽  
Xing Jin ◽  
Zhongfa Xu ◽  
Zengjun Li ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Small Interfering Rna ◽  
Beta Catenin ◽  
Colon Cancer Cells ◽  
Invasion And Migration ◽  
And Migration ◽  
Interfering Rna

scholarly journals Albendazole Exhibits Anti-Neoplastic Actions against Gastric Cancer Cells by Affecting STAT3 and STAT5 Activation by Pleiotropic Mechanism(s)

Biomedicines ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 362
Author(s):  
Min Hee Yang ◽  
In Jin Ha ◽  
Jae-Young Um ◽  
Kwang Seok Ahn
Keyword(s):  
Gastric Cancer ◽  
Reactive Oxygen Species ◽  
Transcription Factors ◽  
Cancer Cells ◽  
Small Interfering Rna ◽  
Oxygen Species ◽  
Gastric Cancer Cells ◽  
Drug Induced ◽  
Cellular Apoptosis ◽  
Interfering Rna

Albendazole (ABZ) has been reported to display anti-tumoral actions against various maliganncies, but possible impact of ABZ on gastric cancer has not been deciphered. As aberrant phosphorylation of STAT3 and STAT5 proteins can regulate the growth and progression of gastric cancer, we postulated that ABZ may interrupt the activation of these oncogenic transcription factors. We found that ABZ exposure abrogated STAT3/5 activation, inhibited phosphorylation of Janus-activated kinases 1/2 and Src and enhanced the levels of SHP-1 protein. Silencing of SHP-1 gene by small interfering RNA (siRNA) reversed the ABZ-promoted attenuation of STAT3 as well as STAT5 activation and cellular apoptosis. In addition, these effects were noted to be driven by an augmented levels of reactive oxygen species caused by drug-induced GSH/GSSG imbalance. Thus, the data indicates that ABZ can modulate the activation of STAT3 and STAT5 by pleiotropic mechanisms in gastric cancer cells.

scholarly journals Anti-neoplastic Effect of Ginkgolide C through Modulating c-Met Phosphorylation in Hepatocellular Carcinoma Cells

2020 ◽  
Vol 21 (21) ◽  
pp. 8303
Author(s):  
Min Hee Yang ◽  
Seung Ho Baek ◽  
Jae-Young Um ◽  
Kwang Seok Ahn
Keyword(s):  
Hepatocellular Carcinoma ◽  
Invasion And Migration ◽  
Oncogenic Pathways ◽  
Tumor Growth And Metastasis ◽  
And Migration ◽  
Induced Apoptosis ◽  
Interfering Rna ◽  
Hepatocyte Growth ◽  
Hcc Cells ◽  
Met Phosphorylation

Ginkgolide C (GGC) derived from Ginkgo biloba, has been reported to exhibit various biological functions. However, the anti-neoplastic effect of GGC and its mechanisms in liver cancer have not been studied previously. Hepatocyte growth factor (HGF)/c-mesenchymal–epithelial transition receptor (c-Met) pathway can regulate tumor growth and metastasis in hepatocellular carcinoma (HCC) cells. This study aimed to evaluate the anti-neoplastic effect of GGC against HCC cells and we observed that GGC inhibited HGF-induced c-Met and c-Met downstream oncogenic pathways, such as PI3K/Akt/mTOR and MEK/ERK. In addition, GGC also suppressed the proliferation of expression of diverse tumorigenic proteins (Bcl-2, Bcl-xL, Survivin, IAP-1, IAP-2, Cyclin D1, and COX-2) and induced apoptosis. Interestingly, the silencing of c-Met by small interfering RNA (siRNA) mitigated c-Met expression and enhanced GGC-induced apoptosis. Moreover, it was noted that GGC also significantly reduced the invasion and migration of HCC cells. Overall, the data clearly demonstrate that GGC exerts its anti-neoplastic activity through modulating c-Met phosphorylation and may be used as an effective therapy against HCC.

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