scholarly journals Wharton Jelly Stem Cells inhibits AGS Gastric Cancer Cells through Induction of Apoptosis and Modification of MAPK and NF‑κB Signaling Pathways

2021 ◽  
Author(s):  
Samaneh Abbasi ◽  
Reza Bazyar ◽  
Mohammad Ali Saremi ◽  
Gholamhoseen Alishiri ◽  
Nasrin Seyyedsani ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Cell Line ◽  
Mapk Signaling ◽  
Dependent Manner ◽  
Induction Of Apoptosis ◽  
Mapk Signaling Pathways

Abstract Background and aim: Gastric cancer) GC) is one of the most common cancer with high mortality worldwide. The human Wharton's jelly stem cells (hWJSCs) can inhibit several cancer cells through several molecular pathways. Therefore, the present study aimed to investigate anticancer effects of hWJSCs conditioned medium (hWJSC-CM) and cell-free lysate (hWJSC-CL) against of GC cell line AGS and underlying signaling pathways. Methods: In this study, we evaluated the effects of hWJSC-CM and hWJSC-CL on viability, proliferation, migration, invasion, apoptosis, and MAPK and NF‑κB signaling pathways in AGS cells. Moreover, mRNA expression of genes involved in apoptosis (BAX, BCL2, SMAC, and SURVIVIN), as well as expression of proteins involved in NF-κB and MAPK signaling pathways were evaluated. Results: The obtained results showed that the hWJSC-CM and hWJSC-CL decreased viability, migration, and invasion of GC cell line AGS in a concentration and time dependent manner. We observed that the hWJSC-CM and hWJSC-CL induced apoptosis pathway through regulation of apoptosis involved genes mRNA expression. In addition, the hWJSC-CM and hWJSC-CL suppressed NF-κB signaling pathways as well as promoted MAPK signaling pathways. Conclusions: In general, our study suggested that the hWJSC-CM and hWJSC-CL inhibits proliferation and viability of GC cell line AGS through induction of apoptosis, as well as modification of NF-κB and MAPK signaling pathways.

scholarly journals Wharton Jelly Stem Cells inhibits AGS Gastric Cancer Cells through Induction of Apoptosis and Modification of MAPK and NF-κB Signaling Pathways

2021 ◽  
pp. 101597
Author(s):  
Samaneh Abbasi ◽  
Reza Bazyar ◽  
Mohammad Ali Saremi ◽  
Gholamhoseen Alishiri ◽  
Nasrin Seyyedsani ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Gastric Cancer Cells ◽  
Induction Of Apoptosis

scholarly journals Expression and Secretion of Cathelicidin LL-37 in Human Epithelial Cells after Infection by Mycobacterium bovis Bacillus Calmette-Guérin

2008 ◽  
Vol 15 (9) ◽  
pp. 1450-1455 ◽  
Author(s):  
Patricia Méndez-Samperio ◽  
Elena Miranda ◽  
Artemisa Trejo
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Mrna Expression ◽  
Signaling Pathways ◽  
Western Blotting ◽  
Mycobacterium Bovis ◽  
A549 Cells ◽  
Mapk Signaling ◽  
Dependent Manner ◽  
Mapk Signaling Pathways

ABSTRACT The antimicrobial cathelicidin LL-37 is considered to play an important role in the innate immune response to tuberculosis infection. However, little is known about the induction and secretion of this antimicrobial peptide in A549 epithelial cells after infection with Mycobacterium bovis bacillus Calmette-Guérin (BCG), the world's most widely used tuberculosis vaccine. In this study, we investigated the effect of M. bovis BCG on LL-37 mRNA levels in A549 cells by real-time PCR and on protein levels by Western blotting. Treatment of cells with M. bovis BCG upregulates LL-37 mRNA expression in a dose- and time-dependent manner. The quantitative analysis of LL-37 gene expression correlated with our Western blotting results. Moreover, our results demonstrated that treatment of cells with the transcriptional inhibitor actinomycin D effectively inhibited in a concentration-dependent manner the ability of M. bovis BCG to induce LL-37 mRNA expression. Finally, inhibition of the MEK1/2 and p38 mitogen-activated protein kinase (MAPK) signaling pathways reduced M. bovis BCG-mediated LL-37 mRNA expression, a reduction that correlated with the observed high level of downregulation of LL-37 protein induction. Thus, these results indicate that the MEK1/2 and p38 MAPK signaling pathways play a critical role in the regulation of inducible LL-37 gene expression in A549 cells infected with M. bovis BCG.

scholarly journals Halofuginone Sensitizes Lung Cancer Organoids to Cisplatin via Suppressing PI3K/AKT and MAPK Signaling Pathways

2021 ◽  
Vol 9 ◽  
Author(s):  
Hefei Li ◽  
Yushan Zhang ◽  
Xiaomei Lan ◽  
Jianhua Yu ◽  
Changshuang Yang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Underlying Mechanism ◽  
Mapk Signaling ◽  
Lung Cancer Cells ◽  
Dependent Manner ◽  
New Strategy ◽  
Resistant Patient ◽  
Mapk Signaling Pathways

Lung cancer is the leading cause of cancer death worldwide. Cisplatin is the major DNA-damaging anticancer drug that cross-links the DNA in cancer cells, but many patients inevitably develop resistance with treatment. Identification of a cisplatin sensitizer might postpone or even reverse the development of cisplatin resistance. Halofuginone (HF), a natural small molecule isolated from Dichroa febrifuga, has been found to play an antitumor role. In this study, we found that HF inhibited the proliferation, induced G0/G1 phase arrest, and promoted apoptosis in lung cancer cells in a dose-dependent manner. To explore the underlying mechanism of this antitumor effect of halofuginone, we performed RNA sequencing to profile transcriptomes of NSCLC cells treated with or without halofuginone. Gene expression profiling and KEGG analysis indicated that PI3K/AKT and MAPK signaling pathways were top-ranked pathways affected by halofuginone. Moreover, combination of cisplatin and HF revealed that HF could sensitize the cisplatin-resistant patient-derived lung cancer organoids and lung cancer cells to cisplatin treatment. Taken together, this study identified HF as a cisplatin sensitizer and a dual pathway inhibitor, which might provide a new strategy to improve prognosis of patients with cisplatin-resistant lung cancer.

scholarly journals Adenosine Triphosphate Prevents Serum Deprivation-Induced Apoptosis in Human Mesenchymal Stem Cells via Activation of the MAPK Signaling Pathways

Stem Cells ◽  
2014 ◽  
Vol 33 (1) ◽  
pp. 211-218 ◽  
Author(s):  
Jessica L. Berlier ◽  
Sabrina Rigutto ◽  
Antoine Dalla Valle ◽  
Jessica Lechanteur ◽  
Muhammad S. Soyfoo ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Signaling Pathways ◽  
Adenosine Triphosphate ◽  
Human Mesenchymal Stem Cells ◽  
Mapk Signaling ◽  
Serum Deprivation ◽  
Induced Apoptosis ◽  
Mapk Signaling Pathways

Berberine inhibits lipopolysaccharide-induced expression of inflammatory cytokines by suppressing TLR4-mediated NF-ĸB and MAPK signaling pathways in rumen epithelial cells of Holstein calves

2019 ◽  
Vol 86 (2) ◽  
pp. 171-176 ◽  
Author(s):  
Chenxu Zhao ◽  
Yazhou Wang ◽  
Xue Yuan ◽  
Guoquan Sun ◽  
Bingyu Shen ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Signaling Pathways ◽  
Inflammatory Cytokines ◽  
Molecular Mechanisms ◽  
Mapk Signaling ◽  
Dependent Manner ◽  
Inflammatory Drug ◽  
Anti Inflammatory ◽  
Mapk Signaling Pathways ◽  
Rumen Epithelial Cells

AbstractSubacute ruminal acidosis (SARA) can increase the level of inflammation and induce rumenitis in dairy cows. Berberine (BBR) is the major active component of Rhizoma Coptidis, which is a type of Chinese anti-inflammatory drug for gastrointestinal diseases. The purpose of this study was to investigate the anti-inflammatory effects of BBR on lipopolysaccharide (LPS)-stimulated rumen epithelial cells (REC) and the underlying molecular mechanisms. REC were cultured and stimulated with LPS in the presence or absence of different concentrations of BBR. The results showed that cell viability was not affected by BBR. Moreover, BBR markedly decreased the concentrations and mRNA expression of pro-inflammatory cytokines, including tumor necrosis factor-α, interleukin-1β, and interleukin-6 in the LPS-treated REC in a dose-dependent manner. Importantly, Western blotting analysis showed that BBR significantly suppressed the protein expression of toll-like receptor 4 (TLR4) and myeloid differentiation primary response protein (MyD88) and the phosphorylation of nuclear factor-κB (NF-κB), inhibitory kappa B (IκBα), p38 mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK) in LPS-treated REC. Furthermore, the results of immunocytofluorescence showed that BBR significantly inhibited the nuclear translocation of NF-κB p65 induced by LPS treatment. In conclusion, the protective effects of BBR on LPS-induced inflammatory responses in REC may be due to its ability to suppress the TLR4-mediated NF-κB and MAPK signaling pathways. These findings suggest that BBR can be used as an anti-inflammatory drug to treat inflammation induced by SARA.

Sign in / Sign up

Export Citation Format

Share Document