scholarly journals Crosstalk of the Wnt/β-Catenin Signaling Pathway in the Induction of Apoptosis on Cancer Cells

2021 ◽  
Vol 14 (9) ◽  
pp. 871
Author(s):  
Cristina Trejo-Solis ◽  
Angel Escamilla-Ramirez ◽  
Dolores Jimenez-Farfan ◽  
Rosa Angelica Castillo-Rodriguez ◽  
Athenea Flores-Najera ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Malignant Tumors ◽  
Cell Renewal ◽  
Stem Cell Renewal ◽  
Wide Range ◽  
Proliferation And Apoptosis ◽  
Cellular Context ◽  
Available Information

The Wnt/β-catenin signaling pathway plays a major role in cell survival and proliferation, as well as in angiogenesis, migration, invasion, metastasis, and stem cell renewal in various cancer types. However, the modulation (either up- or downregulation) of this pathway can inhibit cell proliferation and apoptosis both through β-catenin-dependent and independent mechanisms, and by crosstalk with other signaling pathways in a wide range of malignant tumors. Existing studies have reported conflicting results, indicating that the Wnt signaling can have both oncogenic and tumor-suppressing roles, depending on the cellular context. This review summarizes the available information on the role of the Wnt/β-catenin pathway and its crosstalk with other signaling pathways in apoptosis induction in cancer cells and presents a modified dual-signal model for the function of β-catenin. Understanding the proapoptotic mechanisms induced by the Wnt/β-catenin pathway could open new therapeutic opportunities.

scholarly journals Effect of Daidzein on the Proliferation of Lung Cancer Cells Involved in the Apoptotic Signaling Pathway

2020 ◽  
Author(s):  
Hui Liu ◽  
Xiaobo Wang ◽  
Ouyang Jin ◽  
Denggang Fu ◽  
You Peng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Signaling Pathway ◽  
Tp53 Gene ◽  
Cell Counting ◽  
Pcr Analysis ◽  
Human Embryonic Lung ◽  
Bioactive Substances ◽  
Apoptosis Pathway ◽  
Wide Range ◽  
Proliferation And Apoptosis

Abstract Background: Daidzein is one of the key bioactive substances of soybean isoflavones that has a wide range of health benefits includes antineoplastic. Epidemiological evidence suggests that soy glycogen is associated with the incidence and prognosis of lung cancer. we purposed to assess the effect and molecular mechanism of daidzein on lung cancer, and to maximize therapy outcome for individualized treatment. Methods: In this report, H1299 were cultured in a medium with 10 μM daidzein for 6 hours , we detected the expression level of apoptosis-related genes in H1299 by cDNA microarray analysis. The selected genes were further validated by using RT-PCR analysis and Western blot. Finally, We usedflow cytometry to detect cell cycle alterations, and apoptosis the proliferation and apoptosis in HELF and H1299 cells were detected by Cell counting kit-8 assays. Results: These results indicate that low concentrations of isoflavone crude extract and daidzein could significantly affect the proliferation of H1299 (Human lung adenocarcinoma) and HELF (Human embryonic lung fibroblast) cells. The results of microarray in our study suggest that apoptosis-related genes are up-regulated induced by daidzein in H1299 cells and verified by RT-qPCR, particularly TP53 and caspase9. Western blotting shows the effect of daidzein on P53 and caspase9 in HELF cells be more obvious than it in H1299 cells. While the expression of TP53 was suppressed by pifithrin-α (PFTα) in HELF and H1299 cells, the mRNA and protein expression of TP53 still increase induced by daidzein, also, the effect of apoptosis induced by daidzein is involved in the P53 apoptosis pathway through inhibition of TP53 gene expression by PFTα. Conclusions: In conclusion, daidzein affected proliferation and apoptosis in HELF and H1299 cells, and the mechanism of apoptosis involved in the P53 signaling pathway.

scholarly journals MicroRNAs Differentially Regulated by Akt Isoforms Control EMT and Stem Cell Renewal in Cancer Cells

2009 ◽  
Vol 2 (92) ◽  
pp. ra62-ra62 ◽  
Author(s):  
D. Iliopoulos ◽  
C. Polytarchou ◽  
M. Hatziapostolou ◽  
F. Kottakis ◽  
I. G. Maroulakou ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cancer Cells ◽  
Cell Renewal ◽  
Akt Isoforms ◽  
Stem Cell Renewal

Effects of Amygdalin on TLR4/NF-αB Signaling Pathway-Mediated Proliferation and Apoptosis of Gastric Cancer Cells

2021 ◽  
Vol 20 (1) ◽  
pp. 153-158
Author(s):  
Abulajiang Abudoukelimu ◽  
Xinhui Yang ◽  
Lei Ge ◽  
Xiangyue Zeng ◽  
Yin Shu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
B Cell Lymphoma ◽  
Toll Like Receptor ◽  
Gastric Cancer Cells ◽  
Toll Like Receptor 4 ◽  
Proliferation And Apoptosis ◽  
High Incidence Rate ◽  
Factor Α

Gastric cancer is a highly malignant tumor of the digestive tract with high incidence rate and mortality. In the present study, we have shown decreased cell proliferation, increased apoptosis, and expression of proinflammatory cytokines (Interleukin-6, Interleukin-1β, and Tumor necrosis factor-α) in gastric cancer cells MGC-803 by amygdalin. Also, amygdalin treatment significantly reduced expression of the mRNA and protein for B-cell lymphoma 2 protein, CyclinD1, toll-like receptor 4, and REL-associated protein involved in NF-κB heterodimer formation in MGC-803 cells. In summary, amygdalin inhibits the proliferation of gastric cancer cells MGC-803 and promotes cell apoptosis by regulating the toll-like receptor 4/ nuclear factor-kappa B signaling pathway.

scholarly journals Transcriptomic analysis reveals that bromodomain containing 9 controls signaling pathways in gastric cancer

2020 ◽  
Author(s):  
Yuan Wang ◽  
Chen Wang ◽  
Yu-Ting Mo ◽  
Wen Yi Tan ◽  
Xi-Yong Yu
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
The Cancer Genome Atlas ◽  
Gastric Cancer Cells ◽  
Ags Cells ◽  
R Language ◽  
Gastric Cancers ◽  
Ppi Networks

Abstract Background According to the Cancer Genome Atlas, gastric cancers involve 30% BRD9 changes. Studying the signaling net controlled by BRD9 is important and provides useful information for the treatment of patients with gastric cancer and BRD9 alteration. Objective We performed this study to find the signaling pathways controlled by BRD9 in gastric cancer cells. Methods MGC-803 and AGS cells were selected as BRD9 overexpression and normal expression models, respectively, and added with BRD9 inhibitors BI9564 and BI7273, respectively. RNA-seq and limma R language were used to obtain differentially expressed genes (DEGs), and heatmap R language was employed for cluster analysis. Database for Annotation, Visualization and Integrated Discovery (DAVID) was applied to identify the gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichments, and STRING database was utilized to construct the protein–protein interaction (PPI) networks. Analysis was performed through Cytoscape software to determine the possible signaling pathway and target genes. Results Group MGC-803: 1204 and 1338 DEGs were found in MGC-803 cells added with BI9564 and BI7273, respectively, and 425 DEGs were found in the intersection of these two sets. AGS group: 974 and 1006 DEGs were found in AGS cells added with BI9564 and BI7273, respectively, and 382 DEGs were found in the intersection of these two sets. The DEG number in the intersection of groups MGC-803 and AGS was only 12, and only 3 of which showed the same regulation direction. Hence, these two types of gastric cancers are greatly altered in the signaling network. GO enrichment and KEGG signaling pathway analyses showed that in group MGC-803, BRD9 mainly controls cell adhesion molecule (CAM) pathway, and genes SPP1 and GNAO1 may play important an important role in the BRD9 controlling network. In group AGS, BRD9 mainly controls protein digestion and absorption pathway, and genes AR and GNGT2 have an important function in the BRD9 controlling network. Conclusion Comprehensive bioinformatics analyses were conducted to screen the DEGs and signaling pathways controlled by BRD9 in different gastric cancer cells. The findings provide a theoretical basis in curing patients with clinical gastric cancer.

Exploring the Mechanism of Periplogenin in the treatment of Lung Cancer Based on Network Pharmacology and Molecular Biology

2021 ◽  
Vol 7 (4) ◽  
pp. 765-775
Author(s):  
Junwei Wu ◽  
Mengting Qin ◽  
Hong Pan ◽  
Qi Pan ◽  
Shoufeng Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Survival Rate ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Network Pharmacology ◽  
Peptidase Activity ◽  
Fatty Acid Binding ◽  
The Core ◽  
Core Proteins

Lung cancer (the 5-year survival rate is only about 16%) has a low survival rate, and more-effective drugs are urgently needed. Our team discovered that cortex Periplocae Radicis has obvious toxic effects on various cancer cells, including lung cancer cells. However, the mechanism is not clear. Therefore, we used the PubChem database to obtain periplogenin as the target of therapeutic drugs and the TCGA database to obtain differential genes of lung cancer. The results showed that MMP9, PPARG, BMP2, and TGFB2 were the core proteins of periplogenin acting on lung adenocarcinoma (LUAD), and MMP9, angiotensin-converting enzyme (ACE), BMP2, PPARG, MMP13, MMP3, and TGFB2 were the core proteins of periplogenin acting on lung squamous cell carcinoma (LUCS). Through gene ontology (GO) enrichment analysis, it was found that periplogenin mainly acted on LUAD via fatty acid binding, metallopeptidase activity, and monocarboxylic acid binding, and mainly acted on lung squamous carcinoma (LUSC) via endopeptidase activity, metallopeptidase activity, and serine-type peptidase activity. Kyoto Encyclopedia of Genes, and Genomes (KEGG) analysis revealed that the IL-17 signaling pathway, fluid shear stress, atherosclerosis, hepatocellular carcinoma, and so on, were the main signaling pathways of periplogenin acting on LUSC, whereas glycolysis/gluconeogenesis, and the peroxisome proliferator-activated receptor (PPAR) signaling pathway were major signaling pathways of periplogenin acting on LUAD. This shows that treatment of lung cancer can be achieved through multi-targeted, and multi-channel periplogenin activity.

scholarly journals Berberine Sensitizes Human Ovarian Cancer Cells to Cisplatin Through miR-93/PTEN/Akt Signaling Pathway

2015 ◽  
Vol 36 (3) ◽  
pp. 956-965 ◽  
Author(s):  
Qiaoyun Chen ◽  
Rong Qin ◽  
Yue Fang ◽  
Hao Li
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Ovarian Cancer Cell Line ◽  
Akt Signaling ◽  
Ovarian Cancer Cells ◽  
Control Group ◽  
Akt Signaling Pathway ◽  
Wide Range

Background: Berberine, a well-known component of the Chinese herbal medicine Huanglian, has wide range of biochemical and pharmacological effects, including antineoplastic effect, but the exact mechanisms remain unclear. The aim of the present study was to evaluate the potential chemo-sensitization effect of berberine in ovarian cancer cell line A2780. Methods: The expression of miR-93 was measure by RT-PCR. The target of miR-93 was confirmed by luciferase activity assay. Hoechst 33258 staining, Annexin V and PI double staining were used for apoptosis analysis. Results: In this study, we found A2780/DDP cells that were incubated with berberine combined with cisplatin had a significantly lower survival than the control group. Berberine enhanced cisplatin induced apoptosis and induced G0/G1 cell cycle arrest in A2780 cells. Next, we observed that the miR-93 levels in cisplatin resistant cell lines were higher than that in cisplatin sensitive cell lines. Furthermore, our study found berberine could inhibit miR-93 expression and function in ovarian cancer, as shown by an increase of its target PTEN, an important tumor suppressor in ovarian cancer. A2780 cells that were treated with PTEN siRNA had increased survival compared to NC group and this could be partly alleviated by the AKT inhibitor Triciribine. More importantly, A2780 cells that were treated with PTEN siRNA had a survival pattern that is similar to cells with miR-93 overexpression. Conclusion: The results suggested that berberine modulated the sensitivity of cisplatin through miR-93/PTEN/AKT signaling pathway in the ovarian cancer cells.

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