Pristimerin targeting NF‐κB pathway inhibits proliferation, migration, and invasion in esophageal squamous cell carcinoma cells

Tu, Yuanqing; Tan, Fuxing; Zhou, Jingfeng; Pan, Jingxuan

doi:10.1002/cbf.3335

Cited by 31 publications

(36 citation statements)

References 41 publications

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“…Matrix metallopeptidase (MMP) is considered as an important member of the invasive process, which cancer cell secreted to dissolve the components of ECM or basement membrane [31]. It was previously reported that pristimerin down-regulated MMP2 and matrix metallopeptidase 9 (MMP9) to inhibit migration and invasion of esophageal squamous cell carcinoma (ESCC) [32]. Similarly, we found an obviously decreased expression of MMP2 in our study.…”

Section: Discussionsupporting

confidence: 80%

Pristimerin induces apoptosis and inhibits proliferation, migration in H1299 Lung Cancer Cells

Guo

Lei

et al. 2020

J. Cancer

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Background: The natural occurring pristimerin, a quinonemethide triterpenoid, is extracted from a variety of species of the Celastraceae and Hippocrateaceae family. This research investigated the in vitro anti-cancer potential of pristimerin on NSCLC cells NCI-H1299 and elucidated the molecular mechanism. Methods: Cell growth inhibition by pristimerin was assessed using the MTT assay. Apoptosis was detected using the Annexin V/propidium iodide (PI) test. The colony forming assay was used to investigate the anti-proliferative effects of pristimerin. Wound healing assay and the transwell cell migration assay were utilized to determine the inhibitory effects of migration and invasion, respectively. Western blot was used to detect the protein expression, and real-time-quantitative (RT-q) PCR was used to analyze the mRNA expression. Results: The results showed that pristimerin inhibited the proliferation of H1299 cells with an IC50 value of 2.2 ± 0.34 µM and induced apoptosis in a dose-dependent manner. The colony formation ability was reduced in a dose-dependent manner. A marked inhibition of migration and invasion against H1299 cells was observed in a dose-or time-dependent manner. Moreover, the decreased protein levels of vimentin, F-actin, integrin β1, matrix metalloproteinase (MMP2) and Snail revealed the potential inhibition of epithelial-to-mesenchymal transition (EMT). The regulated mRNA levels of integrin β1, MMP2 and Snail indicated the great potential in the treatment of NSCLC. Conclusion: In conclusion, our study demonstrated that pristimerin suppressed NSCLC cells NCI-H1299 in vitro, exhibited potent activities of proliferation inhibition and apoptosis induction. Furthermore, the treatment of pristimerin decreased migration and invasion of H1299, which was correlated with EMT-related proteins and mRNA.

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Section: Discussionsupporting

confidence: 80%

Pristimerin induces apoptosis and inhibits proliferation, migration in H1299 Lung Cancer Cells

Guo

Lei

et al. 2020

J. Cancer

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“…Pristimerin, a naturally occurring triterpenoid, targets the NF-κB pathway to inhibit the proliferation, migration and invasion of oesophageal squamous cell carcinoma cells. 15,16 Reactive oxygen species (ROS) have important roles in mediating cell proliferation, migration and angiogenesis through the regulation of many key intracellular signalling pathways including Akt, Stat3, and NF-κB. 17 Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs) are an important source of ROS.…”

Section: Introductionmentioning

confidence: 99%

<p>Aloin Inhibits the Proliferation and Migration of Gastric Cancer Cells by Regulating NOX2–ROS-Mediated Pro-Survival Signal Pathways</p>

Wang¹,

Tang²,

Wang³

et al. 2020

DDDT

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Background: Aloin has been reported to have many pharmacological effects including antiinflammatory, anti-oxidant and anti-tumour activities. However, the precise molecular mechanisms underlying the anti-tumour properties of aloin are yet to be elucidated. Methods: HGC-27 and BGC-823 gastric cancer cells were treated with aloin. EdU and colony formation assays were used to detect the proliferation ability of cells. The migration of cells was detected using wound healing and transwell assays. Western blotting was used to detect the levels of cyclinD1, cyclin E1, MMPs, N-cadherin, E-cadherin and NOX2. The phosphorylation of Akt, mTOR, P70S6K, S6, Src, stat3 and IκBα were also detected by Western blotting. Flow cytometry was used to detect the cell cycle distribution.The location of p65 in cells was determined by using a confocal microscopy assay. The total amounts of ROS present in cells were measured using an ROS assay kit. Results: Here, we found that aloin inhibited the proliferation and migration of HGC-27 and BGC-823 gastric cancer cells using a combination of EdU, colony formation, wound healing and transwell assays. Further investigations revealed that aloin decreased the protein expression levels of cyclin D1, N-cadherin, and the matrix metalloproteinases (MMP)-2 and MMP-9; increased E-cadherin expression in a dose-dependent manner; inhibited reactive oxygen species (ROS) generation; and mediated the activation of Akt-mTOR, signal transducer and activator of transcription-3 (Stat3), and NF-κB signalling pathways. Our results also indicated that aloin is able to attenuate the expression levels of the two regulatory proteins of nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2), p47 phox and p22 phox , but had no effect on the level of gp91 phox. N-acetylcysteine treatment of gastric cancer cells inhibited ROS production and Akt-mTOR, Stat3, and IκBα phosphorylation. Taken together, our data suggest that aloin inhibits the proliferation and migration of gastric cancer cells by downregulating NOX2-ROS-mediated activation of the Akt-mTOR, Stat3, and NF-κB signalling pathways. Conclusion: Our findings suggest a potential role for aloin in the prevention of gastric cancer cell proliferation and migration and provide novel insights into the anti-cancer properties of aloin.

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“…It has been known that tumorigenesis is a complex process that involves the interaction of various genes and signaling pathways [26,27]. In ESCC, an increasing number of signaling pathways have been reported to play important roles in the progression of the disease [28][29][30]. Therefore, the analysis of pathways related to neoplasia could provide information regarding tumor development.…”

Section: Discussionmentioning

confidence: 99%

Identification of Differentially Expressed Genes and miRNAs Associated with Esophageal Squamous Cell Carcinoma by Integrated Analysis of Microarray Data

Zhang

Chen

Cheng

et al. 2020

BioMed Research International

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To identify candidate key genes and miRNAs associated with esophageal squamous cell carcinoma (ESCC) development and prognosis, the gene expression profiles and miRNA microarray data including GSE20347, GSE38129, GSE23400, and GSE55856 were downloaded from the Gene Expression Omnibus (GEO) database. Clinical and survival data were retrieved from The Cancer Genome Atlas (TCGA). Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of differentially expressed genes (DEGs) was analyzed via DAVID, while the DEG-associated protein-protein interaction network (PPI) was constructed using the STRING database. Additionally, the miRNA target gene regulatory network and miRNA coregulatory network were constructed, using the Cytoscape software. Survival analysis and prognostic model construction were performed via the survival (version 2.42-6) and rbsurv R packages, respectively. The results showed a total of 2575, 2111, and 1205 DEGs, and 226 differentially expressed miRNAs (DEMs) were identified. Pathway enrichment analyses revealed that DEGs were mainly enriched in 36 pathways, such as the proteasome, p53, and beta-alanine metabolism pathways. Furthermore, 448 nodes and 1144 interactions were identified in the PPI network, with MYC having the highest random walk score. In addition, 7 DEMs in the microarray data, including miR-196a, miR-21, miR-205, miR-194, miR-103, miR-223, and miR-375, were found in the regulatory network. Moreover, several reported disease-related miRNAs, including miR-198a, miR-103, miR-223, miR-21, miR-194, and miR-375, were found to have common target genes with other DEMs. Survival analysis revealed that 85 DEMs were related to prognosis, among which hsa-miR-1248, hsa-miR-1291, hsa-miR-421, and hsa-miR-7-5p were used for a prognostic survival model. Taken together, this study revealed the important roles of DEGs and DEMs in ESCC development, as well as DEMs in the prognosis of ESCC. This will provide potential therapeutic targets and prognostic predictors for ESCC.

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Pristimerin targeting NF‐κB pathway inhibits proliferation, migration, and invasion in esophageal squamous cell carcinoma cells

Cited by 31 publications

References 41 publications

Pristimerin induces apoptosis and inhibits proliferation, migration in H1299 Lung Cancer Cells

Pristimerin induces apoptosis and inhibits proliferation, migration in H1299 Lung Cancer Cells

<p>Aloin Inhibits the Proliferation and Migration of Gastric Cancer Cells by Regulating NOX2–ROS-Mediated Pro-Survival Signal Pathways</p>

Identification of Differentially Expressed Genes and miRNAs Associated with Esophageal Squamous Cell Carcinoma by Integrated Analysis of Microarray Data

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