Baicalein inhibits cell growth and increases cisplatin sensitivity of A549 and H460 cells via miR‐424‐3p and targeting PTEN/PI3K/Akt pathway

Lu, Chenyang; Wang, Huaqi; Chen, Shanshan; Yang, Rui; Li, Hui; Zhang, Guojun

doi:10.1111/jcmm.13556

Cited by 66 publications

(41 citation statements)

References 50 publications

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“…A previous study suggested that the PTEN/PI3K/AKT pathway is involved in cancer progression ( 21 – 25 ), thus, the effect of Pec on the PTEN/PI3K/AKT pathway in A549 and Calu-3 cells was evaluated by western blotting to examine the underlying mechanism of Pec-mediated inhibition of cell proliferation and metastasis. In the present study, the results of western blotting demonstrated that the expression of phospho-PI3K and phospho-AKT was significantly decreased; whereas, the PTEN protein expression level was increased with increasing concentrations of Pec ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Pectolinarigenin inhibits non‑small cell lung cancer progression by regulating the PTEN/PI3K/AKT signaling pathway

Gao

Pan

2018

Oncol Rep

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Lung cancer is the principal cause of cancer-associated mortality. Pectolinarigenin (Pec) reportedly has effective antitumor activity against certain cancer types. Phosphatase and tensin homolog (PTEN) is a well-known tumor suppressor and serves a vital role in cancer progression. However, the effect of Pec on non-small cell lung cancer (NSCLC) cell proliferation and metastasis, and the underlying mechanism, has not yet been elucidated. In the present study, it was demonstrated that Pec inhibited the proliferation of A549 and Calu-3 cells in dose- and time-dependent manners. The apoptosis rate significantly increased with increasing doses of Pec. Apoptosis-associated protein expression was additionally altered by Pec exposure. Pec was able to suppress the metastasis of NSCLC cells; it upregulated the mRNA and protein expression levels of E-cadherin, and downregulated the mRNA and protein expression levels of vimentin. Additionally, Pec was able to activate PTEN and subsequently downregulate the PI3K/protein kinase B (AKT) signaling pathway. In summary, Pec was able to inhibit cell proliferation, promote apoptosis and suppress metastasis in NSCLC cells through the PTEN/PI3K/AKT signaling pathway, indicating that Pec is a potential agent for NSCLC therapy.

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Section: Resultsmentioning

confidence: 99%

Pectolinarigenin inhibits non‑small cell lung cancer progression by regulating the PTEN/PI3K/AKT signaling pathway

Gao

Pan

2018

Oncol Rep

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“…Traditional Chinese or Korean medicine is widely accepted as an alternative treatment for cancer [24][25][26]. Furthermore, research on traditional Chinese and Korean medicinal and herbal formulations has been recognized internationally by medical researchers [27], and several studies elucidated the molecular and cellular mechanisms of herbal medicine-derived phytochemicals in the context of cancer research [28][29][30]. In this study, we investigated the effect of oriental medicinal herbs on PAK-1 signaling.…”

Section: Discussionmentioning

confidence: 99%

HMT Inhibits Prostate Cancer Progression by Targeting PAK-1.

Lee¹,

Xu²,

Lee³

et al. 2020

Preprint

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Background: Heamatang (HMT) is a classic medicinal formula used in traditional Chinese and Korean medicine; it contains seven distinct components, mainly of herbal origin. HMT is used as an anti-aging remedy, in the treatment of urinary disorders, and to increase energy and vitality. However, the therapeutic applications of this formula have not been evaluated with evidence-based science. Methods: Therefore, we assessed HMT through various in vitro methods, including cell viability assay, fluorescence-activated cell sorting assay (FACS), western blotting, migration assay, three-dimensional (3D) cell culture, siRNA-mediated PAK-1 knockdown, and crystal violet assays. Results: HMT decreased PAK-1 expression in PC-3 cells and inhibited cell viability, growth, and motility. The inhibition of cell motility by HMT was correlated with PAK-1-mediated inhibition of Lim domain kinase (LIMK) and cofilin. HMT induced G1 arrest and apoptosis through the transcriptional regulation of cell cycle regulatory proteins (inhibition of cyclin-dependent kinase (CDK) 4, 6, and cyclin D1) and apoptosis-related proteins (increase in cleaved caspase-3 (c-cas3) and inhibition of poly ADP-ribose polymerase (PARP) and B-cell lymphoma 2 (BCL-2)). Moreover, HMT suppressed P21-activated kinase (PAK-1) expression, leading to the inhibition of AKT activities. Finally, we showed that Decursin was the active ingredient involved in the inhibitory effect of HMT on PAK-1. Conclusion: Our findings demonstrated that HMT exerts its anticancer influence through the inhibition of PAK-1 expression. The HMT formula could be applied in various fields, including functional health food and pharmaceutical development.

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“…50 In our study, the expression of miR-424 in DDP resistant group was significantly decreased in compared with the DDP chemosensitive group, which was consistent with other research. 51,52 In present study, hub genes were screened by the plug-in CytoHubba, among the top 10 hubgenes in downregulation miRNA group, 8 of them were identified as the target genes of miRNA-424(CDC27, CDC23, RNF213, SMURF1, SMURF2, UBE4A, LMO7, WSB1), the hub gens were continued to be screened by Coremine Medical online database. Coremine Medical is a domainspecific search engine for medical information, which was based on a new search concept that offers the user domainspecific networks.…”

Section: Discussionmentioning

confidence: 99%

<p>MicroRNA-424 regulates cisplatin resistance of gastric cancer by targeting SMURF1 based on GEO database and primary validation in human gastric cancer tissues</p>

Lü¹,

Wu²,

Lu³

et al. 2019

OTT

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Purpose: Cisplatin (DDP) based chemotherapy regimens are widely used in advanced gastric cancer (GC). Drug resistance often limited the clinical benefits of cisplatin regimen. The mechanisms of cisplatin resistance have not been fully revealed. Therefore, further exploration of the relevant molecular mechanisms is urgently needed. Patients and methods: DDP resistance associated miRNA of GC microarray dataset GSE86195 was obtained from the National Center for Biotechnology Information (NCBI) GEO database, GEO2R was applied to compare the samples in two different groups under the same experimental conditions. |log 2 (Fold Change) | (log 2 (FC)) was selected as the criteria to screen the statistically significant DE-miRNAs. StarBaseV3.0 was used to predict the target genes of the DE-miRNAs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses of target genes of DE-miRNAs were carried out using DAVID. The STRING database was applied to estimate the correlations between target genes. Analysis of hubgenes by coremine and The Human Protein Atlas (THPA). Initial expression validations of miR-424 and miR-491-5p, SMURF1 and BCL2L1 were carried out using clinical pathological specimens by RT-PCR. Results: A total of 13 Differential expression-miRNAs (DE-miRNAs) were identified in DDP chemoresistant cells, including 9 upregulated miRNAs and 4 downregulated miRNAs. SMURF1 and BCL2L1 were screened as the critical genes in DDP-resistant GC, which were regulated by miR-424 and miR-491-5p respectively. The results of validation of hub genes expression in GC tissues indicated that in DFS<1-year group, the expression of miR-424 decreased significantly, notably upregulated expression of SMURF1 was also detected. Conclusion: Our results implied that miR-424, as a tumor suppressor, could deregulate SMURF1 in DDP-resistant GC cells.

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Baicalein inhibits cell growth and increases cisplatin sensitivity of A549 and H460 cells via miR‐424‐3p and targeting PTEN/PI3K/Akt pathway

Cited by 66 publications

References 50 publications

Pectolinarigenin inhibits non‑small cell lung cancer progression by regulating the PTEN/PI3K/AKT signaling pathway

Pectolinarigenin inhibits non‑small cell lung cancer progression by regulating the PTEN/PI3K/AKT signaling pathway

HMT Inhibits Prostate Cancer Progression by Targeting PAK-1.

<p>MicroRNA-424 regulates cisplatin resistance of gastric cancer by targeting SMURF1 based on GEO database and primary validation in human gastric cancer tissues</p>

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