scholarly journals NCAPG upregulation mediated by four microRNAs combined with activation of the p53 signaling pathway is a predictor of poor prognosis in patients with breast cancer

2021 ◽  
Vol 21 (4) ◽  
Author(s):  
Menglu Dong ◽  
Tao Xu ◽  
Xiaoqing Cui ◽  
Hanning Li ◽  
Xingrui Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Signaling Pathway ◽  
Poor Prognosis ◽  
P53 Signaling ◽  
P53 Signaling Pathway

scholarly journals Exploring the Mechanism of Baicalin Intervention in Breast Cancer Based on MicroRNA Microarrays and Bioinformatics Strategies

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Anqi Ge ◽  
Lifang Liu ◽  
Xian’guang Deng ◽  
Jun Luo ◽  
Yanghua Xu
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
Enrichment Analysis ◽  
Dependent Manner ◽  
P53 Signaling ◽  
Microrna Microarrays ◽  
P53 Signaling Pathway ◽  
Mcf 7

Objective. To explore the mechanism of baicalin intervention in breast cancer based on microRNA microarrays. Methods. The inhibitory rate of baicalin intervention in MCF-7 breast cancer cells was determined by MTT. Then, the miRNA microarrays were used to validate the key microRNAs. After that, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to validate microRNA, hsa-miR-15a, hsa-miR-100, hsa-miR-16, and hsa-miR-7t. Finally, the potential targets of these key microRNAs are predicted by miRWalk, and DAVID was utilized for gene ontology (GO) enrichment analysis and pathway enrichment analysis. Results. Baicalin may inhibit the proliferation of MCF-7 cells in a dose-dependent and time-dependent manner. The concentration of baicalin 150 μmol/L was determined for the subsequent miRNA chip research. A total of 92 upregulated microRNAs and 35 downregulated microRNAs were obtained. The upregulated miRNAs include hsa-miR-6799-5p, hsa-miR-6126, hsa-miR-4792, hsa-miR-6848-5p, hsa-miR-3197, hsa-miR-6779-5p, and hsa-miR -654-5p. The downregulated miRNAs include hsa-miR-3911, hsa-miR-504-5p, hsa-miR-30a-3p, hsa-miR-193b-3p, and hsa-miR-181b-5p. Then, differentially expressed miRNA was verified by qRT-PCR. The results showed that the expression of hsa-miR-15a, hsa-miR-100, hsa-miR-16, and hsa-let-7c was upregulated ( P < 0.05 ), which was consistent with the results of the miRNA microarray. The enrichment analysis showed that baicalin might regulate the DNA-templated proliferation, DNA-templated transcription, p53 signaling pathway, etc., of MCF-7 breast cancer cells through miRNA. Conclusion. Baicalin inhibits the proliferation of breast cancer cells. It may achieve antitumor effects through regulating microRNAs so as to affect the DNA replication (such as cellular response to DNA damage stimulus and DNA binding), RNA transcription (such as regulation of transcription, DNA-templated, transcription from RNA polymerase II promoter, and transcription factor binding), protein synthesis (such as mRNA binding, Golgi apparatus, and protein complex), endocytosis, pathways in cancer, p53 signaling pathway, and so on.

scholarly journals Folate-targeted PTEN/AKT/P53 signaling pathway promotes apoptosis in breast cancer cells

Pteridines ◽  
2020 ◽  
Vol 31 (1) ◽  
pp. 158-164
Author(s):  
Hexian Wang ◽  
Qiang Fan ◽  
Longlong Zhang ◽  
Danli Shi ◽  
Haibo Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Folic Acid ◽  
Cell Viability ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
P53 Protein ◽  
Specific Inhibitor ◽  
P53 Signaling ◽  
P53 Signaling Pathway

AbstractObjective Folate deficiency is closely related to the occurrence of human tumors and plays an important role in cell growth, differentiation, repair, and host defense. We studied the effects of folic acid on the apoptosis of breast cancer cells (MDA-MB-231) and on the activity of the PTEN/AKT/P53 signaling pathway in breast cancer cells.Methods Breast cancer cells (MDA-MB-231) were treated with folate alone or in combination with a PTEN specific inhibitor, SF1670. Cell viability was detected by a MTT assay, and the expression levels of apoptosis-related proteins and PTEN/AKT/P53 signaling pathway were detected via Western blot analysis. Rate of apoptosis was measured via cytometry.Results Folic acid inhibited the cell viability of MDAMB-231 cells and the expressions of Bcl-2 and p-AKT proteins and upregulate the expression of Bax, PTEN, and P53 proteins, thereby inducing apoptosis in these cells. SF1670 treatment inhibited the expressions of Bcl-2 and p-AKT protein and upregulate Bax, PTEN, and P53 protein expression.Conclusion Folic acid has cytotoxic effects on MDAMB-231 cells and can induce apoptosis by targeting the PTEN/AKT/P53 signaling pathway.

scholarly journals Evaluation of clinical value and potential mechanism of MTFR2 in lung adenocarcinoma via bioinformatics

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Cheng Chen ◽  
Yang Tang ◽  
Wen-Dong Qu ◽  
Xu Han ◽  
Jie-Bin Zuo ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Replication ◽  
Homologous Recombination ◽  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Poor Prognosis ◽  
Neoplasm Staging ◽  
Smoking History ◽  
P53 Signaling ◽  
P53 Signaling Pathway

Abstract Background Mitochondrial fission regulator 2 (MTFR2) was involved in the progression and development of various cancers. However, the relationship between MTFR2 with lung adenocarcinoma (LUAD) had not been reported. Herein, this study analyzed the clinical significance and potential mechanisms of MTFR2 in LUAD via bioinformatics tools. Results We found that the level of MTFR2 was increased, and correlated with sex, age, smoking history, neoplasm staging, histological subtype and TP53 mutation status in LUAD patients. Kaplan-Meier survival analysis showed LUAD patients with increased MTFR2 had a poor prognosis. In addition, univariate COX regression analysis showed neoplasm staging, T stage, distant metastasis and MTFR2 level were risk factors for the prognosis of LUAD. A total of 1127 genes were coexpressed with MTFR2, including 840 positive and 208 negative related genes. KEGG and GSEA found that MTFR2 participated in the progression of LUAD by affecting cell cycle, DNA replication, homologous recombination, p53 signaling pathway and other mechanisms. The top 10 coexpressed genes, namely CDK1, CDC20, CCNB1, PLK1, CCNA2, AURKB, CCNB2, BUB1B, MAD2L1 and BUB1 were highly expressed, and were associated with poor prognosis in LUAD. Conclusions Consequently, we elucidated MTFR2 was a biomarker for diagnosis and poor prognosis in LUAD, and might participate in the progression of LUAD via affecting cell cycle, DNA replication, homologous recombination and p53 signaling pathway.

scholarly journals Evaluation of clinical value and potential mechanism of MTFR2 in lung adenocarcinoma via bioinformatics

2020 ◽  
Author(s):  
Cheng Chen ◽  
Yang Tang ◽  
Wendong Qu ◽  
Xu Han ◽  
Jiebin Zuo ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Replication ◽  
Homologous Recombination ◽  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Poor Prognosis ◽  
Neoplasm Staging ◽  
Smoking History ◽  
P53 Signaling ◽  
P53 Signaling Pathway

Abstract Background Mitochondrial fission regulator 2 (MTFR2) was involved in the progression and development of various cancers. However, the relationship between MTFR2 with lung adenocarcinoma (LUAD) had not been reported. Herein, this study analyzed the clinical significance and potential mechanisms of MTFR2 in LUAD via bioinformatic tools. Results We found that the level of MTFR2 was increased, and correlated with sex, age, smoking history, neoplasm staging, histological subtype and TP53 mutation status in LUAD patients. Kaplan-Meier survival analysis showed LUAD patients with increased MTFR2 had a poor prognosis. In addition, univariate COX regression analysis showed neoplasm staging, T stage, distant metastasis and MTFR2 level were risk factors for the prognosis of LUAD. A total of 1127 genes were coexpressed with MTFR2, including 840 positive and 208 negative related genes. KEGG and GSEA found that MTFR2 participated in the progression of LUAD by affecting cell cycle, DNA replication, homologous recombination, p53 signaling pathway and other mechanisms. The top 10 coexpressed genes, namely CDK1, CDC20, CCNB1, PLK1, CCNA2, AURKB, CCNB2, BUB1B, MAD2L1 and BUB1 were highly expressed, and were associated with poor prognosis in LUAD. Conclusions Consequently, we elucidated MTFR2 was a biomarker for diagnosis and poor prognosis in LUAD, and might participate in the progression of LUAD via affecting cell cycle, DNA replication, homologous recombination and p53 signaling pathway.

scholarly journals Evaluation of Clinical Value and Potential Mechanism of MTFR2 in Lung Adenocarcinoma via Bioinformatics

2021 ◽  
Author(s):  
Cheng Chen ◽  
Yang Tang ◽  
Wendong Qu ◽  
Xu Han ◽  
Jiebin Zuo ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Replication ◽  
Homologous Recombination ◽  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Poor Prognosis ◽  
Neoplasm Staging ◽  
Smoking History ◽  
P53 Signaling ◽  
P53 Signaling Pathway

Abstract Background: Mitochondrial fission regulator 2 (MTFR2) was involved in the progression and development of various cancers. However, the relationship between MTFR2 with lung adenocarcinoma (LUAD) had not been reported. Herein, this study analyzed the clinical significance and potential mechanisms of MTFR2 in LUAD via bioinformatics tools.Results: We found that the level of MTFR2 was increased, and correlated with sex, age, smoking history, neoplasm staging, histological subtype and TP53 mutation status in LUAD patients. Kaplan-Meier survival analysis showed LUAD patients with increased MTFR2 had a poor prognosis. In addition, univariate COX regression analysis showed neoplasm staging, T stage, distant metastasis and MTFR2 level were risk factors for the prognosis of LUAD. A total of 1127 genes were coexpressed with MTFR2, including 840 positive and 208 negative related genes. KEGG and GSEA found that MTFR2 participated in the progression of LUAD by affecting cell cycle, DNA replication, homologous recombination, p53 signaling pathway and other mechanisms. The top 10 coexpressed genes, namely CDK1, CDC20, CCNB1, PLK1, CCNA2, AURKB, CCNB2, BUB1B, MAD2L1 and BUB1 were highly expressed, and were associated with poor prognosis in LUAD. Conclusions: Consequently, we elucidated MTFR2 was a biomarker for diagnosis and poor prognosis in LUAD, and might participate in the progression of LUAD via affecting cell cycle, DNA replication, homologous recombination and p53 signaling pathway.

scholarly journals Identifying the Effect of Ursolic Acid Against Triple-Negative Breast Cancer: Coupling Network Pharmacology With Experiments Verification

2021 ◽  
Vol 12 ◽  
Author(s):  
Yubao Zhang ◽  
Xiaoran Ma ◽  
Huayao Li ◽  
Jing Zhuang ◽  
Fubin Feng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Signaling Pathway ◽  
Ursolic Acid ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Gene Set Enrichment Analysis ◽  
Dependent Manner ◽  
P53 Signaling ◽  
P53 Signaling Pathway

Triple negative breast cancer (TNBC) is a subtype of breast cancer with complex heterogeneity, high invasiveness, and long-term poor prognosis. With the development of molecular pathology and molecular genetics, the gene map of TNBC with distinctive biological characteristics has been outlined more clearly. Natural plant extracts such as paclitaxel, vinblastine, colchicine etc., have occupied an important position in the treatment of hormone-independent breast cancer. Ursolic acid (UA), a triterpenoid acid compound derived from apple, pear, loquat leaves, etc., has been reported to be effective in a variety of cancer treatments, but there are few reports on the treatment of TNBC. This study performed comprehensive bioinformatics analysis and in vitro experiments to identify the effect of UA on TNBC treatment and its potential molecular mechanism. Our results showed that UA could not only reduce the proliferation, migration, and invasion in MDA-MB-231 and MDA-MB-468 cell lines with a dose-dependent manner but also induce cell cycle arrest and apoptosis. Meanwhile, we collected the gene expression data GSE45827 and GSE65194 from GEO for comparison between TNBC and normal cell type and obtained 724 DEGs. Subsequently, PLK1 and CCNB1 related to TNBC were screened as the key targets via topological analysis and molecular docking, and gene set enrichment analysis identified the key pathway as the p53 signaling pathway. In addition, quantitative real-time PCR and western blot verified the key genes were PLK1 and CCNB1. In vivo and in vitro experiments showed that UA could inhibit the growth of TNBC cells, and down-regulate the protein expression levels of PLK1 and CCNB1 by mediating p53 signaling pathway. These findings provide strong evidence for UA intervention in TNBC via multi-target therapy.

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