Microarray data analysis reveals gene expression changes in response to ionizing radiation in MCF7 human breast cancer cells

Bai, Jing; Luo, Youzhen; Zhang, Shengchu

doi:10.1186/s41065-020-00151-z

Cited by 7 publications

(4 citation statements)

References 50 publications

(48 reference statements)

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“…Forkhead box D1 (FOXD1), a member of the Forkhead family, was first identified in the forebrain neuroepithelium and has been demonstrated to be a vital gene participating in the development of the kidney and retina [ 4 ]. Previous studies have shown that FOXD1 also participates in the development of various cancers, including liver cancer [ 5 ], cervical cancer [ 6 ], pancreatic cancer [ 7 ], breast cancer [ 8 ], and glioma [ 9 ]. For instance, Sun et al found that lncRNA NORAD promotes cell stemness and angiogenesis in liver cancer by regulating the miR-211-5p/FOXD1/VEGF-A axis [ 5 ]; Cheng et al found that FOXD1 can determine the renewal ability and tumorigenicity of glioma through transcriptional regulation of ALDH1A3 [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

FOXD1 promotes EMT and cell stemness of oral squamous cell carcinoma by transcriptional activation of SNAI2

et al. 2021

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Background Epithelial-mesenchymal transition (EMT) and cell stemness are implicated in the initiation and progression of oral squamous cell carcinoma (OSCC). Revealing the intrinsic regulatory mechanism may provide effective therapeutic targets for OSCC. Results In this study, we found that Forkhead box D1 (FOXD1) was upregulated in OSCC compared with normal samples. Patients with a higher FOXD1 expression had a poorer overall survival and disease-free survival. Immunohistochemical staining results showed that FOXD1 expression was related to the clinical stage and relapse status of OSCC patients. When FOXD1 expression was knocked down in CAL27 and SCC25 cells, the migration, invasion, colony formation, sphere formation, and proliferation abilities decreased. Moreover, EMT and stemness-related markers changed remarkably, which indicated that the EMT process and cell stemness were inhibited. Conversely, overexpression of FOXD1 promoted EMT and cell stemness. Further study demonstrated that FOXD1 could bind to the promoter region and activate the transcription of SNAI2. In turn, the elevated SNAI2 affected EMT and cell stemness. An in vivo study showed that FOXD1-overexpressing CAL27 cells possessed a stronger tumorigenic ability. Conclusions Our findings revealed a novel mechanism in regulating EMT and cell stemness and proposed FOXD1 as a potential marker for the diagnosis and treatment of OSCC.

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Section: Introductionmentioning

confidence: 99%

FOXD1 promotes EMT and cell stemness of oral squamous cell carcinoma by transcriptional activation of SNAI2

et al. 2021

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“…Interestingly, microarray analysis demonstrated that STAT1 is co-expressed with ESCO2 and may regulate its transcription in breast cancer [24]. These ndings indicate a positive regulatory loop in which STAT1 increases ESCO2 expression, which further activates STAT1.…”

Section: Discussionmentioning

confidence: 94%

“…So far, our data have indicated that ESCO2 depletion signi cantly suppressed tumor growth in vitro and in vivo. In addition, a recent bioinformatics study indicated the potential signi cance of the STAT1/ESCO2 pathway in breast cancer [24]. It is reasonable to speculate that STAT1 may also be involved in ESCO2-associated tumorigenesis in HPC.…”

Section: Stat1-overexpression Suppressed Esco2-de Ciencymediated Tumo...mentioning

confidence: 98%

ESCO2 promotes hypopharyngeal carcinoma progression in a STAT1-dependent manner

Yan

Chen

et al. 2023

Preprint

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Background: The establishment of sister chromatid cohesion N-acetyltransferase 2 (ESCO2) is involved in the development of multiple malignancies. However, its role in hypopharyngeal carcinoma (HPC) progression remains uncharacterized. Methods: This study employed bioinformatics to determine the ESCO2 expression in head and neck squamous cell carcinoma (HNSC) and normal tissues. In vitro cell proliferation, migration, apoptosis, and/or cell cycle distribution assays were used to determine the function of ESCO2 and its relationship with STAT1. Xenograft models were established in nude mice to determine ESCO2 in HPC growth in vivo. Coimmunoprecipitation/mass spectrometry (Co-IP/MS) was conducted to identify the potential ESCO2 binding partners. Results: We found that ESCO2 expression was elevated in HNSC tissues, and ESCO2 depletion suppressed tumor cell migration in vitro and inhibited tumor growth in vitro and in vivo. Co-IP/MS and immunoblotting assays revealed the interaction between ESCO2 and STAT1 in HPC cells. ESCO2-mediated suppressive effects on HPC cell proliferation, viability, and migration were compromised by STAT1-overexpression. Conclusions: These findings suggest that ESCO2 is crucial in promoting HPC malignant progression through the STAT1 pathway, and provide novel therapeutic targets for HPC treatment.

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“… 30 Bai et al , revealed identified potential therapeutic target genes for breast cancer (BC) by the investigation of gene expression changes after ionizing radiation (IR) in BC cells, and found FOXD1 was one of the hub nodes in the transcriptional regulatory network of the overlapping DEGs. 31 Another bioinformatics analysis also revealed FOXD1 was the breast cancer survival related gene. 32 Zhao et al reported that FOXD1 was up-regulated in breast cancer tissues, and depletion of FOXD1 expression decreases the ability of cell proliferation and chemoresistance in MDA-MB-231 cells.…”

Section: Discussionmentioning

confidence: 99%

Investigation of Candidate Genes and Pathways in Basal/TNBC Patients by Integrated Analysis

Liu

Song

Liu

et al. 2021

Technol Cancer Res Treat

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Purpose: This study aims to identify the key pathway and related genes and to further explore the potential molecular mechanisms of triple negative breast cancer (TNBC). Methods: The transcriptome data and clinical information of breast cancer patients were downloaded from the TCGA database, including 94 cases of paracancerous tissue, 225 cases of Basal like type, 151 cases of Her2 type, 318 cases of Luminal type A, 281 cases of Luminal type B, and 89 cases of Normal Like type. The differentially expressed genes (DEGs) were identified based on the criteria of |logFC|≥1.5 and adjust P < 0.001.Their functions were annotated by gene ontology (GO) analysis and Kyoto Encyclopedia of differentially expressed genes & Genomes (KEGG) pathway analysis. Cox regression univariate analysis and Kaplan-Meier survival curves (Log-rank method) were used for survival analysis. FOXD1, DLL3 and LY6D were silenced in breast cancer cell lines, and cell viability was assessed by CCK-8 assay. Further, the expression of FOXD1, DLL3 and LY6D were explored by immunohistochemistry on triple negative breast tumor tissue and normal breast tissue. Results: A total of 533 DEGs were identified. Functional annotation showed that DEGs were significantly enriched in intermediate filament cytoskeleton, DNA−binding transcription activator activity, epidermis development, and Neuroactive ligand−receptor interaction. Survival analysis found that FOXD1, DLL3, and LY6D showed significant correlation with the prognosis of patients with the Basal-like type ( P < 0.05). CCK-8 assay showed that compared with Doxorubicin alone group, the cytotoxicity of Doxorubicin combined with siRNA-knockdown of FOXD1, DLL3, or LY6D was much significant. Conclusion: The DEGs and their enriched functions and pathways identified in this study contribute to the understanding of the molecular mechanisms of TNBC. In addition, FOXD1, DLL3, and LY6D may be defined as the prognostic markers and potential therapeutic targets for TNBC patients.

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Microarray data analysis reveals gene expression changes in response to ionizing radiation in MCF7 human breast cancer cells

Cited by 7 publications

References 50 publications

FOXD1 promotes EMT and cell stemness of oral squamous cell carcinoma by transcriptional activation of SNAI2

FOXD1 promotes EMT and cell stemness of oral squamous cell carcinoma by transcriptional activation of SNAI2

ESCO2 promotes hypopharyngeal carcinoma progression in a STAT1-dependent manner

Investigation of Candidate Genes and Pathways in Basal/TNBC Patients by Integrated Analysis

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