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WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE113289 | GEO | 2019/12/17

REPOSITORIES: GEO

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WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway [ChIP-seq]

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WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway [RNA-seq PDX]

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WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway [RNA-seq CCL]

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WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway

Project description:WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway

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WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway [ChIP-seq]

Project description:WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway [ChIP-seq]

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WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway [RNA-seq CCL]

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WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway [RNA-seq PDX]

Project description:WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway [RNA-seq PDX]

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HMGA2/TET1/HOXA9 pathway regulates breast cancer growth and metastasis.

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-06-03 | E-GEOD-43741 | biostudies-arrayexpress

KIN17 promotes tumor metastasis by activating EMT signaling in luminal-A breast cancer.

Project description:BackgroundBreast cancer (BC), the most common cause of cancer death in women, overtook lung cancer as the leading cause of cancer worldwide in 2020. Although many studies have proposed KIN17 as a biomarker of tumorigenesis in different cancer types, its role in tumor metastasis, particularly in BC metastasis, has been underexplored. This study aimed to explore the role of KIN17 in BC metastasis.MethodsSurvival analyses was performed to identify the association between KIN17 expression and BC patient survival in silico. Using lentivirus constructs, we developed bidirectional KIN17 expression (KD, knockdown; OE, overexpression) cellular models of luminal-A (Lum-A) breast cancer MCF-7 cells. We performed in vitro wound healing, transwell with and without Matrigel assays, and in vivo tail-vein metastasis assay to evaluate the migration and invasion abilities of MCF-7 with stable KIN17 knockdown or overexpression. Western blotting was performed to compare the changes in protein expression.ResultsWe found that KIN17 expression was associated with poor overall survival (OS), relapse-free survival (RFS), distant metastasis-free survival (DMFS) and post-progression survival (PPS), particularly in Lum-A breast cancer patients. Later, we found that KIN17 knockdown inhibited migration and invasion of MCF-7 cells via regulating EMT-associated signaling pathways in vitro and decreases metastatic spread of the disease in vivo. In contrast, KIN17 overexpression promoted migration and invasion of MCF-7 cells in vitro and increased the metastatic spread of the disease in vivo.ConclusionsOverall, our findings provide preliminary data which suggests KIN17 of importance to target in metastatic Lum-A patients.

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RUNX1 promotes tumour metastasis by activating the Wnt/?-catenin signalling pathway and EMT in colorectal cancer.

Project description:BACKGROUND:Runt-related transcription factor 1 (RUNX1) plays the roles of an oncogene and an anti-oncogene in epithelial tumours, and abnormally elevated RUNX1 has been suggested to contribute to the carcinogenesis of colorectal cancer (CRC). However, the mechanism remains unclear. METHODS:The expression of RUNX1 in CRC and normal tissues was detected by real-time quantitative PCR and Western blotting. The effect of RUNX1 on CRC migration and invasion was conducted by functional experiments in vitro and in vivo. Chromatin Immunoprecipitation assay verified the direct regulation of RUNX1 on the promoter of the KIT, which leads to the activation of Wnt/?-catenin signaling. RESULTS:RUNX1 expression is upregulated in CRC tissues. Upregulated RUNX1 promotes cell metastasis and epithelial to mesenchymal transition (EMT) of CRC both in vitro and in vivo. Furthermore, RUNX1 can activate Wnt/?-catenin signalling in CRC cells by directly interacting with ?-catenin and targeting the promoter and enhancer regions of KIT to promote KIT transcription. These observations demonstrate that RUNX1 upregulation is a common event in CRC specimens and is closely correlated with cancer metastasis and that RUNX1 promotes EMT of CRC cells by activating Wnt/?-catenin signalling. Moreover, RUNX1 is regulated by Wnt/?-catenin. CONCLUSION:Our findings first demonstrate that RUNX1 promotes CRC metastasis by activating the Wnt/?-catenin signalling pathway and EMT.

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