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Gene expression data from BM1 (1833) tumors that are wild type or overexpressing RKIP in a xenograft mouse model

ABSTRACT: RKIP is a metastasis suppressor that is lost or silenced in most metastatic cancers. Here we reintroduce RKIP exogenously into BM1 cells (bone-tropic derivative of MDA-MB-231 cells, also known as 1833) that lack RKIP expression, in order to study transcriptomic changes that lead to metastasis in vivo and identify actionable targets to be used in anti-metastatic treatment strategies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE128983 | GEO | 2021/05/12

REPOSITORIES: GEO

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MicroRNA expression array for 1833 cells expressing RKIP vs. control

Project description:RKIP has been implicated in suppression of breast tumor metastasis. Identification of microRNAs regulated by RKIP helps us to understand how RKIP suppresses tumor metastasis via its downstream target mircoRNAs and genes. Total RNA was extracted from 1833 cells expressing RKIP or control, respectively. Exiqon miRCURY LNA array v.11.0. was performed to identify the microRNAs regulated by RKIP.

2014-07-01 | E-GEOD-47366 | biostudies-arrayexpress

Gene expression data from 1833 cells expressing RKIP vs control

Project description:RKIP regulates human breast tumor metastasis. We use gene expression array analysis to identify genes regulated by RKIP in human breast cancer cells. Total RNAs were extracted from 1833 cells expressing mutant RKIP (S153E-RKIP, a more potent Raf-1 inhibitor) and vector control. Affymetrix GeneChip hgu133plus2.0 Arrays were performed to detail the gene expression and identify the genes regulated by RKIP in human breast cancer cells.

2014-07-01 | E-GEOD-47378 | biostudies-arrayexpress

1833 cells expressing RKIP vs control

Project description:1833 cells expressing RKIP vs control

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MicroRNA expression array for 1833 cells expressing RKIP vs. control

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Project description:The transcription factor BACH1 is a master regulator of human breast cancer metastasis. Here we use gene expression array analysis to identify and compare the genes regulated by BACH1 depletion in a metastatic human breast cancer cell line. Total RNAs were extracted from vector control 1833 cells or 1833 cells with shBACH mRNA BACH1 depletion. Affymetrix GeneChip Human Gene 1.0 ST Arrays were performed to detail the gene expression and identify the genes regulated by BACH1in metastatic human breast cancer cells.

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Effect of knockdown of RKIP(=PEBP1) on gene expression in mouse breast cancer cells

Project description:Raf-1 kinase inhibitor protein (RKIP = PEBP1) has been shown to negatively regulate signaling pathways including the MAPK and NFkappaB pathways involved in cancer progression and metastasis. RKIP acts as a suppressor of metastasis, but the exact mechanisms are unclear. In this study, knockdown of RKIP expression was used to identify the targets of RKIP expression. GSEA analysis identified interferon response genes as downregulated in the RKIP knockdown cells.

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Gene expression data from THP-1 cells expressing RKIP shRNA vs control

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Gene expression data from BM1 (1833) tumors that are wild type or overexpressing RKIP in a xenograft mouse model

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RKIP regulates differentiation-related features in melanocytic cells

Project description:Raf Kinase Inhibitor Protein (RKIP) has been extensively reported as an inhibitor of key signaling pathways involved in the aggressive tumor phenotype and shows decreased expression in several types of cancers. However, little is known about RKIP in melanoma or regarding its function in normal cells. We examined the role of RKIP in both primary melanocytes and malignant melanoma cells and evaluated its diagnostic and prognostic value. IHC analysis revealed a significantly higher expression of RKIP in nevi compared with early-stage (stage I-II, AJCC 8th) melanoma biopsies. Proliferation, wound healing, and collagen-coated transwell assays uncovered the implication of RKIP on the motility but not on the proliferative capacity of melanoma cells as RKIP protein levels were inversely correlated with the migration capacity of both primary and metastatic melanoma cells but did not alter other parameters. As shown by RNA sequencing, endogenous RKIP knockdown in primary melanocytes triggered the deregulation of cellular differentiation-related processes, including genes (i.e., ZEB1, THY-1) closely related to the EMT. Interestingly, NANOG was identified as a putative transcriptional regulator of many of the deregulated genes, and RKIP was able to decrease the activation of the NANOG promoter. As a whole, our data support the utility of RKIP as a diagnostic marker for early-stage melanomas. In addition, these findings indicate its participation in the maintenance of a differentiated state of melanocytic cells by modulating genes intimately linked to the cellular motility and explain the progressive decrease of RKIP often described in tumors.

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