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SIPA1 Functions as a Transcription Regulator to Sustain Progression of Triple-Negative Breast Cancer

ABSTRACT: SIPA1 Functions as a Transcription Regulator to Sustain Progression of Triple-Negative Breast Cancer

PROVIDER: PRJNA915946 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22892100_1.fastq.gz	Fastqsanger.gz
	SRR22892100_2.fastq.gz	Fastqsanger.gz
	SRR22892101_1.fastq.gz	Fastqsanger.gz
	SRR22892101_2.fastq.gz	Fastqsanger.gz
	SRR22892102_1.fastq.gz	Fastqsanger.gz

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SIPA1 Functions as a Transcription Regulator to Sustain Progression of Triple-Negative Breast Cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-12-31 | GSE221743 | GEO

Exploring mechanism the transcription factor SIPA1 promote the progression of triple-negative breast cancer

Project description:To further study the regulation of SIPA1 on cells, the transcriptome sequencing on BT549 cells, BT549/shSIPA1 cells and si-dDBR cells were performed. We then performed gene expression profiling analysis using data obtained from RNA-seq of BT549 cells, BT549/shSIPA1 cells and si-dDBR cells to find the genes regulated by SIPA1.

2022-12-31 | GSE221742 | GEO

SIPA1 expression in breast cancer patient

Project description:To study the expression of SIPA1 in patients with metastatic triple-negative breast cancer, we obtained a subcutaneous metastatic sample from a patient with stage III triple-negative breast cancer and performed single-cell transcriptome sequencing

2022-12-31 | GSE221731 | GEO

Role of SIPA1 in chemotherapy resistance in breast cancer cells

Project description:SIPA1 is a potential transcriptional modulator of tumor metastasis and recurrence. Here we showed that the breast cancer patients with higher SIPA1 expression have a higher relapse rate and worse prognosis, especially for triple-negative breast cancer (TNBC) patients. Moreover, SIPA1 expression was found positively correlated with relapse of breast cancer patients receiving adjuvant chemotherapy. In a TNBC cell line MDA-MB-231, we identified the possible tumorigenesis and metastasis processes regulated by SIPA1, and demonstrated that SIPA1 promoted cancer stem-like feature to form tumourspheres. Tumoursphere-formed MDA-MB-231 cells were shown to be resistant to epirubicin. Then we confirmed that SIPA1 could particularly activate the CD44 promoter and upregulate CD44 expression. Furthermore, SIPA1 could promote ABCB1 expression and strengthen chemoresistance of MDA-MB-231 cells to epirubicin. In conclusion, SIPA1 is a risk factor for highly-relapse in TNBC patients and a transcriptional regulator to maintain cancer stem-like features and promote chemoresistance in breast cancer cells.

2018-12-25 | GSE124344 | GEO

Exploring mechanism the transcription factor SIPA1 promote the progression of triple-negative breast cancer

Project description:Exploring mechanism the transcription factor SIPA1 promote the progression of triple-negative breast cancer

| PRJNA915947 | ENA

Cilia locally synthesize proteins to sustain their ultrastructure and functions

Project description:Cilia locally synthesize proteins to sustain their ultrastructure and functions

| PRJNA745942 | ENA

SIPA1 Regulates LINC01615 to Promote Metastasis in Triple-Negative Breast Cancer.

Project description:Long non-coding RNAs (lncRNAs) are reported to play an important regulatory effect in carcinogenesis and malignancy. We found by high-throughput sequencing that LINC01615 is upregulated in breast cancer patients and reduces patients' overall survival. In vivo and in vitro experiments, we clarified that overexpression of LINC01615 can promote breast cancer cell metastasis ability. The expression of LINC01615 is regulated by the transcriptional activator SIPA1, thereby promoting carcinogenesis in breast cancer cells. Our research clarified that LINC01615 can act as an oncogenic factor in promoting the development of breast cancer.

| S-EPMC9562673 | biostudies-literature

SIPA1 expression in breast cancer patient

Project description:SIPA1 expression in breast cancer patient

| PRJNA915622 | ENA

A novel transcription factor SIPA1: identification and verification in triple-negative breast cancer.

Project description:Transcription factors (TFs) regulate the expression of genes responsible for cell growth, differentiation, and responses to environmental factors. In this study, we demonstrated that signal-induced proliferation-associated 1 (SIPA1), known as a Rap-GTPase-activating protein, bound DNA and served as a TF. Importin β1 was found to interact with SIPA1 upon fibronectin treatment. A TGAGTCAB motif was recognized and bound by DNA-binding region (DBR) of SIPA1, which was confirmed by electrophoretic mobility shift assay. SIPA1 regulated the transcription of multiple genes responsible for signal transduction, DNA synthesis, cell adhesion, cell migration, and so on. Transcription of fibronectin 1, which is crucial for cell junction and migration of triple-negative breast cancer (TNBC) cells, was regulated by SIPA1 in a DBR-dependent manner both in vivo and in vitro. Furthermore, single-cell transcriptome sequencing analysis of specimens from a metastatic TNBC patient revealed that SIPA1 was highly expressed in metastatic TNBC. Hence, this study demonstrated that SIPA1 served as a TF, promoting TNBC migration, invasion, and metastasis.

| S-EPMC10457189 | biostudies-literature

HMGA1: A master regulator of tumor progression in triple-negative breast cancer cells

Project description:Emerging evidence suggests that tumor cells metastasize by co-opting stem cell transcriptional networks, although the molecular underpinnings of this process are poorly understood. Here, we show for the first time that the high mobility group A1 (HMGA1) gene drives metastatic progression in triple negative breast cancer cells (MDA-MB-231) by reprogramming cancer cells to a stem-like state. We discovered an HMGA1 signature in triple negative breast cancer cells that is highly enriched in embryonic stem cells. Together, these findings indicate that HMGA1 is a master regulator of tumor progression in breast cancer by reprogramming cancer cells through stem cell transcriptional networks. Future studies are needed to determine how to target HMGA1 in therapy. HMGA1 was knocked-down in MDA-MB-231 cells using siRNA as we previously described (Tesfaye A 2007). RNA from three independent knockdown experiements along with 3 control populations were collected by Rneasy miniprep (Qiagen) and analyzed by Affymetrix Human Exon 1.0 ST platform.

2015-02-18 | E-GEOD-45483 | biostudies-arrayexpress

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