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

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

PROVIDER: PRJNA915947 | 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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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

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

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

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

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

| PRJNA915946 | ENA

SIPA1 expression in breast cancer patient

Project description:SIPA1 expression in breast cancer patient

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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.

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Triple therapy reduced metastasis in triple-negative breast cancer.

Project description:Triple therapy reduced metastasis in triple-negative breast cancer.

| PRJNA832953 | ENA

ADAR1 regulates growth & invasion in triple-negative breast cancer

Project description:ADAR1 catalyzes Adenosine-to-Inosine (A-to-I) editing of double-stranded RNA and regulates global expression output through its interactions with RNA and other proteins. ADARs play important roles in development and disease, and previous work has shown that ADAR1 is oncogenic in a growing list of cancer types. Here we show that ADAR1 is important for growth and invasion in triple negative breast cancer cells, as ADAR1 loss yields reduced growth, migration & invasion, and mammosphere formation. Global RNA-seq analyses demonstrate that ADAR1 regulates both coding and non-coding targets via expression level and/or A-to-I editing. We demonstrated that a recoding edit in FLNB (chr3:58156064) inhibits the tumor suppressive activities of the protein to promote growth & invasion. We show that several tumor suppressor microRNAs are also downregulated by ADAR1 to promote cell cycle progression and invasion. This work describes several novel mechanisms of ADAR1-mediated oncogenesis in triple negative breast cancer, providing support to strategies for targeting ADAR1 in this aggressive cancer type with few treatment options.

2022-03-14 | GSE177056 | GEO

Exploring the biological behavior and underlying mechanism of KITLG in triple-negative breast cancer.

Project description:The tyrosine-kinase receptor that is specified by the KIT locus is demarcated by KITLG. This multifaceted factor is instrumental during in-utero germ and neural cell maturation and hematopoiesis, ostensibly reflecting its role in facilitating cell migration. Concurrently, KITLG is prone to a mutation in germ cell tumors, entailing a presumed connection to tumorigenesis. Despite this, the intricacies of its function in breast cancer and the relevant mechanisms remain elusive. Multiple independent databases depict a consistently low expression of KITLG within tissues affected by triple-negative breast cancers (TNBC), a trend strongly coupled with reduced survival rates. Interestingly, non-triple-negative breast cancers exhibit a markedly high expression of KITLG compared to the norm. An initial analysis of the GEO database speculates that KITLG may serve as an oncogene suppressor in TNBC, hinting at varied roles for KITLG isoforms within this disease context. In conclusion, our preliminary analysis offers valuable insights into the role and expression pattern of KITLG in TNBC. We provide evidence supporting its consideration as a promising new prognostic marker, thereby potentially enriching therapeutic strategies for TNBC. Indeed, given the limited advances in molecularly targeted therapy for TNBC, a significant need exists for a more precise therapeutic approach and a comprehensive understanding of its inherent mechanisms of action.

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