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Functional Characterization of lncRNA152 as an Angiogenesis-Inhibiting Tumor Suppressor in Triple-Negative Breast Cancers

ABSTRACT: Functional Characterization of lncRNA152 as an Angiogenesis-Inhibiting Tumor Suppressor in Triple-Negative Breast Cancers

PROVIDER: PRJNA797014 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17609683.fastq.gz	Fastqsanger.gz
	SRR17609684.fastq.gz	Fastqsanger.gz
	SRR17609685.fastq.gz	Fastqsanger.gz
	SRR17609686.fastq.gz	Fastqsanger.gz
	SRR17609687.fastq.gz	Fastqsanger.gz

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Functional Characterization of lncRNA152 as an Angiogenesis-Inhibiting Tumor Suppressor in Triple-Negative Breast Cancers

Project description:Long non-coding RNAs have been implicated in many of the hallmarks of cancer. We previously annotated lncRNA152 (lnc152; a.k.a. DRAIC) and demonstrated its roles in proliferation, cell cycle progression, and regulation of the estrogen signaling pathway in breast cancer cells. Herein, we found that lnc152 is highly upregulated in luminal breast cancers, but is downregulated in triple-negative breast cancers (TNBC). Using a set of complementary experimental approaches, we found that knockdown of lnc152 promotes cell migration and invasion in luminal breast cancer cell lines. In contrast, ectopic expression of lnc152 inhibits growth, migration, invasion, and angiogenesis in TNBC cell lines. In xenograft studies in mice, lnc152 inhibited the growth and metastasis of TNBC cells. Transcriptome analysis of the xenografts indicated that lnc152 downregulates genes regulating cancer-related phenotypes, including angiogenesis. Using RNA-pull down assays coupled with LC-MS/MS analysis, we identified RBM47, a known tumor suppressor protein in breast cancer, as a lnc152-interacting protein. We found that lnc152 suppresses the aggressive phenotypes of TNBC cells by regulating the expression of RBM47. Collectively, our results demonstrate that lnc152 is an angiogenesis-inhibiting tumor suppressor that attenuates the aggressive cancer-related phenotypes found in TNBC.

2022-11-09 | GSE193634 | GEO

Functional Characterization of lncRNA152 as an Angiogenesis-Inhibiting Tumor Suppressor in Triple-Negative Breast Cancers.

Project description: Not available

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Loss of the Tumor Suppressor FLCN Promotes Breast Tumor Growth by Inducing a TFE3-Dependent Program Driving Warburg Effect and Angiogenesis

Project description:Growing tumors exist in metabolically compromised environments that require activation of multiple pathways to scavenge nutrients to support accelerated rates of growth. The FLCN tumor suppressor complex (FLCN, FNIP1, FNIP2) has been implicated in the regulation of energy homeostasis via two metabolic master kinases: AMPK and mTORC1. Loss-of-function mutations of the FLCN tumor suppressor complex have only been reported in renal tumors in patients with the rare Birt-Hogg-Dube syndrome. Here we reveal that FLCN, FNIP1, and FNIP2 are downregulated in many human cancers including poor prognosis invasive basal-like breast carcinomas where AMPK and TFE3 targets are activated compared to the luminal, less aggressive subtypes. We show that FLCN loss in luminal subtypes promotes tumor growth through TFE3 activation and subsequent induction of several pathways including autophagy, lysosomal biogenesis, aerobic glycolysis, and angiogenesis. Strikingly, induction of aerobic glycolysis and angiogenesis in FLCN deficient cells was dictated by the activation of PGC-1⍺/HIF-1⍺ pathway, which we show to be TFE3-dependent, directly linking TFE3 to Warburg metabolic reprogramming and angiogenesis. Thus, FLCN loss induces TFE3-dependent breast tumor growth through activation of multiple mechanisms, including previously unreported roles in aerobic glycolysis and angiogenesis. These findings could point to a general role of a deregulated FLCN/TFE3 tumor suppressor pathway in human cancers.

2020-12-23 | GSE163791 | GEO

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Transcriptional regulation by Fra-1 in triple negative breast cancers

Project description:This SuperSeries is composed of the SubSeries listed below. All the data are described in the article "Fra-1 regulates its target genes via binding to remote enhancers without exerting major control on chromatin architecture in triple negative breast cancers" by Bejjani et al.

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Transcriptional regulation by Fra-1 in triple negative breast cancers

Project description:Transcriptional regulation by Fra-1 in triple negative breast cancers

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Project description:Expression data from patient-derived xenografts of human triple-negative breast cancers

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Moringa oleifera concentrate as a complementary treatment in triple negative breast cancer

Project description:Using a rodent xenograft model of triple negative breast cancer (MDA-MB-231 cells), diet induced obesity, and insulin resistance, the aim of this study is to evaluate the effects of moringa (MC) on improving insulin sensitivity and inhibiting angiogenesis as a dual mechanism by which the efficacy of antineoplastic treatment by standard of care chemotherapy is augmented in vivo.

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CUL4B functions as a tumor suppressor in KRAS-driven lung tumor by inhibiting recruitment of myeloid-derived suppressor cells

Project description:Lung cancer is the leading cause of cancer-related death worldwide. KRAS mutations are the most common oncogenic alterations found in lung cancer. Unfortunately, treating KRAS-mutant lung adenocarcinoma (ADC) remains a major challenge in cancer treatment of directly inhibiting the KRAS oncoprotein, indicating the need for understanding the regulatory mechanism with this molecular profile. Here, we used both autochthonous and transplantable KRAS mutant tumor models to investigate the role of tumor-derived CUL4B in KRAS-driven lung cancers. We show that knockout or knockdown of CUL4B promotes lung adenocarcinoma growth and progression in both two models. Mechanistically, CUL4B directly binds to the promoter of Cxcl2 and epigenetically represses its transcription. CUL4B deletion increases the expression of CXCL2, which binds to CXCR2 on myeloid-derived suppressor cells (MDSCs) and promotes their migration to the tumor microenvironment, and in turn, suppresses anti-tumor immunity. Targeting MDSCs with anti-Gr-1 neutralizing antibody or treatment with CXCR2 antagonist SB265610 significantly suppresses MDSCs infiltration and delayed the growth of CUL4B knockdown KRAS mutant lung adenocarcinoma tumors. Moreover, a negative correlation between CUL4B and CXCL2 expression was observed in high-stage KRAS mutant lung ADC patients. Collectively, our study provides mechanistic insights into the novel tumor suppressor-like functions of CUL4B in regulating the KRAS-driven lung tumor development.

2026-01-15 | GSE222940 | GEO

Comparative Characterization of 3D Chromatin Organization in Triple-Negative Breast Cancers

Project description:Comparative Characterization of 3D Chromatin Organization in Triple-Negative Breast Cancers

| PRJNA703390 | ENA