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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:Long noncoding RNAs have been implicated in many of the hallmarks of cancer. Herein, we found that the expression of lncRNA152 (lnc152; a.k.a. DRAIC), which we annotated previously, is highly upregulated in luminal breast cancer (LBC) and downregulated in triple-negative breast cancer (TNBC). Knockdown of lnc152 promotes cell migration and invasion in LBC cell lines. In contrast, ectopic expression of lnc152 inhibits growth, migration, invasion, and angiogenesis in TNBC cell lines. In mice, lnc152 inhibited the growth of TNBC cell xenografts, as well as metastasis of TNBC cells in an intracardiac injection model. Transcriptome analysis of the xenografts indicated that lnc152 downregulates genes controlling angiogenesis. Using pull down assays followed by LC/MS-MS, we identified RBM47, a known tumor suppressor in breast cancer, as a lnc152-interacting protein. The effects of lnc152 in TNBC cells are mediated, in part, 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.ImplicationsThis study identifies lncRNA152 as an angiogenesis-inhibiting tumor suppressor that attenuates the aggressive cancer-related phenotypes found in TNBC by upregulating the expression of the tumor suppressor RBM47. As such, lncRNA152 may serve as a biomarker to track aggressiveness of breast cancer, as well as therapeutic target for treating TNBC.

| S-EPMC9633386 | biostudies-literature

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

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.

2021-02-23 | GSE146825 | GEO

BRCAness, SLFN11 and RB1 loss predict response to topoisomerase I inhibitors in triple negative breast cancers

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

2019-12-28 | GSE142639 | GEO

Transcriptional regulation by Fra-1 in triple negative breast cancers

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

| PRJNA612051 | ENA

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.

2021-10-06 | GSE178973 | 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

ACE2 Enhances Sensitivity to PD-L1 Blockade by Inhibiting Macrophage-Induced Immunosuppression and Angiogenesis

Project description:ACE2 Enhances Sensitivity to PD-L1 Blockade by Inhibiting Macrophage-Induced Immunosuppression and Angiogenesis

| PRJNA1170888 | ENA

Single cell RNA-seq of 25 thousand epithelial cells from xenografts of triple-negative breast cancers

Project description:Patient derived xenografts (PDX) were created from two triple-negative breast cancers (PDX-110 and PDX-332) taken at the time of surgery from drug-naive patients. Freshly sorted epithelial cells were profiled by single-cell RNA-seq (scRNA-seq) using a 10X Genomics Chromium System.

2019-02-26 | GSE123926 | GEO

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