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KRAS drives lung cancer metastasis through lncRNA-mediated transcriptional and post-transcriptional regulation

ABSTRACT: KRAS drives lung cancer metastasis through lncRNA-mediated transcriptional and post-transcriptional regulation

PROVIDER: PRJNA512868 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8392900_1.fastq.gz	Fastqsanger.gz
	SRR8392900_2.fastq.gz	Fastqsanger.gz
	SRR8392910_1.fastq.gz	Fastqsanger.gz
	SRR8392910_2.fastq.gz	Fastqsanger.gz
	SRR8392920.fastq.gz	Fastqsanger.gz

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KRAS drives lung cancer metastasis through lncRNA-mediated transcriptional and post-transcriptional regulation

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

2020-12-17 | GSE124631 | GEO

Oncogenic KRAS drives lipo-fibrogenesis to promote angiogenesis and colon cancer progression

Project description:Oncogenic KRAS (KRAS*) contributes to many cancer hallmarks. In colorectal cancer (CRC), KRAS* has been shown to suppress anti-tumor immunity which promotes tumor metastasis. Here, we show that the protumor actions of KRAS* extend to the adipogenic transformation of fibroblasts into lipid-laden cancer-associated fibroblasts (CAFs), which spur angiogenesis. Mechanistically, KRAS*-mediated activation of the transcription factor CP2 (TFCP2) resulted in TFCP2-mediated transcriptional upregulation of pro-adipogenic factors BMP4 and WNT5B to drive lipid-rich CAF transformation. Functionally, these lipid-rich CAFs promoted tumor growth via their production of vascular endothelial growth factor A (VEGFA). Correspondingly, genetic and pharmacological neutralization of TFCP2 decreased the abundance of lipid-rich CAFs, reduced tumor angiogenesis, and increased survival in an autochthonous KRAS*–driven CRC mouse model. These murine findings mirror translational profiles in human CRC. Thus, KRAS* transforms the stromal cell state to promote tumor angiogenesis and disease progression, providing an actionable therapeutic intervention for KRAS*–driven CRC.

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KRas targeting by clinically significant miR-193a-3p inhibits mutant KRas lung cancer growth, circulating tumor cells and metastasis in vivo

Project description:Ras family oncogenes are mutated in approximately 30% of human cancers and cause resistance to multiple treatment modalities. While identifying methods to directly target mutant KRas have been challenging, targeting regulators of KRas may be beneficial. Using a systems approach of integrating a genome-wide miRNA screen with patient data of a phospho-proteomic signature of the KRas downstream pathway, we identified miR-193a-3p as a potent tumor suppressor capable of reversing KRas-related signaling, whereby the 3’UTR of KRas is directly targeted via two miR-193a-3p binding sites. Mechanistic studies revealed that miR-193a-3p inhibited the KRas protein signature, KRas downstream transcriptomic network, proliferation, induced a G1 arrest, and reduced colony formation in 3D cultures through direct targeting of KRas. An ex vivo lung cancer model showed that miR-193a-3p significantly reduced the viability of circulating tumor cells as well as decreased metastasis. In vivo studies revealed that miR-193a-3p significantly reduced tumor growth as well as metastasis of a KRas-mutant lung cancer xenograft model.

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Genome-wide analysis of long noncoding RNA (lncRNA) expression in colorectal cancer tissues from patients with liver metastasis

Project description:We performed a genome-wide analysis of lncRNA expression to identify novel targets for the further study of liver metastasis in CRC. Samples obtained from CRC patients were analyzed using Arraystar human 8Ã?60K lncRNA/mRNA v3.0 microarrays chips to find differentially expressed lncRNAs and mRNAs; The results were confirmed by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The differentially expressed lncRNAs and mRNAs were identified through fold-change filtering. Gene ontology (GO) and pathway analyses were performed using standard enrichment computational methods. Twelve primary CRC samples were obtained from six patients with CRC and liver metastasis (Exp G) and six patients with CRC without metastasis (Ctrl G).

2016-05-18 | E-GEOD-75050 | biostudies-arrayexpress

A novel metastasis–associated lncRNA destabilizes p21 through cooperative interactions with the NF90/NF45 complex

Project description:Long non-coding RNAs (lncRNA) have emerged as important regulators of gene expression at both the transcriptional and post-transcriptional levels. While altered expressions of lncRNAs have been observed in breast cancer (BCa) development, their roles in BCa progression and metastasis are still poorly understood. To identify novel BCa-associated lncRNA candidates, we have employed a high-density SNP array based approach to uncover lncRNA genes at intergenic region that are aberrantly expressed in BCa. Here we report the role of a novel lncRNA, LincIN, in breast cancer progression and metastasis. High levels of LincIN expression are frequently observed in tumors compared to adjacent normal tissues, and are strongly associated with aggressive breast cancers. Importantly, analysis of The Cancer Genome Atlas (TCGA) data further suggested that high LincIN expression was associated with poor overall survival in patients with breast cancer (P<0.05). Our gain-and-loss experiments demonstrate that LincIN play a role in tumor cell migration and invasion and knockdown of LincIN diminishes tumor cell invasion in vitro and lung metastasis in a mouse xenograft model. We also identified a LincIN-binding protein complex, NF90/NF45, through which LincIN destabilizes tumor suppressor p21 mRNA post-transcriptionally and thereby represses its protein expression. In summary, our findings delineated an oncogenic role of LincIN in breast tumor progression-metastasis, and mechanistically uncovered its cooperative actions with NF90/NF45 in regulating tumor suppressor gene expression at the post-transcriptional level.

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2016-01-12 | E-GEOD-67647 | biostudies-arrayexpress

lncRNA expression of CRC liver metastasis

Project description:The purpose of this study is to identify lncRNAs involved in the pathology of colorectal cancer (CRC) liver metastasis and investigate their underlying mechanisms. A total of 439 miRNAs were identified to be differentially expressed between 7 primary CRC tissues with liver metastases and 8 CRC tissues without liver metastases from 15 patients by Arraystar lncRNA microarrays

2017-02-28 | GSE95423 | GEO

LHX9 rescues KRAS suppression through transcriptional regulation of YAP1 [RNA-Seq]

Project description:Oncogenic KRAS signaling is required for tumor survival in cancers that harbor KRAS mutations. We recently performed a genome-scale expression screen to identify genes that bypass KRAS dependency. Here we demonstrate that the developmental transcription factor LHX9 rescues KRAS suppression in vitro and xenograft models. Furthermore, LHX9 decreases cell sensitivity to KRASG12C and MEK1/2 inhibitors. LHX9 promotes transcriptional changes associated with KRAS. Importantly, YAP1 upregulation by LHX9 is required for the rescue of KRAS suppression. Together we identify LHX9 as a YAP1 transcriptional regulator that permits KRAS-dependent cells to proliferate without KRAS expression.

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LHX9 rescues KRAS suppression through transcriptional regulation of YAP1 [ChIP-Seq]

2018-12-01 | GSE116822 | GEO

Comparison of KRas;Atg5fl/+ and KRas;Atg5fl/fl pneumocytes

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