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Homo sapiens

ABSTRACT: MicroRNA-224 promotes tumor progression in non-small cell lung cancer

PROVIDER: PRJNA272417 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1752090.fastq.gz	Fastqsanger.gz
	SRR1752091.fastq.gz	Fastqsanger.gz
	SRR1752092.fastq.gz	Fastqsanger.gz
	SRR1752093.fastq.gz	Fastqsanger.gz
	SRR1752094.fastq.gz	Fastqsanger.gz

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MicroRNA-224 promotes tumor progression in non-small cell lung cancer

Project description:Lung cancer is the leading cause of cancer-related deaths worldwide. Despite advancements and improvements in surgical and medical treatments, the survival rate of lung cancer patients remains frustratingly poor. Local control for early stage non-small cell lung cancer (NSCLC) has dramatically improved over the last decades for both operable and inoperable patients. However, the molecular mechanisms of NSCLC invasion leading to regional and distant disease spread remain poorly understood. Here we identify miR-224 to be significantly up-regulated in NSCLC tissues, in particular in resected NSCLC metastasis. Increased miR-224 expression promotes cell migration, invasion and proliferation by directly targeting the tumor suppressors, TNFAIP1 and SMAD4. In concordance with in vitro studies, mouse xenograft studies validated that miR-224 function as a potent oncomiR in NSCLC in vivo. Moreover, we found promoter hypomethylation and activated ERK signaling to be involved in the regulation of miR-224 expression in NSCLC. Up-regulated mir-224 thus facilitates tumor progression by shifting the equilibrium of the partially antagonist functions of SMAD4 and TNFAIP1 towards enhanced invasion and growth in NSCLC. Our findings indicate that targeting miR-224 could be effective in the treatment of certain lung cancer patients Oncogenic role of miR-224 in lung cancer

2015-07-01 | E-GEOD-64859 | biostudies-arrayexpress

MicroRNA-224 promotes tumor progression in non-small cell lung cancer

2015-07-01 | GSE64859 | GEO

TMT-based phosphoproteomic analysis of ALK-positive patient-derived lung cancer cell lines with GUK1 phospho-null mutation and ALK TKI treatment

Project description:The metabolic adaptations observed in cancer are widely recognized, yet the precise mechanisms of how these metabolic adjustments support tumor growth remain unclear. This study explores the impact of guanine nucleotide metabolism on cancer progression in ALK-driven lung cancer. We showed that GUK1 phosphorylation at Y74 augments guanine nucleotide synthesis and promotes tumor growth in ALK-driven lung cancer both in vitro and in vivo. Using 16-plex TMT-phosphoproteomics, we investigated the effect of the ALK tyrosine kinase inhibitor lorlatinib on patient-derived non-small cell lung cancer cell lines with and without GUK1 Y74F mutation, thus shedding light on signaling and metabolic pathways reliant on GUK1 phosphorylation in ALK-driven lung cancer cells.

2025-02-03 | PXD049284 | Pride

Dickkopf-1 promotes tumor progression of gefitinib- resistant non-small cell lung cancer through cancer cell-fibroblast interactions

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Postoperative circulating tumor DNA monitoring for stage I-III non-small cell lung cancer

Project description:The target sequecing vcf data of tumor and curculating tumor DNA for non-small cell lung cancer patients.

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Homo sapiens

Project description:CKAP2L promotes non-small cell lung cancer progression through regulation of transcription elongation

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Project description:Heterogeneous Tumor Microenvironment of Non-Small Cell Lung Cancer

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Project description:Heterogeneous Tumor Microenvironment of Non-Small Cell Lung Cancer

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Project description:Heterogeneous Tumor Microenvironment of Non-Small Cell Lung Cancer

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NFIB is a driver of SCLC initiation, progression and metastasis in mouse and marks metastatic disease in patients

Project description:Small Cell Lung Cancer (SCLC) is the most aggressive type of lung cancer with early metastatic dissemination and invariable development of resistant disease for which no effective treatment is available to date. Mouse models of SCLC based on inactivation of Rb1 and Trp53 developed earlier showed frequent amplifications of two transcription factor genes: Nfib and Mycl. Overexpression of Nfib but not Mycl in SCLC mouse results in an enhanced and altered metastatic profile, and appears to be associated with genomic instability. NFIB promotes tumor heterogeneity with the concomitant expansive growth of poorly differentiated, highly proliferative, and invasive tumor cell populations. Consistent with the mouse data, NFIB expression in high-grade human neuroendocrine carcinomas correlates with advanced stage III/IV disease warranting its further assessment as a potentially valuable progression marker in a clinical setting. Genomic DNA from mouse small cell lung tumor samples was analyzed by mate pair sequencing and low coverage sequencing. And RNA from Nfib overexpressing mouse small cell lung cancer cell lines was further analyzed for high quality RNA profiles using Illumina Hiseq2500. This series contains only RNA-seq data.

2016-07-29 | E-GEOD-82005 | biostudies-arrayexpress

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