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Comprehensive molecular characterization of lung tumors implicates AKT and MYC signaling in adenocarcinoma to squamous cell transdifferentiation

ABSTRACT: Comprehensive molecular characterization of lung tumors implicates AKT and MYC signaling in adenocarcinoma to squamous cell transdifferentiation

PROVIDER: PRJNA938458 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23613208_1.fastq.gz	Fastqsanger.gz
	SRR23613208_2.fastq.gz	Fastqsanger.gz
	SRR23613209_1.fastq.gz	Fastqsanger.gz
	SRR23613209_2.fastq.gz	Fastqsanger.gz
	SRR23612410_1.fastq.gz	Fastqsanger.gz

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Comprehensive molecular characterization of lung tumors implicates AKT and MYC signaling in adenocarcinoma to squamous cell transdifferentiation [EPIC]

Project description:Comprehensive molecular characterization of lung tumors implicates AKT and MYC signaling in adenocarcinoma to squamous cell transdifferentiation [EPIC]

| PRJNA938466 | ENA

Comprehensive molecular characterization of lung tumors implicates AKT and MYC signaling in adenocarcinoma to squamous cell transdifferentiation [RNA-seq]

Project description:Comprehensive molecular characterization of lung tumors implicates AKT and MYC signaling in adenocarcinoma to squamous cell transdifferentiation [RNA-seq]

| PRJNA938465 | ENA

Comprehensive molecular characterization of lung tumors implicates AKT and MYC signaling in adenocarcinoma to squamous cell transdifferentiation

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

2023-02-28 | GSE226070 | GEO

Comprehensive molecular characterization of lung tumors implicates AKT and MYC signaling in adenocarcinoma to squamous cell transdifferentiation [EPIC]

Project description:To investigate molecular changes occurring during lung adenocarcinoma to squamous carcinoma transformation.

2023-02-28 | GSE226068 | GEO

Comprehensive molecular characterization of lung tumors implicates AKT and MYC signaling in adenocarcinoma to squamous cell transdifferentiation [RNA-seq]

Project description:To investigate molecular changes occurring during lung adenocarcinoma to squamous carcinoma transformation.

2023-02-28 | GSE226069 | GEO

Transdifferentiation of Rat Keratinocyte Progenitors to Corneal Epithelial Cells by Limbal Niche via the STAT3/PI3K/AKT signaling pathway

Project description:PURPOSE. To develop a method for enriching keratinocyte progenitor cells (KPCs) and establish a limbal niche (LN)-mediated transdifferentiation protocol to induce KPCs transdifferentiation into corneal epithelial cells. METHODS. Limbal niche cells (LNCs) were isolated from limbal tissues through enzymatic digestion and characterized. Conditioned medium from LNCs cultures was collected. KPCs were enriched by rapid adhesion of Matrigel and subsequently cultured in either an LNCs-conditioned medium supplemented with KSFM (LN-KS) or SHEM (LN-SH) for 14 days. Corneal-specific marker expression was assessed to evaluate transdifferentiation efficiency. Key transcription factors and signaling pathways involved in the transdifferentiation process were identified through single-cell and RNA sequencing, and validated using western blot and quantitative real-time PCR. RESULTS. Both LN-KS and LN-SH protocols successfully induced corneal epithelial cell transdifferentiation from KPCs, with LN-KS demonstrating higher efficiency in generating CK12+ and p63+ cells (p<0.001). RNA sequencing analysis and western blot have revealed significant activation of STAT3 and PI3K/AKT signaling pathways. Inhibition of STAT3 blocked PI3K/AKT activation and impaired corneal epithelial cell transdifferentiation. CONCLUSIONS. This study demonstrates the ability of LN to promote KPCs transdifferentiation into corneal epithelial cells in vitro, a process partially mediated by the STAT3 and PI3K/AKT signaling pathways.

2024-12-22 | GSE284499 | GEO

Transdifferentiation of lung adenocarcinoma in mice with Lkb1 deficiency to squamous cell carcinoma.

Project description:Lineage transition in adenocarcinoma (ADC) and squamous cell carcinoma (SCC) of non-small cell lung cancer, as implicated by clinical observation of mixed ADC and SCC pathologies in adenosquamous cell carcinoma, remains a fundamental yet unsolved question. Here we provide in vivo evidence showing the transdifferentiation of lung cancer from ADC to SCC in mice: Lkb1-deficient lung ADC progressively transdifferentiates into SCC, via a pathologically mixed mAd-SCC intermediate. We find that reduction of lysyl oxidase (Lox) in Lkb1-deficient lung ADC decreases collagen disposition and triggers extracellular matrix remodelling and upregulates p63 expression, a SCC lineage survival oncogene. Pharmacological Lox inhibition promotes the transdifferentiation, whereas ectopic Lox expression significantly inhibits this process. Notably, ADC and SCC show differential responses to Lox inhibition. Collectively, our findings demonstrate the de novo transdifferentiation of lung ADC to SCC in mice and provide mechanistic insight that may have important implications for lung cancer treatment.

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AKT but not MYC promotes reactive oxygen species-mediated cell death in oxidative culture

Project description:In addition to driving tumorigenesis, oncogenes can create metabolic vulnerabilities in cancer cells. Here, we tested how the oncogenes AKT and MYC affect the ability to shift between respiration and glycolysis. Using immortalized mammary epithelial cellsMCF10A, we discovered constitutively active AKT but not MYC induced cell death in galactose culture, where cells must rely on oxidative phosphorylation for energy generation. However, the negative effects of AKT were short-lived, and AKT-expressing cells recommenced growth after ~15 days in galactose culture. To identify the mechanisms regulating AKT-mediated cell death, we first used metabolomics and found that AKT cells dying in galactose culture exhibited upregulated glutathione metabolism. Next, using shotgun proteomics, we discovered AKT cells dying in galactose upregulated proteins related to nonsense-mediated mRNA decay (NMD), a known response to oxidative stress. We therefore measured levels of reactive oxygen species (ROS) and discovered galactose culture induced ROS only in cells expressing AKT. Additionally, we found thatdiscovered the ROS scavenger catalase rescued AKT-expressing cells from galactose culture-induced cell death. We then demonstrated that breast cancer cell lines with constitutively active AKT signaling also exhibited cell death in galactose culture and rescue by catalase. Together, our results demonstrate that AKT but not MYC induces a metabolic vulnerability in cancer cells, namely the that restricted flexibility to use oxidative phosphorylation.

2020-03-19 | PXD015122 | Pride

Histone modifications along transdifferentiation from B cell to macrophage

Project description:Transdifferentiation of BLaER1 B cell into macrophages is an appropriate model to understand how chromatin behaves along a dynamic process. With this purpose, we have performed chromatin immunoprecipitation experiments of two histone modifications associated to active enhancer activity along 4 time points of BLaER1 transdifferentiation.

2020-05-08 | E-MTAB-9010 | biostudies-arrayexpress

Study of Akt Inhibitor MK2206 in Patients With Relapsed Lymphoma

Project description:This phase II clinical trial studies how well Akt inhibitor MK2206 works in treating patients with relapsed lymphoma. Akt inhibitor MK2206 may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth.

| 2099453 | ecrin-mdr-crc

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