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SRCAP mutation promotes cutatneous squamous cell carcinoma invasion [RNA-Seq]

ABSTRACT: SRCAP mutation promotes cutatneous squamous cell carcinoma invasion [RNA-Seq]

PROVIDER: PRJNA1237315 | ENA |

REPOSITORIES: ENA

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SRCAP mutation promotes cutatneous squamous cell carcinoma invasion [RNA-Seq]

Project description:In this study, we identify a mutational hotspot affecting SRCAP in cancer and that SRCAP is recurrently mutated in keratinocyte carcinomas. When introduced to primary human epidermal keratinocytes, the SRCAP hotspot mutation dysregulates gene expression in the differentiated state far more than the progenitor state. Gene dysregulation occurs without a change in H2A.Z chromatin occupancy. Finall, the presence of the SRCAP mutation in a RAS-CDK4 driven model of cSCC increases invasion significantly.

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SRCAP mutation promotes cutatneous squamous cell carcinoma invasion [ChIP-Seq]

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SRCAP mutation promotes cutatneous squamous cell carcinoma invasion [ChIP-Seq]

Project description:SRCAP mutation promotes cutatneous squamous cell carcinoma invasion [ChIP-Seq]

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Apolipoprotein E promotes invasion in oral squamous cell carcinoma

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Downregulation of miR-218-5p promotes invasion of oral squamous cell carcinoma cells via activation of CD44-ROCK signaling

Project description:The invasion front of oral squamous cell carcinoma (OSCC) harbors the most aggressive cells of the tumor and is critical for cancer invasion and metastasis. MicroRNAs (miRNAs) play an important role in regulating OSCC invasion. In this study, we modeled the OSCC invasion front on a microfluidic chip and investigated differences in miRNA profiles between cells in the invasion front and those in the tumor mass by small RNA sequencing and bioinformatic analysis. We found that miR-218-5p was downregulated in invasion front cells; a luciferase reporter assay confirmed that cluster of differentiation (CD)44 was a direct target of miR-218-5p. Inhibiting miR-218-5p in invasion front cells activated CD44- Rho-associated protein kinase (ROCK) signaling and promoted cell invasion by inducing cytoskeletal reorganization. These findings indicate that miR-218-5p negatively regulates OSCC invasiveness by targeting the CD44–ROCK pathway and may be a useful therapeutic target for OSCC. Moreover, our method of modeling and isolating invasion front cells using a microfluidic chip is a time-saving alternative to in vivo models.

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SRCAP ChIP-sequencing of mouse intestinal stem cells (ISCs)

Project description:We previously demonstrated that SRCAP regulates the self-renewal of ESCs and modulates lymphoid lineage commitment. We further validated that SRCAP was mainly distributed in liver, spleen and intestine by Northern blot. SRCAP was also highly expressed in Lgr5+ ISCs. We then sought to explore the physiological role of SRCAP in the regulation of self-renewal maintenance of ISCs.We identified that Srcap deficiency impairs the self-renewal of ISCs and intestinal epithelial regeneration. Through SRCAP ChIP-sequencing, we sough to identify the key gene regulated by SRCAP in ISC self-renewal.

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Human squamous cell carcinoma HSC-4 betaine treatment

Project description:This study aims to examine the effects of betaine on the survival, proliferation, and invasion of human oral squamous carcinoma cells (HSC) and further elucidate the potential function of betaine via the utilisation of proteomic analysis.

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Growth signaling promotes H2A.Z deposition by SRCAP to sustain somatic tissue regeneration [ChIP-Seq]

Project description:In this study, we find that H2A.Z expression and chromatin occupancy dramatically decrease during normal epidermal differentiation. While the chromatin remodeler SRCAP is necessary and sufficient to maintain H2A.Z deposition in epidermal progenitors, EP400 is dispensable. Growth factor signaling mediated by the MAPK and PI3K signaling pathways is necessary to maintain both the expression and deposition of H2A.Z. Loss of SRCAP, H2AZ1, or H2AZ2 induces nuclear deformation and cytoplasmic DNA in progenitor keratinocytes which impairs DNA repair and proliferation.

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Growth signaling promotes H2A.Z deposition by SRCAP to sustain somatic tissue regeneration [RNA-Seq]

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