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KLF5 regulates actin remodeling to enhance the metastasis of nasopharyngeal carcinoma [ChIP-seq]

ABSTRACT: KLF5 regulates actin remodeling to enhance the metastasis of nasopharyngeal carcinoma [ChIP-seq]

PROVIDER: PRJNA1020788 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26161376.fastq.gz	Fastqsanger.gz
	SRR26161377.fastq.gz	Fastqsanger.gz
	SRR28435071_1.fastq.gz	Fastqsanger.gz
	SRR28435071_2.fastq.gz	Fastqsanger.gz
	SRR28435072_1.fastq.gz	Fastqsanger.gz

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KLF5 regulates actin remodeling to enhance the metastasis of nasopharyngeal carcinoma [RNA-seq]

Project description:Transcription factors (TFs) engage in various cellular essential processes including differentiation, growth and migration. However, the master TF involved in distant metastasis of nasopharyngeal carcinoma (NPC) remains largely unclear. Here we show that KLF5 regulates actin remodeling to enhance NPC metastasis. We analyzed the msVIPER algorithm-generated transcriptional regulatory networks and identified KLF5 as a master TF of metastatic NPC linked to poor clinical outcomes. KLF5 regulates actin remodeling and lamellipodia formation to promote the metastasis of NPC cells in vitro and in vivo. Mechanistically, KLF5 preferentially occupies distal enhancer regions of ACTN4 to activate its transcription, whereby decoding the informative DNA sequences. ACTN4, extensively localized within actin cytoskeleton, facilitates dense and branched actin networks and lamellipodia formation at the cell leading edge, empowering cells to migrate faster. Collectively, our findings reveal that KLF5 controls robust transcription program of ACTN4 to modulate actin remodeling and augment cell motility which enhances NPC metastasis, and provide new potential biomarkers and therapeutic interventions for NPC.

2024-04-18 | GSE243952 | GEO

KLF5 regulates actin remodeling to enhance the metastasis of nasopharyngeal carcinoma [ChIP-seq]

2024-04-18 | GSE243951 | GEO

KLF5 regulates actin remodeling to enhance the metastasis of nasopharyngeal carcinoma

Project description:KLF5 regulates actin remodeling to enhance the metastasis of nasopharyngeal carcinoma

| PRJNA1020786 | ENA

KLF5 regulates actin remodeling to enhance the metastasis of nasopharyngeal carcinoma [RNA-seq]

Project description:KLF5 regulates actin remodeling to enhance the metastasis of nasopharyngeal carcinoma [RNA-seq]

| PRJNA1020789 | ENA

KLF5 regulates actin remodeling to enhance the metastasis of nasopharyngeal carcinoma

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

2024-04-18 | GSE243953 | GEO

Interuption of Klf5 acetylaiton at K358 affects tumor microenvironment in Pten deficient mouse prostates

Project description:PTEN deficiency induces KLF5 acetylation; and the interruption of KLF5 acetylation orchestrates intricate interactions between cancer cells and CAFs that enhance FGFR1 signaling and promote tumor growth. Deacetylated KLF5 promotes tumor cells to secrete TNF, which stimulates inflammatory CAFs to release FGF9. Single-cell transcriptomic analysis reveals an enhanced FGF signaling from fibroblasts to cancer cells after the interruption of Klf5 acetylation.

2024-06-24 | GSE262893 | GEO

MicroRNA Signatures Correlate with Diagnosis, Distant Metastasis and Prognosis in nasopharyngeal carcinoma

Project description:microRNA signatures with diagnosis, distant metastasis and prognosis for nasopharyngeal carcinoma 62 nasopharyngeal carcinoma and 6 non-cancer nasopharyngitis fresh tissues were detected by microRNA microarray

2012-05-09 | E-GEOD-36682 | biostudies-arrayexpress

Interuption of Klf5 acetylaiton at K358 affects gene expression profiles in Pten deficient mouse prostates

Project description:Cancer associated fibroblasts (CAFs) play a pivotal role in tumor progression, but it remains elusive whether and how PTEN-deficient prostate cancers reprogram CAFs to overcome the barriers for tumor progression. Herein, we report that PTEN deficiency induces KLF5 acetylation; and interruption of KLF5 acetylation orchestrates intricate interactions between cancer cells and CAFs that enhance FGFR1 signaling and promote tumor growth. Deacetylated KLF5 promotes tumor cells to secrete TNF-α, which stimulates inflammatory CAFs to release FGF9. CX3CR1 inhibition blocks FGFR1 activation triggered by FGF9 and sensitizes PTEN-deficient prostate cancer to AKT inhibitor capivasertib.

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Human nasopharyngeal carcinoma cells : S18 with high metastasis potential vs. S26 with low metastasis potential

Project description:Metastasis is the major reason of treatment failure in nasopharyngeal carcinoma. miRNAs have been identified to regulate tumor metastasis. We aimed to identify metastasis-associated miRNAs in nasopharyngeal carcinoma.

2020-02-24 | GSE137312 | GEO

Over-expression and knockdown of KLF5

Project description:Activation of the Ras/Erk pathway upregulates expression of the Kruppel-like Factor 5 (KLF5) transcription factor, and KLF5 is a downstream mediator of Ras oncogenic signaling. Specifically, in bladder and colon cancer cell lines KLF5 upregulates the Ras-pathway target gene cyclin D1, and facilitates entry into the S phase of the cell cycle. Ras mutations are common in lung cancer, but a role for KLF5 in lung tumorigenesis has not been defined. To this end, we manipulated KLF5 expression in four Ras-mutant human lung adenocarcinoma cell lines to find that KLF5 significantly modulates anchorage-independent growth, a mutant Ras phenotype. However, in a mouse model of human lung adenocarcinoma, K-RasG12D does not critically require Klf5 to mediate oncogenesis or induce cyclin D1 expression. Patients with lung tumors expressing high levels of KLF5 have significantly better prognosis than those with low or no KLF5 expression (opposite of mutant Ras prognosis). The latter may be explained by KLF5 transcriptional repression of the ATP-binding cassette, sub-family G (WHITE), member 2 (ABCG2), an anthracycline transporter. In agreement with this, KLF5 knockdown cells display significantly more Hoechst “side population” and resistance to doxorubicin. In summary, while KLF5 is not an obligate partner in Ras oncogenic signaling, KLF5 control of ABCG2 expression is significant to patient survival.

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