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Loss of DLX3 tumor suppressive function promotes progression of SCC through EGFR-ERBB2 pathway.

ABSTRACT: Loss of DLX3 tumor suppressive function promotes progression of SCC through EGFR-ERBB2 pathway.

PROVIDER: PRJNA677975 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13049332.fastq.gz	Fastqsanger.gz
	SRR13049333.fastq.gz	Fastqsanger.gz
	SRR13049334.fastq.gz	Fastqsanger.gz
	SRR13049335.fastq.gz	Fastqsanger.gz
	SRR13049336.fastq.gz	Fastqsanger.gz

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Loss of DLX3 tumor suppressive function promotes progression of SCC through EGFR-ERBB2 pathway.

Project description:Emerging evidence suggests that homeoproteins can act as modulators of tumor initiation and progression. Our findings show that loss of DLX3 tumor suppressive function acts as a tumor promoter through regulation of ERBB2 and EGFR signaling and also support an important inhibitory role of DLX3 in skin cancer promotion and progression, that may potentially be used as a promising prognostic marker.

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Loss of DLX3 tumor suppressive function promotes progression of SCC through EGFR-ERBB2 pathway.

Project description:Cutaneous squamous cell carcinoma (cSCC) ranks second in the frequency of all skin cancers. The balance between keratinocyte proliferation and differentiation is disrupted in the pathological development of cSCC. DLX3 is a homeobox transcription factor which plays pivotal roles in embryonic development and epidermal homeostasis. To investigate the impact of DLX3 expression on cSCC prognosis, we carried out clinicopathologic analysis of DLX3 expression which showed statistical correlation between tumors of higher pathologic grade and levels of DLX3 protein expression. Further, Kaplan-Meier survival curve analysis demonstrated that low DLX3 expression correlated with poor patient survival. To model the function of Dlx3 in skin tumorigenesis, a two-stage dimethylbenzanthracene (DMBA)/12-O-tetradecanoylphorbol 13-acetate (TPA) study was performed on mice genetically depleted of Dlx3 in skin epithelium (Dlx3cKO). Dlx3cKO mice developed significantly more tumors, with more rapid tumorigenesis compared to control mice. In Dlx3cKO mice treated only with DMBA, tumors developed after ~16 weeks suggesting that loss of Dlx3 has a tumor promoting effect. Whole transcriptome analysis of tumor and skin tissue from our mouse model revealed spontaneous activation of the EGFR-ERBB2 pathway in the absence of Dlx3. Together, our findings from human and mouse model system support a tumor suppressive function for DLX3 in skin and underscore the efficacy of therapeutic approaches that target EGFR-ERBB2 pathway.

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