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HCAR1 nuclear transportation is critical for cell function

ABSTRACT: HCAR1 nuclear transportation is critical for cell function

PROVIDER: PRJNA1064959 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27554369_1.fastq.gz	Fastqsanger.gz
	SRR27554369_2.fastq.gz	Fastqsanger.gz
	SRR27554370_1.fastq.gz	Fastqsanger.gz
	SRR27554370_2.fastq.gz	Fastqsanger.gz
	SRR27554371_1.fastq.gz	Fastqsanger.gz

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HCAR1 nuclear transportation is critical for cell function

Project description:Membrane receptor nuclear translocation play some novel role in cancer pathology. In the current studies, we demonstrate HCAR1 distributes in cancer cell nucleus in Lung cancer; Lactate promote HCAR1 nuclear translocation. Proteomics analysis found there are a set of nuclear proteins binds with HCAR1; interaction of HCAR1 with SFPQ etc other proteins promote cell self-renewal and cell invasion in lung cancer. ChIP sequencing analysis discovered there are a set of genes were targeted by HCAR1.

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Project description:The involvement of G-Protein-Coupled Receptors’ (GPCR) location bias in diverse cellular functions and their misregulation in pathology is an underexplored territory. HCAR1, a GPCR for lactate is linked to cancer progression, mainly due to Warburg effect, but its mechanism of action remains elusive. Here, we show HCAR1 has a nuclear localization, capable of signaling intranuclearly to induce nuclear-ERK and AKT phosphorylation concomitant with higher cancer cell proliferation and survival. We determine its nuclear interactome, proving its involvement in protein-translation and DNA-damage repair. Nuclear HCAR1 (N-HCAR1) directly interacts with chromatin/DNA promoting expression of genes involved in cellular migration. Notably, we show N-HCAR1 particularly regulates a broader transcriptomic signature than its PM counterpart, emphasizing on the facts that functional output of N-HCAR1 is larger than PM localized HCAR1. Our study presents several unprecedented processes by which a GPCR through location-biased activity regulate various cellular functions and how cancer cells exploit these.

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