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CCDC50 promotes tumor growth through regulation of lysosome homeostasis

ABSTRACT: CCDC50 promotes tumor growth through regulation of lysosome homeostasis

PROVIDER: PRJNA785985 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17121000_1.fastq.gz	Fastqsanger.gz
	SRR17121000_2.fastq.gz	Fastqsanger.gz
	SRR17121001_1.fastq.gz	Fastqsanger.gz
	SRR17121001_2.fastq.gz	Fastqsanger.gz
	SRR17121002_1.fastq.gz	Fastqsanger.gz

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CCDC50 promotes tumor growth through regulation of lysosome homeostasis

Project description:Cutaneous melanoma is characterized by lineage-specific lysosome-associated vesicular trafficking. Specifically, we report a melanoma enrichened lysophagy receptor, CCDC50, controlling lysosomal homeostasis and autolysosomal activity. We reveal that targeting CCDC50 in melanoma may be a promising therapeutic strategy, as nearly 70% of human melanomas highly express CCDC50. Moreover, targeting CCDC50 together with BRAFV600E inhibition induces synergistic function in regression of melanoma tumors, representing an alternative strategy for melanoma therapy. We performed transcriptome profiling (RNA-seq) and quantitative reverse transcription polymerase chain reaction (qRT–PCR) in shCtrl and shCCDC50 cells to evaluate the melanoma growth and metastasis controlled by CCDC50. The deep sequencing results showed that CCDC50 defciency caused increased lysosome and vacuolar memebrane and blocked autophagy flux.

2021-12-06 | GSE190144 | GEO

Carnosine Regulation of Intracellular pH Homeostasis Promotes Lysosome-dependent Tumor Immunoevasion

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CCDC50 promotes tumor growth through regulation of lysosome homeostasis.

Project description:The maintenance of lysosome homeostasis is crucial for cell growth. Lysosome-dependent degradation and metabolism sustain tumor cell survival. Here, we demonstrate that CCDC50 serves as a lysophagy receptor, promoting tumor progression and invasion by controlling lysosomal integrity and renewal. CCDC50 monitors lysosomal damage, recognizes galectin-3 and K63-linked polyubiquitination on damaged lysosomes, and specifically targets them for autophagy-dependent degradation. CCDC50 deficiency causes the accumulation of ruptured lysosomes, impaired autophagic flux, and superfluous reactive oxygen species, consequently leading to cell death and tumor suppression. CCDC50 expression is associated with malignancy, progression to metastasis, and poor overall survival in human melanoma. Targeting CCDC50 suppresses tumor growth and lung metastasis, and enhances the effect of BRAFV600E inhibition. Thus, we demonstrate critical roles of CCDC50-mediated clearance of damaged lysosomes in supporting tumor growth, hereby identifying a potential therapeutic target of melanoma.

| S-EPMC10561174 | biostudies-literature

CCDC50 promotes tumor growth through regulation of lysosome homeostasis

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CCDC50 promotes glioblastoma progression through regulating EGFR cell-surface recycle

Project description:Glioblastomas (GBM) are a kind of malignant tumor with high mortality. However, the mechanism of tumor progression remains poorly understood. Specifically, we find that the expression of autolysosome-associated protein CCDC50, is positively correlated with tumor malignancy, and poor survival of GBM patients. CCDC50 functions as a specific cargo adaptor to assist EGFR recycling back to the plasma membrane, leading to prolonged activation of the downstream signaling pathways. We reveal that targeting CCDC50 in GBM may be a promising therapeutic strategy, as CCDC50 deficiency significantly inhibited the proliferation and migration of tumor cells in vitro and in vivo. Moreover, targeting CCDC50 together with alkylating agent temozolomide (TMZ) induces synergistic function in regression of GBM tumors, representing an alternative strategy for malignant tumor therapy. We performed transcriptome profiling (RNA-seq) and quantitative reverse transcription polymerase chain reaction (qRT–PCR) in shCtrl and shCCDC50 cells to evaluate the GBM tumor growth and metastasis controlled by CCDC50.

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A cascade for zinc mediated transcriptional activation by the zinc-sensing nuclear receptor HIZR-1 on the regulator of lysosome biogenesis HLH-30 to achieve homeostasis

Project description:Zinc is an essential element for animals and stored in de novo synthesized lysosome related organelles called bilobed granules in Caenorhabditis elegans. Defining how zinc regulated transcription drives the observed lysosome remodeling is key to understand zinc homeostasis processes. Here we describe a positively regulated zinc network controlled by HIZR-1 and HLH-30, the zinc sensor and the master regulator of the autophagy-lysosomal pathway in Caenorhabditis elegans, respectively; essential for connecting zinc homeostasis to lysosome biogenesis. Our studies indicate that either hizr-1 and hlh-30 are necessary and sufficient to activate transcription of lysosome-genes under high dietary zinc conditions. Consistent with the hizr-1 and hlh-30 dependency for high zinc response, we found DNA enhancer elements corresponding to the high zinc activation element consistently adjacent to E-boxes in the promoter regions of lysosome-genes. We defined a regulatory network based on the contribution of each transcription factor. Since zinc cannot be degraded, the autophagy-lysosomal pathway could play a key role in removing zinc excess

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Lysosome-coupled mRNA transport maintains mitochondrial and ribosomal homeostasis in the axon

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CCDC50 promotes glioblastoma progression through regulating EGFR cell-surface recycle

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Carnosine Regulation of Intracellular pH Homeostasis Promotes Lysosome-dependent Tumor Immunoevasion

Project description:To explore which genes are suppressed by NFX1 under hypoxic conditions, we performed RNA-seq analysis in PLC cells overexpressing EV or NFX1 under hypoxia.

2023-11-16 | GSE198881 | GEO

β2-adrenergic agonists rescue lysosome acidification and function in PSEN1 deficiency by reversing defective ER to lysosome delivery of ClC-7

Project description:Lysosomal dysfunction is considered pathogenic in Alzheimer Disease (AD). Loss of Presenilin-1(PSEN1) function causing early onset AD impedes acidification via defective vATPase V0a1 subunit delivery to lysosomes. We report that isoproterenol and related β2-adrenergic agonists re-acidify lysosomes in PSEN1 KO cells and fibroblasts from PSEN1 familial AD(FAD) patients, restores lysosomal calcium homeostasis and proteolysis, and reverses impaired autophagy flux. We identify a novel rescue mechanism involving PKA-mediated facilitated delivery of ClC-7 to lysosomes, which stimulates chloride influx and reverses markedly lowered Cl- content of PSEN1 KO lysosomes. Notably, PSEN1 loss-of-function impedes ER-to-lysosome delivery of ClC-7, thus accounting for lysosomal Cl- deficits that compound pH deficits due to deficient vATPase function. Transcriptomics of PSEN1-deficient cells reveal strongly down-regulated ER-to-lysosome transport pathways and reversibility by isoproterenol. Our findings uncover a broadened PSEN1 role in lysosomal ion homeostasis and novel pH modulation of lysosomes through β-adrenergic regulation of ClC-7, which can be therapeutically modulated.

2020-02-29 | GSE136894 | GEO

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