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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.

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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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MALT1 paracaspase controls cholesterol homeostasis in glioblastoma stem-like cells through lysosome proteome shaping

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MALT1 paracaspase controls cholesterol homeostasis in glioblastoma stem-like cells through lysosome proteome shaping

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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

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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

Project description:CCDC50 promotes glioblastoma progression through regulating EGFR cell-surface recycle

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