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CCDC50 promotes tumor growth through regulation of lysosome homeostasis

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE190144 | GEO | 2021/12/06

REPOSITORIES: GEO

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CCDC50 suppresses NLRP3 inflammasome activity by mediating the autophagic degradation of NLRP3

Project description:Autophagy and autophagy-associated genes are closely linked to NLRP3-mediated inflammation in inflammatory disorders. This study determined that the functions of CCDC50, the novel autophagy receptor, in regulating the activation of NLRP3 inflammasome and associated inflammatory diseases. We performed transcriptome profiling (RNA-seq) and quantitative reverse transcription polymerase chain reaction (qRT–PCR) in shCtrl and shCCDC50 cells to evaluate the inflammatory responses regulated by CCDC50. The deep sequencing results showed that CCDC50 defciency caused increased NLRP3 inflammasome assembly and upregulation of associated disease pathways.

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CCDC50 promotes glioblastoma progression through regulating EGFR cell-surface recycle

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Project description: Not available

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