IndraLab

Statements



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"CSN6 recovery rescued the cell proliferation, migration, and invasion of CSN6-knockdown melanoma cells."

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"Here, we report that GBM tumors overexpressed CSN6 compared with normal brain tissues and that CSN6 promoted GBM cell proliferation, migration, invasion and tumorigenesis."

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"Here, we identified that CSN6 promoted melanoma cell migration and invasion in vivo."

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"In this study, we show that CSN6 promotes the growth, migration and invasion of melanoma cells via CDK9 mediated signaling pathways."

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"In melanoma cells , CSN6 knockdown remarkably inhibited cell proliferation , tumorigenicity , migration , and invasion , whereas CSN6 recovery rescued the proliferative and metastatic abilities ."

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"Here , we identified that CSN6 promoted melanoma cell migration and invasion in vivo ."

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"Also, WT CSN6 increased cell migration and invasion in a wound healing assay (p < 0.001, XREF_FIG) and in transwell migration and invasion assays (XREF_FIG), whereas CSN6 S148A lost such capability, demonstrating that the CSN6 promoted migration and invasion of colon cancer cells requires a phosphorylation event."

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"CSN6 Promotes the Migration and Invasion of Cervical Cancer Cells by Inhibiting Autophagic Degradation of Cathepsin L."

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"In vitro and in vivo data showed that loss of CSN6 attenuated cell proliferation, migration, and invasion of PTC cells, confirming the vital function of CSN6 in PTC."

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"These results suggest that CSN6 robustly modulates PTC migration and invasiveness."

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"Overexpression of CSN6 promoted processes of HCC cell proliferation, migration, and invasion, while these processes were inhibited when CSN6 was silenced."

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"Moreover, we demonstrated that CSN6 promoted invasion and metastasis through regulating forkhead box protein A1 (FOXA1) in PAAD cells."

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"In summary , these findings demonstrated that downregulation of CSN6 expression could inhibit cell proliferation , migration and invasion ."

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"Furthermore, migration and invasion assays showed that knockdown of CSN6 reduced cell migration and invasion in DLD-1."