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Suppression of CCT3 inhibits tumor growth by downregulating CDK1 expression in melanoma

ABSTRACT: Suppression of CCT3 inhibits tumor growth by downregulating CDK1 expression in melanoma

PROVIDER: PRJNA604922 | ENA |

REPOSITORIES: ENA

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Suppression of CCT3 inhibits tumor growth by downregulating CDK1 expression in melanoma

Project description:The members of the eukaryotic chaperonin family are essential for cell survival. The dysregulation of chaperonin-containing TCP-1 subunit 3 (CCT3) is implicated in the development of several types of malignant tumors. However, its functional role in melanoma remains unknown. Herein, we elucidated the functional contribution of CCT3 to melanoma progression. The results indicated that CCT3 was frequently upregulated in melanoma tissues, and high level of CCT3 is correlated with clinical stage in melanoma patients. Knockdown of CCT3 in melanoma cells markedly inhibited cell proliferation and induced cell apoptosis in vitro and suppressed tumorigenesis in a mouse xenograft model. We also identified the cyclin-dependent kinase 1 (CDK1) as a downstream effector of CCT3 and further evaluation demonstrated that suppression of CCT3 attenuates cell proliferation via downregulating CDK1 expression and CCT3-mediated regulation of cell cycle signaling pathway in melanoma. Collectively, our results provide compelling evidence that CCT3 contributes to melanoma progression via CDK1 and is a potential therapeutic target for melanoma A-375 cells infected with NC lentivirus and CCT3 knockdown lentivirus were prepeared and cultured for RNA extraction and hybridization on Affymetrix microarrays.

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Suppression of Ca2+ Signaling Enhances Melanoma Progression

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Suppression of type I interferon signaling overcomes the oncogene-induced senescence and mediates melanoma development and progression

Project description:Activation of oncogenes often leads to induction of the DNA damage responses and onset of the cell senescence. Given that DNA damage can also trigger production of type I interferons (IFN) that contribute to senescence development, we sought to determine the role of IFN in the oncogene-induced senescence. Our data in mouse model demonstrate that inactivation of IFN signaling is sufficient for inducing melanomas in melanocytes harboring mutant Braf. Restoration of IFN signaling in IFN-deficient melanoma cells induces cell senescence and suppresses melanoma progression. In addition, data in human patients that received high dose IFN therapy and in mouse transplanted tumor models strongly suggest the importance of the non-cell-autonomous IFN signaling. Suppression of IFN signaling mediated by the downregulation of IFN receptor IFNAR1 invariably occurs during development of mouse melanoma. Mice harboring the IFNAR1 mutant, which is relatively resistant to downregulation, delay melanoma development, suppress the metastatic disease, and better respond to treatment with BRAF or PD1 inhibitors. These results suggest that IFN signaling is an important tumor suppressive pathway that inhibits melanoma development and progression. Accordingly, the inhibition of IFN pathway via IFNAR1 downregulation plays a key role in melanoma pathogenesis. Conversely, these data also argue for targeting IFNAR1 downregulation to prevent the metastatic disease and improve the efficacy of molecularly targeted and immune-targeted therapies. Two genotypes of mice were examined at 2 to 3 times after tamoxifen adminstration, with 2 replicates for each condition, yielding 8 samples in total.

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Tight CDK1 inhibition elicits domain-specific pre-RC setting in S-phase, suppressing CFS instability

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TSPO deficiency promotes the progression of malignant peripheral sheath tumors by regulating the G2/M phase of the cell cycle via CDK1

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Cyclosporin A inhibits prostate cancer growth through suppression of E2F8

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Suppression of ANGPTL4 Reprograms Endothelial Cell Metabolism and Inhibits Angiogenesis

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