Emerging roles of Jab1/CSN5 in DNA damage response, DNA repair, and cancer

Pan, Yunbao; Yang, Huiling; Claret, Francois-Xavier

doi:10.4161/cbt.27823

Cited by 57 publications

(42 citation statements)

References 86 publications

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“…Elevated deposition of Jab1 has been particularly associated with cell proliferation, cell cycle, and therapy response and correlated with worse cancer prognosis [8]. It has also been reported that Jab1 is elevated in breast cancer tissues compared with normal tissues [7,10].…”

Section: Discussionmentioning

confidence: 99%

“…Jab1 is aberrantly expressed in a number of cancer types and contributes to the cancer progression [8]. Elevated deposition of Jab1 has been particularly associated with cell proliferation, cell cycle, and therapy response and correlated with worse cancer prognosis [8].…”

Section: Discussionmentioning

confidence: 99%

“…It has also been reported that overexpression of Jab1 enhances pro-survival pathways in breast cancer [7,10]. In breast carcinogenesis, Jab1 is associated with EGFR and HER-2 receptors and their downstream signaling factors that contribute to the cancer progress [8]. However, whether the increased expression of Jab1 is regulated by non-coding RNAs has not been elucidated in breast cancer.…”

Section: Introductionmentioning

confidence: 98%

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Let-7d Inhibits Growth and Metastasis in Breast Cancer by Targeting Jab1/Cops5

Wei

Liu

et al. 2018

Cell Physiol Biochem

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Background/Aims: MicroRNAs (miRNAs) regulate the expressions of cancer-related genes, and are involved in the development and progression of various human cancers. Here, we performed further analyses to determine whether let-7d is functionally linked to Jab1 in breast cancer. Methods: In situ hybridization and immunohistochemical analyses were used to determine the level of let-7d and Jab1 in breast cancer clinical specimens and its correlation with clinicopathological data. Let-7d overexpressing breast cancer cell lines combined with mouse models bearing cell-derived xenografts were used to assess the functional role of let-7d both in vitro and in vivo. Results: In this study, we found that let-7d was downregulated in breast cancer tissues, coupled with the elevations of Jab1 protein expressions, compared with paired adjacent noncancerous breast tissues. Let-7d overexpression significantly suppressed the proliferation and invasion in MCF-7 and MDA-MB-231 cells. Dual luciferase reporter assay indicated that Jab1 was the direct target of let-7d. Stepwise studies from in vitro and in vivo experiments indicated that let-7d overexpression inhibited cell growth and decreased Jab1 expressions in breast cancer cells and nude mice tumor tissues. Statistical analyses demonstrated that breast cancer patients with low levels of let-7d or high levels of Jab1 had a significant correlation with worse prognosis. Conclusion: These findings provide novel insights into molecular mechanism of let-7d and Jab1 in tumor development and progression of breast cancer, and thus let-7d/Jab1 are novel potential therapeutic targets for breast cancer patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

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Let-7d Inhibits Growth and Metastasis in Breast Cancer by Targeting Jab1/Cops5

Wei

Liu

et al. 2018

Cell Physiol Biochem

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“…MIF has also been shown to mitigate p53-mediated apoptosis via its binding to c-Jun activation domain-binding protein-1 (JAB1) to modulate AP-1-mediated transcription factors (68,104). JAB1 is a key component of the COP9 signalasome and the MIF-JAB1 interaction has been implicated in the regulation of integrins, cell-cycle regulatory proteins, and apoptosis (79,103,107). MIF can activate other signaling pathways that have been implicated in cell survival.…”

Section: Mif: Structure and Functionmentioning

confidence: 99%

Role of macrophage migration inhibitory factor in age-related lung disease

Sauler

Bucala

Lee

2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…It is conceivable that CSN5 plays a significant role in cancer since many key tumor suppressors and oncogene products are regulated by ubiquitination-and proteasome-mediated protein degradation, such as MYC, p27, TGFb1, MIF, c-Jun, E2F1, p53, Cullin, Smad4 and HIF1alpha. 3,4,[12][13][14] CSN5 has an emerging role in cancer. Actually, CSN5 was found to be overexpressed in a variety of human cancers, such as ovarian cancer, 15 breast carcinoma, 16 pancreatic cancer, 17 hepatocellular carcinoma, 18 nasopharyngeal carcinoma, 19 colorectal cancer, 20 neuroblastoma 21 and lung adenocarcinoma.…”

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confidence: 99%