USP35 activated by miR let-7a inhibits cell proliferation and NF-κB activation through stabilization of ABIN-2

Liu, Chunyan; Wang, Lina; Chen, Weiwen; Zhao, Shihu; Yin, Chunli; Lin, Yani; An-li, Jiang; Zhang, Pengju

doi:10.18632/oncotarget.4451

Cited by 28 publications

(36 citation statements)

References 40 publications

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“…More and more reports showed that miRNAs play an important role in regulating various biological behaviours, including cancer cell survival, apoptosis, oxygen stress, and maintenance of cell phenotype [6, 8, 10]. Altered expression of miRNAs is usually related to different kinds and types of tumors, sunch as breast cancer, gliomas, and liver cancer.…”

Section: Discussionmentioning

confidence: 99%

MiR-let-7a inhibits cell proliferation, migration, and invasion by down-regulating PKM2 in cervical cancer

et al. 2017

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In recent decades, miRNA has been reported as a crucial modulator in some biology progressions. This work aims to assess the expression and role of miR-let-7a and pyruvate kinase muscle isozyme M2 (PKM2) in CC tissues and cell lines. Here, we identified that miR-let-7a expression was decreased in CC tissues, and SiHa and HeLa cells (all P < 0.001), however, PKM2 expression was increased in these samples. Statistically, miR-let-7a was inversely associated with PKM2 mRNA or protein (p = 0.013, p = 0.015, respectively). In-vitro assays revealed that ectopic miR-let-7a expression repressed SiHa and HeLa cell proliferation, migration and invasion, and enhanced SiHa and HeLa cell apoptosis. Furthermore, luciferase reporter assays revealed the 3′-UTR of PKM2 was identified a target of miR-let-7a, by which miR-let-7a affected the expression of PKM2 in SiHa and HeLa cells. Besides, PKM2 plasmids partially abrogated the inhibitory effects of miR-let-7a, while si-PKM2 enhanced the inhibitory effects of miR-let-7a. In vivo, miR-let-7a mimics indeed repressed tumor growth in mice xenograft model. In conclusion, our results demonstrated that miR-let-7a inhibits cell proliferation, migration and invasion by down-regulation of PKM2 in cervical cancer. miR-let-7a/PKM2 pathway may be a useful therapeutic target for CC patients.

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Section: Discussionmentioning

confidence: 99%

MiR-let-7a inhibits cell proliferation, migration, and invasion by down-regulating PKM2 in cervical cancer

et al. 2017

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“…39,40 Although NF-κβ signaling has not been studied in the context of scleral remodeling and myopia, regulation of type I collagen is directly relevant because it is the main component of the scleral matrix, and myopic scleras show reduced collagen levels. 41 Other members of the Let-7 family also showed differential expression in our study, including Let-7b, previously shown to be involved in COL1A1 and COL1A2 regulation in skin fibroblasts.…”

Section: Discussionmentioning

confidence: 99%

Genome-Wide Scleral Micro- and Messenger-RNA Regulation During Myopia Development in the Mouse

Metlapally

Park

Chakraborty

et al. 2016

Invest. Ophthalmol. Vis. Sci.

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PurposeMicroRNA (miRNAs) have been previously implicated in scleral remodeling in normal eye growth. They have the potential to be therapeutic targets for prevention/retardation of exaggerated eye growth in myopia by modulating scleral matrix remodeling. To explore this potential, genome-wide miRNA and messenger RNA (mRNA) scleral profiles in myopic and control eyes from mice were studied.MethodsC57BL/6J mice (n = 7; P28) reared under a 12L:12D cycle were form-deprived (FD) unilaterally for 2 weeks. Refractive error and axial length changes were measured using photorefraction and 1310-nm spectral-domain optical coherence tomography, respectively. Scleral RNA samples from FD and fellow control eyes were processed for microarray assay. Statistical analyses were performed using National Institute of Aging array analysis tool; group comparisons were made using ANOVA, and gene ontologies were identified using software available on the Web. Findings were confirmed using quantitative PCR in a separate group of mice (n = 7).ResultsForm-deprived eyes showed myopic shifts in refractive error (−2.02 ± 0.47 D; P < 0.01). Comparison of the scleral RNA profiles of test eyes with those of control eyes revealed 54 differentially expressed miRNAs and 261 mRNAs fold-change >1.25 (maximum fold change = 1.63 and 2.7 for miRNAs and mRNAs, respectively) (P < 0.05; minimum, P = 0.0001). Significant ontologies showing gene over-representation (P < 0.05) included intermediate filament organization, scaffold protein binding, detection of stimuli, calcium ion, G protein, and phototransduction. Significant differential expression of Let-7a and miR-16-2, and Smok4a, Prph2, and Gnat1 were confirmed.ConclusionsScleral mi- and mRNAs showed differential expression linked to myopia, supporting the involvement of miRNAs in eye growth regulation. The observed general trend of relatively small fold-changes suggests a tightly controlled, regulatory mechanism for scleral gene expression.

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“…Data provided by Zhang et al indicated that overexpression of USP28 in lung cancer and silencing of USP28 expression in A549 lung cancer cells inhibited cell proliferation and induced apoptosis. In contrast, Liu et al found that USP35 was downregulated in breast and lung cancer. Ectopic expression of USP35 in H1299 lung cancer cells inhibited cell proliferation.…”

Section: Introductionmentioning

confidence: 86%

Ubiquitin‐specific protease 3 overexpression promotes gastric carcinogenesis and is predictive of poor patient prognosis

et al. 2018

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Although gastric cancer (GC) is one of the most common cancers, knowledge of its development and carcinogenesis is limited. To date, expression of ubiquitin‐specific protease 3 (USP3) in all types of cancer, including GC, is still unknown. The present study explored the involvement of USP3 in the carcinogenesis and prognosis of GC. We measured USP3 expression in normal and GC tissues and cell lines. Correlations between USP3 protein level and clinicopathological parameters, as well as the significance of USP3 protein level for disease‐free survival were assessed. Small hairpin RNA technology and transfection were used to investigate the effect of USP3 manipulation on cell proliferation and spreading. Moreover, xenograft proliferation and metastasis were used to explore the influence of USP3 on tumor growth and metastasis in animals. An increase in USP3 expression was observed in GC cells and tissues. The overexpression of USP3 was significantly correlated with several clinicopathological parameters and poor disease‐free survival. Multivariate Cox regression analysis showed that the overexpression of USP3 was an independent prognostic biomarker. Silencing of USP3 suppressed GC cell proliferation and spreading in vitro as well as xenograft proliferation and metastasis in vivo; however, opposite results were obtained when USP3 was overexpressed. Further studies showed that USP3 influenced cell proliferation and spreading by regulating the cell cycle control‐ and epithelial‐mesenchymal transition‐related molecules. This study suggests that USP3 overexpression can be a useful biomarker for predicting the outcomes of GC patients and that USP3 targeting represents a potential modality for treating GC.

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USP35 activated by miR let-7a inhibits cell proliferation and NF-κB activation through stabilization of ABIN-2

Cited by 28 publications

References 40 publications

MiR-let-7a inhibits cell proliferation, migration, and invasion by down-regulating PKM2 in cervical cancer

MiR-let-7a inhibits cell proliferation, migration, and invasion by down-regulating PKM2 in cervical cancer

Genome-Wide Scleral Micro- and Messenger-RNA Regulation During Myopia Development in the Mouse

Ubiquitin‐specific protease 3 overexpression promotes gastric carcinogenesis and is predictive of poor patient prognosis

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