Inhibition of WWP2 suppresses proliferation, and induces G1 cell cycle arrest and apoptosis in liver cancer cells

Xu, Shengqian; Qin, Yong; Pan, Debiao; Ye, Guan‐Xiong; Wu, Chengjun; Wang, Shi; Jiang, Jingjing; Fu, Jing; Wang, Chao‐Jun

doi:10.3892/mmr.2016.4771

Cited by 22 publications

(14 citation statements)

References 30 publications

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“…The NEDD4 family members WWP1 and WWP2 are also necessary in regulating apoptosis. Depletion of WWP1 altered Bcl-2-associated X protein (Bax) expression, leading to osteosarcoma cell apoptosis (Wu et al, 2015), while the knockdown of WWP2 promoted G1 cell cycle arrest and apoptosis in liver cancer cells by elevating the expression of apoptosis-associated markers, including caspase-7, caspase-8 and Bax (Xu et al, 2016) (Table S2).…”

Section: Regulation Of Apoptosismentioning

confidence: 99%

HECT E3 ubiquitin ligases – emerging insights into their biological roles and disease relevance

Wang

Argiles-Castillo

Kane

et al. 2020

Journal of Cell Science

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Homologous to E6AP C-terminus (HECT) E3 ubiquitin ligases play a critical role in various cellular pathways, including but not limited to protein trafficking, subcellular localization, innate immune response, viral infections, DNA damage responses and apoptosis. To date, 28 HECT E3 ubiquitin ligases have been identified in humans, and recent studies have begun to reveal how these enzymes control various cellular pathways by catalyzing the post-translational attachment of ubiquitin to their respective substrates. New studies have identified substrates and/or interactors with different members of the HECT E3 ubiquitin ligase family, particularly for E6AP and members of the neuronal precursor cell-expressed developmentally downregulated 4 (NEDD4) family. However, there still remains many unanswered questions about the specific roles that each of the HECT E3 ubiquitin ligases have in maintaining cellular homeostasis. The present Review discusses our current understanding on the biological roles of the HECT E3 ubiquitin ligases in the cell and how they contribute to disease development. Expanded investigations on the molecular basis for how and why the HECT E3 ubiquitin ligases recognize and regulate their intracellular substrates will help to clarify the biochemical mechanisms employed by these important enzymes in ubiquitin biology.

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Section: Regulation Of Apoptosismentioning

confidence: 99%

HECT E3 ubiquitin ligases – emerging insights into their biological roles and disease relevance

Wang

Argiles-Castillo

Kane

et al. 2020

Journal of Cell Science

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“…Overexpression of miR‐188 suppressed glioma cell proliferation and cell cycle G1–S transition, whereas inhibition of miR‐188 promoted glioma cell proliferation (N. Li et al, ). Furthermore, small interfering RNA‐mediated WWP2 knockdown in liver cancer cell lines was demonstrated to inhibit cell proliferation, cause cell cycle arrest in G1 phase and induction of apoptosis as revealed by a CCK‐8 assay and ﬂow cytometric analysis (Xu et al, ). Our results demonstrated that miR‐188 inhibited breast cancer cell growth and proliferation, which might be ascribed to G1 cell cycle arrest, indicating that cell cycle progression is blocked.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐188‐5p promotes apoptosis and inhibits cell proliferation of breast cancer cells via the MAPK signaling pathway by targeting Rap2c

Zhu

Qiu

Zhang

et al. 2019

Journal Cellular Physiology

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Breast cancer is a common malignancy that is highly lethal with poor survival rates and immature therapeutics that urgently needs more effective and efficient therapies.MicroRNAs are intrinsically involved in different cancer remedies, but their mechanism in breast cancer has not been elucidated for prospective treatment.The function and mechanism of microRNA-188-5p (miR-188) have not been thoroughly investigated in breast cancer. In our study, we found that the expression of miR-188 in breast cancer tissues was obviously reduced. Our findings also revealed the abnormal overexpression of miR-188 in 4T1 and MCF-7 cells significantly suppressed cell proliferation and migration and also enhanced apoptosis. miR-188 induced cell cycle arrest in the G1 phase. To illuminate the molecular mechanism of miR-188, Rap2c was screened as a single target gene by bioinformatics database analysis and was further confirmed by dual-luciferase assay. Moreover, Rap2c was found to be a vital molecular switch for the mitogen-activated protein kinase signaling pathway in tumor progression by decreasing apoptosis and promoting proliferation and migration. In conclusion, our results revealed that miR-188 is a cancer progression suppressor and a promising future target for breast cancer therapy. K E Y W O R D S apoptosis, breast cancer, MAPK, miR-188-5p, proliferation, Rap2c

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“…The RUNX3 protein can regulate cell growth and apoptosis, as well as signal transduction and biological processes, through a variety of complex mechanisms. 11,12 The expression of RUNX3 was found to be downregulated or even absent in malignant tumors such as gastric cancer. 13,14 This reduced expression of RUNX3 was accompanied by enhanced proliferation and reduced cell apoptosis in gastrointestinal epithelial cells, leading to their abnormal growth and differentiation, and consequently tumorigenesis.…”

Section: Discussionmentioning

confidence: 99%

<p>Long Noncoding RNA (lncRNA) MT1JP Suppresses Hepatocellular Carcinoma (HCC) in vitro</p>

Mo¹,

Dai²,

Liwei³

et al. 2020

CMAR

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The purpose of this study was to evaluate the effects and mechanisms of the long noncoding RNA (lncRNA) MT1JP on hepatocellular carcinoma (HCC) in vitro. Patients and Methods: Thirty pairs of tumor and adjacent normal tissues were collected from HCC patients. Tissue pathology and MT1JP expression were evaluated by hematoxylin and eosin staining and in situ hybridization (ISH), respectively. The correlation between MT1JP and HCC prognosis was investigated. MTT assays, cloning, flow cytometry, transwell assays, and wound-healing assays were used to evaluate the effects of MT1JP on HCC cell lines. RT-qPCR and Western blot were used to measure the relative mRNA and protein expression levels. Results: The expression of MT1JP was downregulated in HCC tumor tissues compared with that in adjacent normal tissues, while the percent survival was significantly greater in the high MT1JP expression group than in the low MT1JP expression group (P=0.0238). In vitro, overexpression of MT1JP suppressed the proliferation, invasion, and migration, reduced colony cell number, increased cell apoptosis, and induced G1-phase cell cycle arrest in Bel-7402 and Huh-7 cells. Meanwhile, the mRNA and protein expression levels of RUNX3 and P21 were significantly upregulated, whereas those of MMP2 and MMP9 were significantly downregulated, in Bel-7402 and Huh-7 cells overexpressing MT1JP (all P<0.001). Conclusion: LncRNA MT1JP may function as a tumor suppressor in HCC. Overexpression of MT1JP suppressed HCC cell biological activities through the regulation of RUNX3.

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Inhibition of WWP2 suppresses proliferation, and induces G1 cell cycle arrest and apoptosis in liver cancer cells

Cited by 22 publications

References 30 publications

HECT E3 ubiquitin ligases – emerging insights into their biological roles and disease relevance

HECT E3 ubiquitin ligases – emerging insights into their biological roles and disease relevance

MicroRNA‐188‐5p promotes apoptosis and inhibits cell proliferation of breast cancer cells via the MAPK signaling pathway by targeting Rap2c

<p>Long Noncoding RNA (lncRNA) MT1JP Suppresses Hepatocellular Carcinoma (HCC) in vitro</p>

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