Ubiquitin specific protease 21 upregulation in breast cancer promotes cell tumorigenic capability and is associated with the NOD-like receptor signaling pathway

Peng, Liang; Hu, Yi; Chen, Demeng; Linghu, Ruixia; Wang, Yingzhe; Kou, Xiaoxue; Yang, Junlan; Jiao, Shunchang

doi:10.3892/ol.2016.5263

Cited by 23 publications

(22 citation statements)

References 40 publications

(44 reference statements)

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“…USP21 amplification was also observed in several other cancer types ( Fig. 1B), which is consistent with previous reports that USP21 regulates cell proliferation and metastasis in bladder cancer (Chen et al 2017), hepatocellular carcinoma Li et al 2018), triple-negative breast cancer and renal cell carcinoma (Peng et al 2016). However, there were no molecular mechanistic insights as to whether and how USP21 may contribute to oncogenesis.…”

Section: Usp21 Is Highly Amplified In Pdacsupporting

confidence: 89%

USP21 deubiquitinase promotes pancreas cancer cell stemness via Wnt pathway activation

Hou

Zhang

et al. 2019

Genes Dev.

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The ubiquitin-specific protease (USP) family is the largest group of cysteine proteases. Cancer genomic analysis identified frequent amplification of USP21 (22%) in human pancreatic ductal adenocarcinoma (PDAC). USP21 overexpression correlates with human PDAC progression, and enforced expression of USP21 accelerates murine PDAC tumor growth and drives PanIN to PDAC progression in immortalized human pancreatic ductal cells. Conversely, depletion of USP21 impairs PDAC tumor growth. Mechanistically, USP21 deubiquitinates and stabilizes the TCF/LEF transcription factor TCF7, which promotes cancer cell stemness. Our work identifies and validates USP21 as a PDAC oncogene, providing a potential druggable target for this intractable disease.

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Section: Usp21 Is Highly Amplified In Pdacsupporting

confidence: 89%

USP21 deubiquitinase promotes pancreas cancer cell stemness via Wnt pathway activation

Hou

Zhang

et al. 2019

Genes Dev.

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“…USP21 was reported to play a tumor promoting role in some cancers. For example, knockdown of USP21 cells can dampen cell growth, migration, and invasion in triple‐negative breast cancer (TNBC) . In present study, we investigated its expression and found that it was also up‐regulated in OSCC tissues and cell lines.…”

Section: Discussionmentioning

confidence: 75%

“…For example, knockdown of USP21 cells can dampen cell growth, migration, and invasion in triple-negative breast cancer (TNBC). 22 In present study, we investigated its expression and found that it was also up-regulated in OSCC tissues and cell lines. USP21 silencing can attenuate cell growth, migration, and invasion, but promoting cell apoptosis.…”

Section: Discussionmentioning

confidence: 79%

LncRNA FGD5‐AS1 can be predicted as therapeutic target in oral cancer

Liu

Yao

Huang

et al. 2020

J Oral Pathology Medicine

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Background Long non‐coding RNAs (lncRNAs) have been extensively studied to participate in the carcinogenesis of various tumors. LncRNA FGD5‐AS1 has been studied as an oncogene in several cancers; however, the role it plays in oral squamous cell carcinoma (OSCC) still remains unclear. Methods Quantitative real‐time polymerase chain reaction (qRT‐PCR) was used to assess relevant RNAs expression. CCK‐8 and colony formation were combined to investigate cell proliferation. Flow cytometry was implemented to test the apoptosis of cell. Wound healing assay and transwell assays were conducted to investigate cell migration and invasion. Western blot assay was conducted to measure relevant protein expression. Results FGD5‐AS1 expression was aberrantly up‐regulated in OSCC tissue and cells. FDG5‐AS1 up‐regulation induced USP21 overexpression advances OSCC development. Knockdown of FGD5‐AS1 inhibited cell growth, migration, and invasion, yet promoted apoptosis. Conclusion FGD5‐AS1 regulates OSCC via competitively binding to miR‐520b against USP21. It could become a potential diagnostic biomarker for OSCC.

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“…ESCC samples were flash frozen in liquid nitrogen and homogenized with a mortar and pestle, as previously described. 17 , 18 , 19 Total RNA was extracted using TRIzol (Invitrogen, China). 20 Quantitative RT-PCR was performed as previously described.…”

Section: Methodsmentioning

confidence: 99%

Inhibition of glutathione metabolism attenuates esophageal cancer progression

et al. 2017

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Esophageal squamous cell carcinoma (ESCC) is a deadly malignancy with regard to mortality and prognosis, and the 5-year survival rate for all patients diagnosed with ESCC remains poor. A better understanding of the biological mechanisms of ESCC tumorigenesis and progression is of great importance to improve treatment of this disease. In this study, we demonstrated that the glutathione metabolism pathway is highly enriched in ESCC cells compared with normal esophageal epithelial cells in an in vivo mouse model. In addition, treatment with L-buthionine-sulfoximine (BSO) to deplete glutathione decreased the ESCC tumor burden in mice, thus demonstrating the critical role of glutathione metabolism in ESCC progression. BSO treatment also led to decreased cell proliferation and activation of cell apoptosis in ESCC. Finally, BSO treatment blocked NF-kB pathway activation in ESCC. Our study reveals a new pathway that regulates ESCC progression and suggests that inhibition of glutathione metabolism may be a potential strategy for ESCC treatment.

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Ubiquitin specific protease 21 upregulation in breast cancer promotes cell tumorigenic capability and is associated with the NOD-like receptor signaling pathway

Cited by 23 publications

References 40 publications

USP21 deubiquitinase promotes pancreas cancer cell stemness via Wnt pathway activation

USP21 deubiquitinase promotes pancreas cancer cell stemness via Wnt pathway activation

LncRNA FGD5‐AS1 can be predicted as therapeutic target in oral cancer

Inhibition of glutathione metabolism attenuates esophageal cancer progression

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