The USP22 promotes the growth of cancer cells through the DYRK1A in pancreatic ductal adenocarcinoma

Bai, Zhile; Du, Yang; Liu, Cong; Cheng, Yong

doi:10.1016/j.gene.2020.144960

Cited by 21 publications

(15 citation statements)

References 23 publications

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“…For instance, USP22 enhanced cell proliferation via increasing surviving stability in renal cell carcinoma (RCC) cells ( 37 ). In pancreatic ductal adenocarcinoma (PDAC) cells, USP22 stimulated cell growth via targeting dual-specificity tyrosine regulated kinase 1A (DYRK1A) ( 38 ). In breast cancer cells, USP22 positively regulated ERα expression via maintaining its stability ( 39 ).…”

Section: Discussionmentioning

confidence: 99%

Long Intergenic Noncoding RNA00265 Enhances Cell Viability and Metastasis via Targeting miR-485-5p/USP22 Axis in Osteosarcoma

et al. 2022

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Osteosarcoma is one of the bone malignancies in children and adolescents. Long noncoding RNAs (lncRNAs) have been demonstrated to participate in osteosarcoma development and progression. Linc00265 has been shown to involve in osteosarcoma oncogenesis; however, the underlying mechanism is largely unclear. In this study, we investigated the function of linc00265 in osteosarcoma cells, including cell viability, migration and invasion. Moreover, we elucidated mechanistically the involvement of linc00265 in osteosarcoma. We found that linc00265 overexpression promoted viability, migration and invasion of osteosarcoma cells. Notably, linc00265 sponged miR-485-5p and increased the expression of USP22, one target of miR-485-5p, in osteosarcoma cells. Strikingly, linc00265 exerted its oncogenic function via regulating miR-485-5p and USP22 in osteosarcoma. Taken together, targeting linc00265 is a promising approach for treating osteosarcoma patients.

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Section: Discussionmentioning

confidence: 99%

Long Intergenic Noncoding RNA00265 Enhances Cell Viability and Metastasis via Targeting miR-485-5p/USP22 Axis in Osteosarcoma

et al. 2022

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“…USP22 also promoted gastric cancer progression and metastasis through regulating c-Myc/NAMPT/SIRT1-dependent FOXO1 and YAP signaling [ 23 ]. USP22 was also been reported to accelerate the development of cancer cells by targeting the DYRK1A in pancreatic ductal adenocarcinoma [ 24 ]. However, the functions of USP22 in colorectal cancer have not been investigated.…”

Section: Discussionmentioning

confidence: 99%

Ring finger 220 promotes the stemness and progression of colon cancer cells via Ubiquitin specific peptidase 22-BMI1 axis

Yan¹,

Tan²,

Yu³

et al. 2021

Bioengineered

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Colorectal cancer (CRC) is ranked as the third most common malignancy worldwide. Therefore, it is urgent to screen novel and effective molecular drug targets for colorectal cancer therapeutics. In this study, the specific role and related mechanism underlying Ring finger (RNF) 220 in colon cancer were investigated. Firstly, RT-PCR assay was used to compare differences between expression levels of RNF220 in colorectal tumor and normal tissues. Western blot and RT-PCR assays were applied to examine the protein levels of RNF220 in normal colonic mucosa and colorectal cancer cells. We found that RNF220 was upregulated in colorectal cancer in patients and cell models. RNF220 promoted the proliferation and migration, invasion of colorectal cancer cells through BrdU incorporation, clone formation, transwell and wound healing assays. Spheroid formation and western blot assays illustrated that RNF220 promoted the stemness of colorectal cancer cells. Moreover, we found that RNF220 regulated BMI1 expression through USP22 by western blot. Finally, we discovered that RNF220 facilitated tumor growth in vivo through establishment of subcutaneous xenograft tumor mice model. In conclusion, RNF220 promoted the stemness and progression of colon cancer cells via the USP22-BMI1 axis.

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“…In addition, the USP22/SOS1/RAS axis is also a cancer-promoting pathway in gastric cancer ( 106 ). In PDAC, USP22 accelerates cancer cell proliferation by targeting DYRK1A ( 88 ). In retinoblastoma, USP22 depletion induces cancer cell apoptosis by inhibiting the TERT/P53 signaling pathway ( 89 ).…”

Section: Usp22 Is a New Therapeutic Target For Cancermentioning

confidence: 99%

Immune Evasion and Drug Resistance Mediated by USP22 in Cancer: Novel Targets and Mechanisms

Guo

Zhao

et al. 2022

Front. Immunol.

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Regulation of ubiquitination is involved in various processes in cancer occurrence and development, including cell cycle arrest, cell proliferation, apoptosis, invasion, metastasis, and immunity. Ubiquitination plays an important role not only at the transcriptional and post-translational levels but also at the protein level. When ubiquitination is in a pathological state, abnormally activated biological processes will not only induce cancer progression but also induce immune evasion. The main function of deubiquitinases (DUBs) is to remove ubiquitin chains from substrates, changing the biological activity of the substrates. It has great potential to improve the prognosis of cancer by targeting DUB to regulate proteome. Ubiquitin-specific peptidase 22 (USP22) belongs to the ubiquitin-specific protease (USP) family of DUBs and has been reported to be related to various physiological and pathological processes. USP22 is abnormally expressed in various malignant tumors such as prostate cancer, lung cancer, liver cancer, and colorectal cancer, which suggests that USP22 may play an important role in tumors. USP22 may stabilize programmed death ligand 1 (PD-L1) by deubiquitination while also regulating T-cell infiltration into tumors. Regulatory T cells (Tregs) are a unique class of immunosuppressive CD4+ T cells that primarily suppress the immune system by expressing the master transcription factor forkhead box protein 3 (FOXP3). USP22 was found to be a positive regulator of stable FOXP3 expression. Treg-specific ablation of USP22 leads to reduced tumor volume in multiple cancer models. This suggests that USP22 may regulate tumor resistance to immunotherapy. In this article, we review and summarize the biological functions of USP22 in multiple signal transduction pathways during tumorigenesis, immune evasion, and drug resistance. Furthermore, we propose a new possibility of combining USP22 with chemotherapeutic, targeted, and immunosuppressive drugs in the treatment of cancer.

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The USP22 promotes the growth of cancer cells through the DYRK1A in pancreatic ductal adenocarcinoma

Cited by 21 publications

References 23 publications

Long Intergenic Noncoding RNA00265 Enhances Cell Viability and Metastasis via Targeting miR-485-5p/USP22 Axis in Osteosarcoma

Long Intergenic Noncoding RNA00265 Enhances Cell Viability and Metastasis via Targeting miR-485-5p/USP22 Axis in Osteosarcoma

Ring finger 220 promotes the stemness and progression of colon cancer cells via Ubiquitin specific peptidase 22-BMI1 axis

Immune Evasion and Drug Resistance Mediated by USP22 in Cancer: Novel Targets and Mechanisms

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