Ubiquitin-specific peptidase 22 inhibits colon cancer cell invasion by suppressing the signal transducer and activator of transcription 3/matrix metalloproteinase 9 pathway

Ao, Ning; Liu, Yanyan; Bian, Xiaocui; Feng, Hao; Liu, Yuqin

doi:10.3892/mmr.2015.3661

Cited by 16 publications

(11 citation statements)

References 23 publications

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“…Several studies also indicate that USP2 expression is associated with poor survival of breast cancer patients and may serve as a prognostic biomarker and therapeutic target for TNBC. In colon cancer, USP22 was reported to attenuate the invasion capacity of colon cancer cells by inhibiting the STAT3/MMP9 signaling pathway (Ao, Liu, Bian, Feng, & Liu, 2015). …”

Section: Dubs In Regulation Of Critical Steps In Tumor Metastasismentioning

confidence: 99%

Emerging role of DUBs in tumor metastasis and apoptosis: Therapeutic implication

Zhou

et al. 2017

Pharmacology & Therapeutics

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Malfunction of ubiquitin-proteasome system is tightly linked to tumor formation and tumor metastasis. Targeting the ubiquitin-pathway provides a new strategy for anti-cancer therapy. Despite the parts played by ubiquitin modifiers, removal of ubiquitin from the functional proteins by the deubiquitinating enzymes (DUBs) plays an important role in governing the multiple steps of the metastatic cascade, including local invasion, dissemination, and eventual colonization of the tumor to distant organs. Both deregulated ubiquitination and deubiquitination could lead to dysregulation of various critical events and pathways such as apoptosis and epithelial-mesenchymal transition (EMT). Recent TCGA study has further revealed the connection between mutations of DUBs and various types of tumors. In addition, emerging drug design targeting DUBs provides a new strategy for anti-cancer therapy. In this review, we will summarize the role of deubiquitination and highlight the recent discoveries of DUBs with regards to multiple metastatic events including anti-apoptosis pathway and EMT. We will further discuss the regulation of deubiquitination as a novel strategy for anti-cancer therapy.

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Section: Dubs In Regulation Of Critical Steps In Tumor Metastasismentioning

confidence: 99%

Emerging role of DUBs in tumor metastasis and apoptosis: Therapeutic implication

Zhou

et al. 2017

Pharmacology & Therapeutics

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“…USP22 protease has been demonstrated to participate in regulation of the cell cycle progression in many cancer cell types [24,25]. This enzyme removes ubiquitin from histones, thus regulating gene transcription [26]. It is interes ting to note that deubiquitinating enzyme USP25 is involved in endoplasmic reticulum (ER)-associa ted degradation (ERAD) of misfolded/anomalous proteins [27].…”

mentioning

confidence: 99%

Expression of ubiquitin specific peptidase and ATG7 genes in U87 glioma cells upon glutamine deprivation

Halkin¹,

Minchenko²,

Riabovol³

et al. 2017

Ukr.Biochem.J

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We have studied the effect of glutamine deprivation on the expression of genes encoding for ubiquitin specific peptidases (usP) [4][5][6]. A better knowledge of tumor respon ses to glutamine deprivation condition is required to elaborate new therapeutical strategies of cell sensibilization, based on the blockade of survival mechanisms.Ubiquitin is a highly conserved protein involved in regulation of intracellular protein breakdown, cell cycle regulation, chromatin remodeling, and stress response. It is released from degraded proteins by disassembly of the polyubiquitin chains, which is mediated by ubiquitin-specific proteases, members of the ubiquitin-specific processing family of proteases for deubiquitination of proteins [7][8][9]. E3 ubiquitin ligases and deubiquitylases play an important role in cancer [7,10,11]. Our previous results demonstrated possible interaction/cross-talk between unfolding protein response signaling and ubiquitin system during adjustment to episodes of hypoxia during tumor development [12]. Ubiquitin specific peptidases (USPs) and ubiquitin activating enzyme E1-like protein/autophagy related 7 (GSA7/ ATG7) are involved in cancer cells survival and progression [13][14][15]. USP1 and USP7 are responsible for deubiquitination of mono-ubiquitinated PCNA (proliferating cell nuclear antigen), which activates error-prone DNA polymerases and controls an oxidative-stress-induced mutagenesis in human cells [13]. Decreased levels of USP1 in cancer cells have been implicated in lung and glioblastoma tumors growth and progression [14,16]. There is data that serine phosphorylation is critical for the activity of USP1 and its interaction with WD40-repeat protein UAF1; while two nuclear localization signals

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“…STAT3 is a transcription factor that directly regulates a panel of tumor-promoting genes (Ao et al, 2015; Lee et al, 2015). We investigate whether AR affected the expression of STAT3 target genes including Mcl-1, Bcl-xL (involve in cell survival), and MMP-2 (involves in cell migration and invasion).…”

Section: Resultsmentioning

confidence: 99%

An Ethanolic Extract of Ampelopsis Radix Exerts Anti-colorectal Cancer Effects and Potently Inhibits STAT3 Signaling In Vitro

Bai

Chen

et al. 2017

Front. Pharmacol.

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Colorectal cancer (CRC) is a leading cause of cancer-related morbidity and mortality worldwide. Signal transducer and activator of transcription 3 (STAT3) signaling is constantly activated in CRC, and has been proposed as a pathogenic factor and a therapeutic target of CRC. Ampelopsis Radix (AR), a traditional Chinese medicinal herb, possesses low toxicity and has long been used clinically for the treatment of cancers including CRC. Some constituents of AR have been reported to exert anti-cancer properties by targeting STAT3. However, the anti-CRC mode and mechanism of action of AR have not been fully elucidated. Here, we investigated the involvement of STAT3 signaling in the anti-CRC effects of AR. Results showed that AR reduced cell viability, induced cell apoptosis, and suppressed cell migration and invasion in human HCT-116 and SW480 CRC cells. Mechanistic studies showed that AR potently suppressed STAT3 and Src phosphorylation, and inhibited STAT3 nuclear localization in cultured CRC cells. AR also downregulated the expression of STAT3 target genes Mcl-1, Bcl-xL, and MMP-2 that are involved in cell survival and mobility. Moreover, the cytotoxic effect of AR was diminished by overexpressing STAT3C, a persistent active variant of STAT3. In conclusion, AR exerted anti-CRC effects in vitro and these effects are at least in part attributed to the inhibition of STAT3 signaling. Our findings provide a molecular justification for the traditional use of AR in treating CRC, and a pharmacological basis for developing AR-derived modern anti-CRC agent(s).

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Ubiquitin-specific peptidase 22 inhibits colon cancer cell invasion by suppressing the signal transducer and activator of transcription 3/matrix metalloproteinase 9 pathway

Cited by 16 publications

References 23 publications

Emerging role of DUBs in tumor metastasis and apoptosis: Therapeutic implication

Emerging role of DUBs in tumor metastasis and apoptosis: Therapeutic implication

Expression of ubiquitin specific peptidase and ATG7 genes in U87 glioma cells upon glutamine deprivation

An Ethanolic Extract of Ampelopsis Radix Exerts Anti-colorectal Cancer Effects and Potently Inhibits STAT3 Signaling In Vitro

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