Ubiquitin-specific protease 22 (USP22) aberrance has been implicated in several malignancies; however, whether USP22 plays a role in anaplastic thyroid carcinoma (ATC) remains unclear. Here, we report that USP22 expression is highly elevated in ATC tissues, which positively correlated with tumor size, extracapsular invasion, clinical stages, and poor prognosis of ATC patients. In vitro assays showed that USP22 depletion suppressed ATC cell survival and proliferation by decreasing Rb phosphorylation and cyclin D2, inactivating Akt, and simultaneously upregulating Rb; USP22 silencing restrained cell migration and invasion by inhibiting epithelial-mesenchymal transition; USP22 knockdown promoted mitochondrion- mediated and caspase-dependent apoptosis by upregulating Bax and Bid and promoting caspase-3 activation. Consistent with in vitro findings, downregulation of USP22 in ATC cells impeded tumor growth and lung metastasis in vivo. These results raise the applicability for USP22 as a useful predictor of ATC prognosis and a potential therapeutic target for ATC.
Oral squamous cell carcinoma (OSCC) is the most frequent type of oral malignancy with high metastasis and poor prognosis. The deubiquitinating enzyme Ubiquitin Specific Peptidase 44 (USP44) regulates the mitotic checkpoint, and its deficiency leads to aneuploidy and increases tumor incidence. However, the role of USP44 in OSCC is not well understood.
Purpose: To investigate the expression of ubiquitin specific protease 20 (USP20) in oral squamous cell carcinoma (OSCC) and its correlation with clinicopathological parameters.
Methods: OSCC samples and paired paracancerous samples were screened from the TCGA database for differential expression analysis and paired differential analysis. Immunohistochemical staining was used to detect the expression level of USP20 in OSCC tissue, paracancerous tissues and normal tissues.
Ubiquitin‑specific protease 35 (USP35) was found to be involved in various tumor progression, but its role in breast cancer remains largely unknown. USP35 mRNA and protein expression in breast cancer tissues and cells were evaluated by qPCR and Western bolt (WB), respectively. Subsequently, flow cytometry and EDU labeling were used to evaluate breast cancer cell apoptosis and proliferation.
State Key Laboratory of Stress Cell Biology, School of Life Sciences; Institute of Gastrointestinal Oncology, School of Medicine, Xiamen University, Xiamen 361102, China.
Gastric cancer (GC) is an aggressive tumor type with an intricate pathogenesis and limited therapeutic options. Ubiquitin-specific protease 22 (USP22) is a protein implicated in cell proliferation, metastasis, and tumorigenesis. However, the regulatory mechanisms governing USP22 in GC are still not fully understood.
Background: The typical pathological feature of pancreatic ductal adenocarcinoma (PDAC) is a significant increase in stromal reaction, leading to a hypoxic and poorly vascularized tumor microenvironment. Tumor cells undergo metabolic reprogramming, such as the Warburg effect, yet the underlying mechanisms are not fully understood.
Methods: Interference and overexpression experiments were conducted to analyze the in vivo and in vitro effects of USP7 on the growth and glycolysis of tumor cells.
