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Knockdown of GTSE1 obviously suppressed the proliferation, migration, and invasion capacity whereas increasing GTSE1 led to the opposite trend, which suggested that GTSE1 could serve as a potential therapeutic target for bladder cancer. GTSE1 overexpression in bladder cancer might participate in the regulation of FoxM1/CCNB1 expression via the induction of the transfer of p53 to cytoplasm
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High expression of GTSE1 is commonly noted in hepatocellular carcinoma (HCC) and is closely correlated with migration and invasion by epithelial-to-mesenchymal transition modulation. Activated GTSE1 significantly interferes with chemotherapy efficacy and influences the probability of survival of patients with HCC.
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G2 and S-phase expressed 1 (GTSE1) expression promotes AM progression and correlates with clinical outcomes of patients with acral melanoma (AM), and may represent a promising therapeutic target to suppress AM progression.
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GTSE1 is expressed exclusively in late G2 and M phase. From nuclear envelope breakdown until anaphase onset, GTSE1 binds preferentially to the most stable mitotic spindle microtubules and promotes their turnover.
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Results indicated for the first time that overexpression of GTSE1 was involved in the progress of HCC, enhancing proliferation and promoting cell invasion in HCC cells.
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GTSE1 inhibition of MCAK activity regulates the balance of MT stability that determines the fidelity of chromosome alignment, segregation, and chromosomal stability.
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Study identifies GTSE1 as a biomarker for cisplatin resistance in gastric cancer cells and suggests its repressive role in cisplatin induced apoptosis making it a potential therapeutic target for better clinical management of gastric cancer patients.
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GTSE1 is a microtubule plus-end tracking protein that regulates EB1-dependent cell migration.
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GTSE1 is overexpressed dramatically in lung cancer patients' tissues.
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Data show that G2 and S-phase-expressed 1 (GTSE1) protein, a negative regulator of p53, is required for G2 checkpoint recovery and that Plk1 phosphorylation of GTSE1 promotes its nuclear localization.
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hGTSE-1 mediated-p21(CIP1/WAF1) stabilization is clearly involved in the ability of cells to counteract cytotoxicity induced by the microtubule poison paclitaxel.
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GTSE-1 controls DNA damage-induced apoptosis by affecting p53 function
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requires an intact nuclear export signal and functional Mdm2 for the regulation of p53
