Abstract
ObjectiveTo explore the potential role of GSG2 in breast cancer progression.MethodsThe mRNA expression, DNA copy number and clinical data used in this study were obtained from the TCGA data portal. The copy number variations (CNVs) thresholds were determined according to the set of discrete copy number calls provided by Genomic Identification of Significant Targets in Cancer (GISTIC).ResultsThe mRNA expression level of GSG2 in 112 breast cancer tissues was much higher than that in adjacent normal tissues. GSG2 was significantly upregulated in stage II compared with stage I, and there was no differential expression of GSG2 between tumors with or without metastasis. Heterozygous deletion occupied 57.1% of CNVs for GSG2 gene in breast cancer samples. Patients with higher GSG2 expression tended to suffer from poorer prognosis.ConclusionOur profiling analysis indicated the overexpression of GSG2 might play an important role in breast cancer development, suggesting that GSG2 could be a new target for breast cancer treatment, making GSG2 inhibitors becoming potential drugs for breast cancer therapy.
Highlights
According to the Global Cancer statistics, there were an estimated 18.1 million new cancer cases and 9.6 million cancer deaths in 2018 [1]
To investigate the potential function of GSG2 in breast cancer, we focused on its mRNA expression level in breast cancer tissues
The analysis revealed that the mRNA expression level of GSG2 in breast cancer tissues is much higher than that in adjacent normal tissues (Figure 1b)
Summary
According to the Global Cancer statistics, there were an estimated 18.1 million new cancer cases and 9.6 million cancer deaths in 2018 [1]. Breast cancer is the second commonly diagnosed cancer and the second leading cause of cancer death [1], which makes it essential to study the mechanism of breast cancer progression and to find new targets for breast cancer treatment. Haspin localizes in nucleus in interphase cells [2, 3], and is predominantly associated with chromosomes, especially centrosomes in mitosis [4, 5]. Despite the absence of some of the highly conserved motifs found in canonical eukaryotic protein kinases, mammalian HASPIN proteins have been proved definitively to have serine/threonine kinase activity, and its only substrate is histone H3 [4, 6, 7]. Haspin phosphorylates histone H3 during mitosis and plays an important role in regulating chromosome behavior during cell division [8]. Haspin depletion results in a defect in chromosome congression and a delay in exit from mitosis [9, 10]
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