Zheng Ye1, Zhaoyu Zhang1, Lijiao Fang1, Daiquan Tian2, Xin Liu3,1. 1. Tianjin Key Laboratory of Medical Epigenetics; Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education); Department of Biochemistry and Molecular Biology, Tianjin Medical University, Tianjin 300070, China. 2. Tianjin Chest Hospital, Tianjin 300222, China. 3. Department of Biochemistry and Molecular Biology, 22 Qixiangtai Road, Tianjin Medical University, Tianjin 300070, China.
Abstract
OBJECTIVE: To explore the potential role of GSG2 in breast cancer progression. METHODS: The 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). RESULTS: The 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. CONCLUSION: Our 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.
OBJECTIVE: To explore the potential role of GSG2 in breast cancer progression. METHODS: The 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). RESULTS: The 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. CONCLUSION: Our 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.
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