GTSE1 promotes prostate cancer cell proliferation via the SP1/FOXM1 signaling pathway

Lai, Wenjie; Zhu, Weian; Li, Xiaojuan; Han, Yuefu; Wang, Yu; Leng, Qu; Li, Mingzhao; Wen, Xin

doi:10.1038/s41374-020-00510-4

Cited by 24 publications

(22 citation statements)

References 30 publications

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“…In this study, we screened GTSE1 as a key gene in ESCC by bioinformatic analysis and preliminarily revealed the aberrant expression of GTSE1 in ESCC and various malignancies by GEPIA and UALCAN databases. GTSE1 has been reported to be highly expressed in many tumors such as hepatocellular carcinoma, 24 prostate cancer, 25 gastric cancer, 26 and breast cancer, 27 whose high expression is associated with cancer progression and can be used as a prognostic indicator. It is involved in inhibiting cell apoptosis and participating in chemical drug resistance, such as cisplatin resistance, paclitaxel resistance, and so on 7,26 .…”

Section: Discussionmentioning

confidence: 99%

“…Some studies have suggested that the activation of JNK signaling pathway is involved in CIN cells, and the mechanism may be related to excessive ROS production. 23 We performed a series of GTSE1 has been reported to be highly expressed in many tumors such as hepatocellular carcinoma, 24 prostate cancer, 25 gastric cancer, 26 and breast cancer, 27 First, we initially verified the high expression of GTSE1 in ESCC tissues and cell lines, EC109 and KYSE150. Correlations between its protein levels and patients' clinical data were analyzed, leading to the conclusion that high GTSE1 was related to patients' tumor size, grade, and lymph node metastasis.…”

Section: Activation Of Jnk Signaling Pathway In Escc Cells and Apopto...mentioning

confidence: 99%

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G2 and S phase‐expressed‐1 induces chromosomal instability in esophageal squamous cell carcinoma cells and inhibits cell apoptosis through ROS/JNK signaling

Zhang

Wang

Liu

et al. 2022

Molecular Carcinogenesis

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New diagnostic and therapeutic strategies are urgently needed to improve the prognosis of patients with esophageal squamous cell carcinoma (ESCC), which has high morbidity and mortality. Bioinformatics analysis revealed that cell cycle regulation related molecular G2 and S phase-expressed-1 (GTSE1) was dysregulated in ESCC. In this study, the ectopic expression of GTSE1 was verified in ESCC patients' tissues and cell lines. After overexpression or knockdown of GTSE1 using lentiviral transfection, the effects of GTSE1 on the proliferation, migration, invasion, and apoptosis of ESCC cells were detected. The contribution of GTSE1 in inducing chromosomal missegregation in cells leading to chromosome instability (CIN) has been described. Long-term existence of CIN can increase reactive oxygen species (ROS) generation in ESCC cells, followed by inhibition of apoptosis by activating the c-Jun N-terminal kinase (JNK) signaling pathway, and this inhibition could be relieved after treatment with JNK inhibitor. In vivo experiments, we also confirmed the tumor-promoting effect and mechanism of GTSE1 in ESCC using nude mice model.In this study, we demonstrated that GTSE1 induces CIN in ESCC cells, and increases intracellular ROS production, which leads to cellular oxidative stress, contributes to the activation of the JNK signaling pathway, and thereby inhibits apoptosis leading to ESCC tumorigenesis.

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Section: Discussionmentioning

confidence: 99%

Section: Activation Of Jnk Signaling Pathway In Escc Cells and Apopto...mentioning

confidence: 99%

G2 and S phase‐expressed‐1 induces chromosomal instability in esophageal squamous cell carcinoma cells and inhibits cell apoptosis through ROS/JNK signaling

Zhang

Wang

Liu

et al. 2022

Molecular Carcinogenesis

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“…28,29 In cervical cancer, Zhang et al 1 reported that silencing of LDHA significantly attenuated colony formation ability and invasive capacity of SiHa and HeLa cells. In addition, GTSE1 was reported to increase the expression of SP1 in prostate cancer, 30 and knockdown of SP1 could decrease the expression of LDHA in testicular tumor cells, 31 indicating that GTSE1 may modulate LDHA expression through SP1. In the current study, we found that downregulation of GTSE1 decreased LDHA expression.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of GTSE1 leads to the inhibition of proliferation, migration, and Warburg effect in cervical cancer by blocking LHDA expression

Chen

Zhong

Yang

et al. 2021

J of Obstet and Gynaecol

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Aim G2 and S phase‐expressed‐1 (GTSE1) has been identified to play a vital role in several kinds of cancers, but its role in cervical cancer development remains unknown. Herein, we aimed to reveal the role and underlying mechanism of GTSE1 in cervical cancer cell growth, migration, and aerobic glycolysis. Methods GTSE1 expression levels in cervical cancer tissues and normal cervical tissues were determined by real time PCR and immunohistochemistry. Human short hairpin RNA was used to downregulate GTSE1 level in cervical cancer cells SiHa and HeLa cells. Colony formation, cell counting kit‐8, and wound‐healing assays were used for cell function evaluation. Lactate production, lactate dehydrogenase activity, and glucose concentration were tested to assess the Warburg effect. Results GTSE1 expressions at both mRNA and protein levels were significantly elevated in cervical cancer tissues compared with normal tissues. Downregulation of GTSE1 induced significant repressions in cell colony formation, viability and migration, and Warburg effect, as well as reduced expression of lactate dehydrogenase isoform A (LDHA) at mRNA and protein levels. Additionally, downregulation of GTSE1 weakened the tumorigenesis of HeLa and SiHa cells in vivo. Conclusion This study demonstrated that downregulation of GTSE1 led to significant inhibitions in cell proliferation, migration, tumorigenesis, and Warburg effect in cervical cancer by blocking the expression of LHDA.

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“…Through the tumor-suppressive protein p53, GTSE1 has been implicated in the pathogenesis of several malignant tumors. Previous research has proved its negative regulation in malignant tumors ( Lai et al, 2021 ). Moreover, GTSE1 has been linked to the development of chemoresistance in osteosarcoma ( Xie et al, 2021 ) and hepatocellular carcinoma ( Li et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Nine-gene signature and nomogram for predicting survival in patients with head and neck squamous cell carcinoma

et al. 2022

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Background: Head and neck squamous cell carcinomas (HNSCCs) are derived from the mucosal linings of the upper aerodigestive tract, salivary glands, thyroid, oropharynx, larynx, and hypopharynx. The present study aimed to identify the novel genes and pathways underlying HNSCC. Despite the advances in HNSCC research, diagnosis, and treatment, its incidence continues to rise, and the mortality of advanced HNSCC is expected to increase by 50%. Therefore, there is an urgent need for effective biomarkers to predict HNSCC patients’ prognosis and provide guidance to the personalized treatment.Methods: Both HNSCC clinical and gene expression data were abstracted from The Cancer Genome Atlas (TCGA) database. Intersecting analysis was adopted between the gene expression matrix of HNSCC patients from TCGA database to extract TME-related genes. Differential gene expression analysis between HNSCC tissue samples and normal tissue samples was performed by R software. Then, HNSCC patients were categorized into clusters 1 and 2 via NMF. Next, TME-related prognosis genes (p < 0.05) were analyzed by univariate Cox regression analysis, LASSO Cox regression analysis, and multivariate Cox regression analysis. Finally, nine genes were selected to construct a prognostic risk model and a prognostic gene signature. We also established a nomogram using relevant clinical parameters and a risk score. The Kaplan–Meier curve, survival analysis, time-dependent receiver operating characteristic (ROC) analysis, decision curve analysis (DCA), and the concordance index (C-index) were carried out to assess the accuracy of the prognostic risk model and nomogram. Potential molecular mechanisms were revealed by gene set enrichment analysis (GSEA). Additionally, gene correlation analysis and immune cell correlation analysis were conducted for further enriching our results.Results: A novel HNSCC prognostic model was established based on the nine genes (GTSE1, LRRN4CL, CRYAB, SHOX2, ASNS, KRT23, ANGPT2, HOXA9, and CARD11). The value of area under the ROC curves (AUCs) (0.769, 0.841, and 0.816) in TCGA whole set showed that the model effectively predicted the 1-, 3-, and 5-year overall survival (OS). Results of the Cox regression assessment confirmed the nine-gene signature as a reliable independent prognostic factor in HNSCC patients. The prognostic nomogram developed using multivariate Cox regression analysis showed a superior C-index over other clinical signatures. Also, the calibration curve had a high level of concordance between estimated OS and the observed OS. This showed that its clinical net can precisely estimate the one-, three-, and five-year OS in HNSCC patients. The gene set enrichment analysis (GSEA) to some extent revealed the immune- and tumor-linked cascades.Conclusion: In conclusion, the TME-related nine-gene signature and nomogram can effectively improve the estimation of prognosis in patients with HNSCC.

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GTSE1 promotes prostate cancer cell proliferation via the SP1/FOXM1 signaling pathway

Cited by 24 publications

References 30 publications

G2 and S phase‐expressed‐1 induces chromosomal instability in esophageal squamous cell carcinoma cells and inhibits cell apoptosis through ROS/JNK signaling

G2 and S phase‐expressed‐1 induces chromosomal instability in esophageal squamous cell carcinoma cells and inhibits cell apoptosis through ROS/JNK signaling

Downregulation of GTSE1 leads to the inhibition of proliferation, migration, and Warburg effect in cervical cancer by blocking LHDA expression

Nine-gene signature and nomogram for predicting survival in patients with head and neck squamous cell carcinoma

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