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Background: Epithelial ovarian cancer (EOC) ranks first for female gynecological tumor-related deaths.Due to the limited efficacy of traditional chemotherapy strategies, potential therapeutic targets are urgently needed. Previous studies have reported a relationship between abnormal spindle-like microcephalyassociated protein (ASPM) and ovarian cancer based on immunohistochemistry (IHC) and bioinformatics analysis. However, the potential role of ASPM in the proliferation of ovarian cancer cells and its molecular mechanism remain to be elucidated. Therefore, we aimed to further investigate the potential role of ASPM and its underlying mechanism in EOC using integrated online databases, clinical samples, and cell models. Methods:We used online databases (Gene Expression Profiling Interactive Analysis, Cbioportal and Kaplan-Meier Plotter) to analyze differential ASPM expression in ovarian carcinoma and explore its prognostic value in ovarian cancer (OvCa) patients. Immunohistochemistry staining based on a clinical tissue microarray (TMA) comprised 75 cases of EOC tissue and 5 cases of adjacent normal ovary tissue was used to detect the ASPM expression and analyze the relationship between ASPM expression and EOC characteristics. Various cell function experiments related to tumorigenesis were performed including the CCK8 assay, 5-ethynyl-2'-deoxyuridine (EdU), colony formation assay and Transwell assay in EOC cell models (A2780 and OVCAR3) with knocked down ASPM by small interfering RNA (siRNA) to observe its role. Finally, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment was conducted to determine the signaling pathways in which ASPM was involved in the pathogenesis of ovarian cancer.Analysis of cell cycle distribution using flow cytometry was further performed to verify the pathways. Results:The expression profile based on data from The Cancer Genome Atlas (TCGA) database confirmed ASPM expression in EOC was higher compared with normal tissue, and further analysis suggested that higher expression was correlated with worse patient prognosis. Immunohistochemical analysis further indicated that ASPM was highly expressed in OvCa tissues and associated with a higher pathological stage, grade, and positive lymphatic metastasis. Cell models with knocked down ASPM by small interfering RNA (siRNA) significantly inhibited proliferation and migration. KEGG pathway enrichment and cell cycle analysis showed that ASPM silencing could inhibit ovarian cancer cell proliferation via synthesis (S) phase arrest.Conclusions: Our study confirmed that ASPM promoted proliferation and caused S phase arrest in EOC cells. ASPM may become a potential molecular marker for early screening and a valuable therapeutic target in EOC.

Background: Somatic copy number alteration (SCNA) usually accompanies the appearance of tumours; one common example is the 19q13.2 region amplification (AMP), mediator complex subunit 29 (MED29) were an amplified effector gene within this region. In this study, the role and molecular mechanism of MED29 in ovarian cancer (OvCa), one of the three major tumours in gynaecology, were discussed.Results: According to the transcriptome and survival data from the TCGA database, 19q13.2 AMP corresponded with a worse prognosis of OvCa patients (P = 0.0253), and individuals with 19q13.2 AMP showed increased levels of MED29 mRNA. From the GSE29450 dataset, we found that the gene expression of MED29 was significantly upregulated in OvCa and overexpression of MED29 in OvCa was related to shorter survival. Additionally, pathway analysis based on RNA-seq data indicated that MED29 could activate the expression of genes involved in cell proliferation. Moreover, knockdown of MED29 obvious inhibited the proliferation, invasion and migration of OVCAR3 and A2780 cells and arrested the cell cycle at the G2/M transition in vitro.Conclusion: MED29 could be used as a potential therapeutic target for OvCa treatment.

Background: Somatic copy number alteration (SCNA) usually accompanies the appearance of tumours; one common example is the 19q13.2 region amplification (AMP). Studies have shown that the 19q13.2 AMP might worsen the prognosis of patients with pancreatic cancer, and mediator complex subunit 29 (MED29) might be an amplified effector gene within this region. In this study, the role and molecular mechanism of MED29 in ovarian cancer (OvCa), one of the three major tumours in gynaecology, were discussed.Results: According to the transcriptome and survival data from the TCGA database, 19q13.2 AMP corresponded with a worse prognosis of OvCa patients (P = 0.0253), and individuals with 19q13.2 AMP showed increased levels of MED29 mRNA. From the GSE29450 dataset, we found that the gene expression of MED29 was significantly upregulated in OvCa and overexpression of MED29 in OvCa was related to shorter survival. Additionally, pathway analysis based on RNA-seq data indicated that MED29 could activate the expression of genes involved in cell proliferation. Moreover, knockdown of MED29 obvious inhibited the proliferation, invasion and migration of OVCAR3 and A2780 cells and arrested the cell cycle at the G2/M transition in vitro.Conclusion: MED29 could be used as a potential therapeutic target for OvCa treatment.