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Published on: November 2, 2014
Abnormal spindle-like microcephaly-associated protein promotes proliferation by regulating cell cycle in epithelial
Yiguo Wu1, Yujuan You2, Ling Chen1
1Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
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 microcephaly-associated 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.
Keywords:
Abnormal spindle-like microcephaly-associated protein (ASPM); epithelial ovarian cancer (EOC); prognosis; proliferation.
Insights
Abnormal spindle-like microcephaly-associated protein (ASPM) promotes epithelial ovarian cancer (EOC) proliferation and causes S phase arrest. Targeting ASPM may offer a new therapeutic strategy for EOC patients.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Epithelial ovarian cancer (EOC) is a leading cause of gynecological cancer deaths.
- Limited efficacy of current chemotherapy necessitates novel therapeutic targets.
- Previous studies suggest a link between abnormal spindle-like microcephaly-associated protein (ASPM) and ovarian cancer.
Purpose of the Study:
- To investigate the role of ASPM in EOC proliferation.
- To elucidate the molecular mechanisms underlying ASPM's function in EOC.
- To evaluate ASPM as a potential biomarker and therapeutic target for EOC.
Main Methods:
- Analysis of ASPM expression and prognostic value using online databases (TCGA, GEPIA, Cbioportal, KM Plotter).
- Immunohistochemistry on clinical tissue microarrays to assess ASPM expression in EOC tissues.
- In vitro functional assays (CCK8, EdU, colony formation, Transwell) in EOC cell lines with ASPM knockdown via siRNA.
- KEGG pathway enrichment and cell cycle analysis to determine molecular pathways involved.
Main Results:
- ASPM is upregulated in EOC and associated with poorer patient prognosis.
- High ASPM expression correlates with advanced pathological stage, grade, and lymphatic metastasis.
- ASPM knockdown significantly inhibits EOC cell proliferation and migration.
- ASPM silencing leads to S phase arrest in EOC cells, indicating pathway involvement.
Conclusions:
- ASPM promotes proliferation and induces S phase arrest in EOC cells.
- ASPM shows potential as an early screening marker and a therapeutic target for EOC.
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