Publication:
AADAC promotes therapeutic activity of cisplatin and imatinib against ovarian cancer cells

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Wang-37-899-907-2022.pdf(4.14 MB)
Date
2022
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Authors
Wang, Haijing ; Wang, Disong ; Gu, Tingting ; Zhu, Mengjiao ; Cheng, Ling ; Da, Wentao
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Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/ 10.14670/HH-18-460
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info:eu-repo/semantics/article
Description
Abstract
Objective. To explore how AADAC functions in the malignant progression of ovarian cancer, and the effect of AADAC on drug therapeutic activity against ovarian cancer cells. Methods. AADAC level in tumor and normal samples from TCGA-OV dataset and its survival significance were analyzed by bioinformatics methods. Signaling pathway enrichment analysis for the high- and low-AADAC patients was achieved by using GSEA software. AADAC expression in the cell lines with different treatments was evaluated via qRT-PCR. Cell proliferative ability was assessed via MTT assay Cell migratory and invasive abilities were evaluated via transwell assay. Angiogenesis assay was performed to examine the angiogenetic ability. Results. AADAC was upregulated in ovarian cancer tissues, and patients with high expression of AADAC had favorable survival conditions compared to the low AADAC expression ones. Overexpression of AADAC inhibited the malignant progression of ovarian cancer cells. Both cisplatin and imatinib suppressed cancer cell malignant progression, while overexpressed AADAC synergistically enhanced such inhibition. Conclusions. The study demonstrated that AADAC could somehow suppress the malignant progression of ovarian cancer, especially at the cellular level. In addition, synergic tumor-inhibitory effects between AADAC and the anti-cancer drugs were identified. All the above results proposed a novel idea and candidate biomarker for ovarian cancer therapy.
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AADAC , Ovarian cancer , Cisplatin , Imatinib , Malignant progression
Citation
URI
http://hdl.handle.net/10201/128928
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Collections
Histology and histopathology Vol.37, nº9 (2022)
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