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345 The impact of long non-coding RNAs on gene expression regulation and pathogenesis mechanisms in ovarian cancer through emerging molecular and bioinformatic analysis
  1. Shika Hanif Malgundkar1,
  2. Sidika Sevde Yenigun1,
  3. Altan Kara2,
  4. Ikram Burney3 and
  5. Yahya Tamimi1
  1. 1Sultan Qaboos University, Al-Khod, Oman
  2. 2Tubitak institute, Istanbul, Turkey
  3. 3Sultan Qaboos Comprehensive Cancer Care and Research Centre, Al-Khod, Oman


Introduction/Background Ovarian cancer (OC) is a deadly gynecological malignancy, often diagnosed in late stages due to the absence of reliable biomarkers, resulting in poor overall survival rates. Therefore, it is crucial to identify biomarkers for early detection and improved outcomes. Emerging evidences suggest the significance of long non-coding RNAs (lncRNAs) as potential biomarkers and regulators of cancer development. However, the role of lncRNAs in OC remains largely not explored.

Methodology In this study we conducted bioinformatics analysis using data from The Cancer Genome Altas (TCGA) database to identify differentially expressed lncRNAs between recurrent and primary OC samples. Among them, lncRNA AC243964.2 was selected for further validation in epithelial ovarian cancer (EOC) cell lines. Functional assays, including cell proliferation, invasion, and wound healing, were performed to assess the role of AC243964.2 in OC. Additionally, qRT-PCR and western blotting were performed to investigate its impact on cancer-related markers.

Results Silencing AC243964.2 did not affect cell proliferation, invasion, and wound healing. However, it led to decreased expression of ATG5, FOXM1, and the anti-apoptotic marker (BCL2), while CASPASE 9 and TP53 expression increased at the RNA level. Furthermore, BCL2, BCL-XL and the apoptotic marker (CASPASE 3) were downregulated, while FOXM1 was overexpressed at the protein level, suggesting the involvement of AC243964.2 in ovarian carcinogenesis.

Conclusion This study reveals the novel role of lncRNA AC243964.2 in regulating ovarian carcinogenesis through the modulation of apoptotic, and autophagy pathways.

Disclosures The authors have no conflict of interest.

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