Líffræðifélag Íslands - biologia.is
Líffræðiráðstefnan 2023
Höfundar / Authors: Zara Ahmad, Dr. Linda Viðarsdóttir
Starfsvettvangur / Affiliations: University of Iceland
Kynnir / Presenter: Zara Ahmad
Autophagy is responsible for degrading/recycling damaged and redundant cellular components, thereby maintaining vital cell functions, especially under cellular stress. Its dysregulation is associated with various diseases, including cancer. Cancer cells often utilize autophagy as a defense mechanism against anticancer drugs. Hence, inhibiting autophagy has been proposed as a chemotherapeutic strategy. Long non-coding RNAs (LncRNAs) are known to regulate tumor suppressor genes and oncogenes. In this project, we aim to investigate the role of the LncRNA FGD5-AS1 in autophagy, in particularly in osteosarcoma. Our data shows that FGD51-AS is overexpressed in osteosarcoma. Further analysis revealed a strong correlation of FGD51-AS and autophagy related proteins. We analyzed the central autophagy protein LC3 marked with GFP in HOS-GFP-LC3 cells and found enrichment of LC3B binding to FGD5-AS. We further validated this binding by RIP of LC3B. We also examined FGD5-AS1 knockdown cells on protein and gene expression level using western blot, confocal microscopy, and qPCR method. The analysis revealed abnormal expression of LC3B, GABA-RAP-L1, and PINK1. Furthermore, we used proliferation assays, e.g. clonogenic assay and live cell analysis, to analyze survival and the response to anticancer drugs, e. g. doxorubicin or etoposide. These assays consistently demonstrated a rescue of FGD5-AS1 knockdown cells. The results suggest a significant relevance of FGD5-AS1 in autophagy and cancer.