ETA2023 Poster Presentations Translational 2 (9 abstracts)
Study on the role of podoplanin in papillary thyroid carcinoma using rna sequencing
Damian Gawel 1 , Damian Mielecki 1 , Anna Bętkowska 1 , Marcin Rozwadowski 1 , Agata M. Gawel 2 , Natalia Zeber-Lubecka 3 , Maria Kulecka 3 , Ewa Gajda 1 & Marlena Godlewska 4
1Centre of Postgraduate Medical Education, Department of Cell Biology and Immunology, Warsaw, Poland; 2Medical University of Warsaw, Histology and Embryology Students’ Science Association Hesa, Warsaw, Poland; 3Centre of Postgraduate Medical Education, Department of Gastroenterology, Hepatology and Clinical Oncology, Warsaw, Poland; 4Centre of Postgraduate Medical Education, Department of Cell Biology and Immunology, Department of Cell Biology and Immunology, Warsaw, Poland
Introduction: Podoplanin (PDPN) is a transmembrane protein linked with metastases of various cancers, including papillary thyroid carcinoma (PTC). PDPN is significantly upregulated in PTC specimens and PTC- derived cell lines: TPC1 and BCPAP, harboring RET/PTC and BRAF V600E alterations, respectively. We observed that depletion of PDPN impairs migration of TPC1 cells, but surprisingly, augments metastases of BCPAP cells. To elucidate this phenomenon we aimed to further investigate the role of PDPN in the biology of PTC cells using NGS-based RNA sequencing (RNAseq).
Material and Methods: BCPAP (BRAF V600E) and TPC1 (RET/PTC) cell lines were used in the study. siRNA was used for knockdown of PDPN expression. Cells transfected with negative siRNA served as controls. Total RNA extracted from the cells was sequenced using the RNAseq technique. The expressional profile of the cells and GO terms were assessed. Statistical significance was considered at P < 0.05.
Results: Depletion of PDPN was found to have a significant, but disparate effect on the tested PTC cells. In TPC1/siPDPN cells, GO terms of negative regulation of transcription, regulation of mitotic nuclear division and cell cycle regulation were the most abundant. In contrast, in BCPAP/siPDPN cells, the assigned GO terms referred to positive regulation of transcription, protein phosphorylation and migration. Also, depletion of PDPN resulted in decreased levels of NF-κB and cIAP2 in TPC1 cells, but increased levels of IRAK1 and STAT2 in BCPAP cells.
Conclusion: We conclude that the role of PDPN in PTCs likely depends on the mutational status of the cells. Silencing of PDPN in TPC1 cells leads to promotion of signaling pathways related to the control of cell stability and adhesion processes, while in BCPAP cells – paths involved in cell proliferation and migration. This research was supported by: National Science Centre (No. 2018/29/B/NZ3/02642) Centre of Postgraduate Medical Education (No. 501-1-26-02-22)
Volume 92
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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