Poster Session 2.E - Pathological and Oncological Sciences
Szakadáti, Helga, MSc
CUKMVQ
Semmelweis University, Department of Pathology and Experimental Cancer Research
+36209533225
szakadati.helga@phd.semmelweis.hu
Investigating SPOCK1 as an Oncogenic Driver and Diagnostic Biomarker in Human Liver Disease
Helga Szakadáti1, Lóránd Váncza2, Dávid Bárdos3, Ilona Kovalszky1, Kornélia Baghy1
1: Semmelweis University, Department of Pathology and Experimental Cancer Research
2: Pediatric Center, Tűzoltó utca Department, Semmelweis University, Faculty of Medicine, Budapest
3: Department of Surgery, Transplantation and Gastroenterology, Semmelweis University, Faculty of Medicine, Budapest
Poszter
Poster Session 2.E - Pathological and Oncological Sciences
English
Pathological and Oncological Sciences
Introduction
Hepatocellular carcinoma (HCC) remains one of the most prevalent primary liver cancers and is a leading cause of cancer-related mortality globally. The tumor microenvironment (TME), comprising cellular and molecular components like the extracellular matrix (ECM), plays a critical role in cancer progression. SPOCK1, a proteoglycan found within the ECM, has emerged as a significant oncogene. Understanding SPOCK1's role in HCC is essential for developing improved diagnostic and therapeutic strategies.
Aims
This research aims to clarify SPOCK1’s pathophysiological role in human liver diseases and assess its potential as a diagnostic marker. Objectives include investigating the effects of SPOCK1 on tumorigenesis, signaling pathways, and apoptosis; quantifying differences in SPOCK1 expression across various liver tissues; and measuring circulating levels in patient blood to evaluate its clinical utility.
Methods
Stable SPOCK1-overexpressing hepatoma cell lines were established and examined. Proliferation and DNA synthesis were measured via SRB and BrdU assays; signaling pathway activation was assessed using cyclin B1 and phospho-histone H3 markers. Migration was analyzed using a transwell assay; apoptosis was measured by flow cytometry. In vivo tumor growth was studied using SCID mouse xenograft models. Human liver samples and plasma were analyzed using in silico tools, immunostaining, and ELISA.
Results
In vitro assays showed that SPOCK1 overexpression enhanced proliferation and DNA synthesis by activating the Akt-mTOR and MAPK-ERK1/2 signaling pathways. In HLE cells, overexpression enhanced migration and inhibited apoptosis. The in vivo mouse model showed that SPOCK1-overexpressing tumors grew at an accelerated rate compared to controls. Analysis of human samples confirmed these findings; SPOCK1 mRNA and protein levels were significantly elevated in HCC tissue compared to healthy controls. While tissue expression was high, ELISA showed a significant decrease in circulating SPOCK1 specifically in patients with hepatitis B.
Conclusion
SPOCK1 is a potent oncogene in liver cancer, driving malignant behavior through key signaling pathways. Its correlation with poor prognosis highlights its potential as a clinical biomarker for HCC.
Funding
This work was supported by NKFI-OTKA FK 138593 and SE 250+.
Semmelweis University
Baghy Kornélia
I do not give consent to the publication of my abstract on the website of the congress.
in doctoral studies after complex exam (PhD)
Szabad
elfogadva
poszter
nem rendelkezett róla
9174
18:06
18:09