56 - Promoter Hypermethylation as a Novel Regulator of Galectin-1 Mediated Progression After Thermal Ablation in Early-Stage Hepatocellular Carcinoma

Monday, April 13, 2026

12:10 PM - 1:10 PM ET

Location: Poster Hall (800 level)

Poster Presenter(s)

YS

Yongwan Shin, PhD

Research Associate
Department of Radiology, Ronald Reagan UCLA Medical Center, Los Angeles, California, USA, United States

Author/Co-author(s)

Tu Nguyen (he/him/his)

Medical Student
Department of Radiology, Ronald Reagan UCLA Medical Center, Los Angeles, California, USA, United States
Janet Pham

Staff Research Associate 2
UCLA Health, United States
Po-Chun Chen, MS, DVM (she/her/hers)

PhD Candidate
UCLA, United States
Jason Chiang, MD, PhD (he/him/his)

Assistant Professor
Interventional Radiology, UCLA, United States

Purpose: To investigate the epigenetic regulation of Galectin-1 (Gal-1) expression, highlighting its role in promoting metastatic potential and post-ablation response in hepatocellular carcinoma (HCC)

Materials and Methods: Gal-1 expression was analyzed by RT-qPCR, Western blotting in heat-resistant SNU423 and SNU449 cells. To assess the role of promoter CpG methylation, cells were treated with the DNA methyltransferase inhibitor 5-aza-2’-deoxycytiding (5-Aza-CdR). DNA methylation status and patterns were examined using methylation specific PCR (MSP) and bisulfite sequencing. Cell motility and invasion assay were performed in SNU423 and SNU449 cells with or without 5-Aza-CdR treatment. The metastasis-related gene expression levels were evaluated by RT-qPCR in Gal-1 knockdown SNU423 with or without 5-Aza-CdR treatment. An in vivo xenograft model was established to evaluate the metastatic potential of HCC cells.

Results: Gal-1 was minimally expressed in SNU423 but overexpressed in SNU449 cells (SNU423: 1.00 ± 0.06 versus SNU449: 64.87 ± 1.70, p= 0.001). The treatment of SNU423 and SNU449 cells with 5-Aza-CdR potentiated Gal-1 expression. Consistent with this notion, hypermethylation was detected at the CpG island of Gal-1 promoter region in SNU423 cells by MSP, and 5-Aza-CdR treatment resulted in a drastic demethylation at promoter CpG methylation sites. Upon 5-Aza-CdR treatment, metastatic indexes, such as cell motility, invasion, and metastasis-related gene expression, were significantly altered in SNU423 cells. These 5-Aza-CdR-induced metastatic hallmarks were, however, almost completely silenced by stable knockdown of Gal-1.

Conclusion: Collectively, our results help elucidate the critical role of Gal-1 expression in HCC in post-ablation progression, which is epigenetically modulated by promoter CpG methylation.