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Oral Sessions
Day 2, June 23(Mon.) 14:40-14:55
Room A (Maesato West)
- 2A-O2-1440
LncRNA HIFCAR Sequesters ER Resident Protein to Hinder Antigen Presentation Process in Pancreatic Ductal Adenocarcinoma
(1R&D, NDMC, 2PhD CBDD, TMU, 3GIMS, NDMC, 4CBDD, TMU)
Tze-Ting Kuo1,2, Jia-Jun He3, Bai-Chia Liu4, Tsui-Chin Huang2,4, oHsin-Yi Chang1,3
Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with limited treatment options. The hypoxia-induced long non-coding RNA (lncRNA) LncHIFCAR is significantly overexpressed in PDAC patients. This study explores its oncogenic role and involvement in immune evasion by regulating antigen presentation.
PDAC cell lines with LncHIFCAR overexpression and knockdown were generated to assess cancer stemness features, including epithelial-mesenchymal transition, migration, and anchorage-independent growth. Quantitative proteome analyses identified differentially expressed proteins (DEPs), while RNA affinity purification revealed LncHIFCAR's protein interaction network.
LncHIFCAR overexpression enhances cancer stemness, whereas knockdown reverses these effects. Proteome analysis showed downregulation of innate immunity-related proteins, particularly MHC class I molecules (HLA-A, HLA-B, HLA-C). LncHIFCAR suppresses TAP1 and TAP2, key antigen presentation mediators, potentially leading to immune checkpoint blockade resistance. RNA affinity purification identified interactions with paraspeckle-associated proteins, filamins, and ER proteins, implicating LncHIFCAR in mRNA stability, migration, and protein sorting.
LncHIFCAR modulates ER-associated antigen presentation and downregulates MHC class I molecules, contributing to immune evasion in PDAC. These findings reveal a novel immune regulatory mechanism and suggest LncHIFCAR as a potential therapeutic target to improve immunotherapy efficacy.