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Updated: Jan 23, 2026

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Oncogenic lncRNA downregulates cancer cell antigen presentation and intrinsic tumor suppression

Qingsong Hu1, Youqiong Ye2, Li-Chuan Chan1,3

  • 1Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.

Nature Immunology
|June 5, 2019
PubMed

Insights

The long noncoding RNA LINK-A drives triple-negative breast cancer (TNBC) by reducing tumor antigen presentation and immune evasion. Targeting LINK-A may improve immunotherapy response in PD-1 blockade-resistant TNBC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Tumor cells evade immune surveillance by losing antigenicity and immune checkpoints, a mechanism not fully understood.
  • Triple-negative breast cancer (TNBC) is an aggressive subtype with limited treatment options.

Purpose of the Study:

  • To investigate the role of the long noncoding RNA LINK-A in TNBC development and immune evasion.
  • To explore potential therapeutic strategies targeting LINK-A for improved immunotherapy outcomes.

Main Methods:

  • Utilized mouse models with tissue-specific LINK-A expression to induce mammary gland tumors.
  • Investigated molecular pathways involving phosphatidylinositol-(3,4,5)-trisphosphate, G-protein-coupled receptors (GPCRs), and TRIM71.
  • Assessed the impact of LINK-A on the antigen peptide-loading complex (PLC), Rb, and p53.
  • Evaluated therapeutic interventions using LINK-A locked nucleic acids and GPCR antagonists.
  • Correlated LINK-A levels and PLC components with patient responses to PD-1 blockade in TNBC.

Main Results:

  • LINK-A expression initiated metastatic mammary tumors resembling human TNBC.
  • LINK-A disrupted signaling pathways, leading to enhanced degradation of PLC, Rb, and p53.
  • Therapeutic targeting of LINK-A or GPCRs restored PLC, Rb, and p53 levels, sensitizing tumors to immune checkpoint blockers.
  • Elevated LINK-A and reduced PLC components were observed in PD-1 blockade-resistant TNBC patients.

Conclusions:

  • lncRNA-dependent downregulation of antigenicity and tumor suppression contributes to TNBC immune evasion.
  • LINK-A represents a potential therapeutic target for enhancing immunotherapy efficacy in TNBC.
  • Findings suggest combinational immunotherapy and early TNBC prevention strategies targeting LINK-A.

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