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Updated: Jan 30, 2026

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Targeting the LHX1-LDB1 Complex Restores STING-dependent Senescence Surveillance and Inhibits Head and Neck Cancer

Mingshu Long1, Yang Chen1,2, Ruixue Du1

  • 1State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.

International Journal of Biological Sciences
|January 29, 2026
PubMed

Insights

LIM homeobox 1 (LHX1) suppresses STING and senescence-associated secretory phenotype (SASP) in head and neck cancer. Targeting LHX1 reactivates SASP, inhibiting tumor growth and improving prognosis for HNSCC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • The senescence-associated secretory phenotype (SASP) has complex roles in cancer, but its regulation in head and neck squamous cell carcinoma (HNSCC) is not fully understood.
  • Understanding SASP regulation is crucial for developing novel cancer therapies.

Purpose of the Study:

  • To investigate the role of LIM homeobox 1 (LHX1) in regulating the SASP in HNSCC.
  • To explore the therapeutic potential of targeting the LHX1-LDB1 complex in HNSCC.

Main Methods:

  • Utilized human and mouse HNSCC cell lines and xenograft models.
  • Assessed the impact of LHX1 expression and depletion on STING signaling and SASP.
  • Employed clinical HNSCC samples to correlate LHX1 expression with patient prognosis.
  • Investigated therapeutic disruption of the LHX1-LDB1 complex using engineered peptides.

Main Results:

  • Identified LHX1 as a transcriptional suppressor of STING, inhibiting SASP activation.
  • Demonstrated that high LHX1 expression correlates with poor prognosis in HNSCC patients.
  • Showed that LHX1 depletion restores STING-dependent SASP and impairs cancer stem cell self-renewal.
  • Confirmed that therapeutic disruption of the LHX1-LDB1 complex re-activates STING, induces SASP, and suppresses tumor growth.

Conclusions:

  • LHX1 acts as a master transcriptional repressor of STING-mediated senescence in HNSCC.
  • Targeting the LHX1-LDB1 axis offers a promising therapeutic strategy to restore tumor-suppressive SASP in HNSCC.
Keywords:
LHX1SASPSTING signalingcancer stem cellspeptide therapeutics

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