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Metastasis02:30

Metastasis

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Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
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Development of Compendium for Esophageal Squamous Cell Carcinoma
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FSTL3-Driven Cuproptosis Resistance and EPCs Promote OSCC Metastasis.

S-R Li1, Z-Z Wu1, W-D Wang1

  • 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, Frontier Science Center for Immunology and Metabolism, Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China.

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Summary

Follistatin-like 3 (FSTL3) drives oral cancer metastasis by enabling cancer cell survival and immune evasion. Targeting FSTL3 inhibits metastasis and enhances immunotherapy effectiveness, offering a new therapeutic strategy for oral squamous cell carcinoma (OSCC).

Keywords:
cell deatherythroid progenitor cellsfollistatin-like 3immunotherapylymphatic metastasisoral carcinogenesis

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Area of Science:

  • Oncology
  • Cancer Metastasis
  • Immunotherapy

Background:

  • Lymph node metastasis in oral squamous cell carcinoma (OSCC) is linked to cancer cell death evasion and poor prognosis.
  • Identifying key regulators of metastasis is crucial for developing effective therapeutic strategies.

Purpose of the Study:

  • To identify master regulators of lymph node metastasis in OSCC.
  • To elucidate the mechanisms by which FSTL3 promotes metastasis and immune evasion.
  • To evaluate FSTL3 as a therapeutic target, alone and in combination with immunotherapy.

Main Methods:

  • CRISPR-Cas9 screening in OSCC cell lines with varying metastatic potential.
  • Analysis of FSTL3's role in cuproptosis, mitochondrial metabolism, and immune cell recruitment.
  • Assessment of FSTL3 depletion effects on tumor immunity and immunotherapy response in vivo.

Main Results:

  • Follistatin-like 3 (FSTL3) was identified as a master regulator of OSCC lymph node metastasis.
  • FSTL3 loss induced cuproptosis by suppressing SLC25A10, leading to succinate accumulation and DLAT upregulation.
  • FSTL3 promoted an immunosuppressive tumor microenvironment by recruiting EPCs expressing CCR5, CD73, and PD-L1.
  • FSTL3 depletion sensitized immunotherapy-resistant tumors, unleashed antitumor immunity, and synergized with immunotherapy.

Conclusions:

  • FSTL3 is a pivotal node coordinating cuproptosis resistance and immune evasion in OSCC metastasis.
  • Targeting FSTL3 disrupts these adaptive programs, effectively inhibiting lymph node metastasis.
  • Combining FSTL3 inhibition with immunotherapy presents a promising dual-targeting strategy to improve OSCC outcomes.