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Related Experiment Video

Updated: Jun 25, 2025

Modeling Oral-Esophageal Squamous Cell Carcinoma in 3D Organoids
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LINC00330/CCL2 axis-mediated ESCC TAM reprogramming affects tumor progression.

Lijun Zhao1, Gengchao Wang2, Haonan Qi3

  • 1Henan Key Laboratory of Immunology and Targeted Drugs, Xinxiang Key Laboratory of Tumor Microenvironment and Immunotherapy, School of Medical Technology, Xinxiang Medical University, Xinxiang, Henan, China. lijun_zhao123@163.com.

Cellular & Molecular Biology Letters
|May 20, 2024
PubMed
Summary

Long noncoding RNA LINC00330 inhibits esophageal squamous cell carcinoma (ESCC) progression by reprogramming tumor-associated macrophages (TAMs) via the CCL2 pathway. This discovery offers new therapeutic strategies for ESCC patients.

Keywords:
CCL2ESCCLINC00330TAM reprogramming

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Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Tumor-associated macrophages (TAMs) are critical in esophageal squamous cell carcinoma (ESCC) progression, metastasis, and recurrence.
  • While aberrant long noncoding RNA (lncRNA) expression is known in ESCC, their role in TAM reprogramming remains unclear.

Purpose of the Study:

  • To investigate the role of lncRNAs in TAM reprogramming during ESCC progression.
  • To identify specific lncRNAs involved in TAM regulation and their impact on ESCC.
  • To elucidate the molecular mechanisms underlying LINC00330's function in ESCC and TAMs.

Main Methods:

  • Identified ESCC TAM-related lncRNAs by intersecting differentially expressed and immune-related lncRNAs.
  • Analyzed LINC00330 expression and clinical relevance using TCGA and patient samples.
  • Investigated LINC00330's effect on ESCC progression and TAM reprogramming through in vitro and in vivo experiments, including co-culture and transcriptomic analysis.

Main Results:

  • LINC00330 was significantly downregulated in ESCC and associated with poor outcomes.
  • LINC00330 overexpression inhibited ESCC proliferation, invasion, EMT, and tumorigenicity.
  • LINC00330 promoted TAM reprogramming, which subsequently inhibited ESCC progression by binding to CCL2 and affecting downstream signaling.

Conclusions:

  • LINC00330 inhibits ESCC progression by disrupting the CCL2/CCR2 axis in both autocrine and paracrine manners.
  • LINC00330 impedes CCL2-mediated TAM reprogramming, offering a novel mechanism.
  • The LINC00330/CCL2 axis presents potential targets for novel immunotherapies in ESCC.