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  11. Hypoxia Drives Estrogen Receptor Β-mediated Cell Growth Via Transcription Activation In Non-small Cell Lung Cancer

Hypoxia drives estrogen receptor β-mediated cell growth via transcription activation in non-small cell lung cancer

Qi Su1, Kun Chen1, Jiayan Ren1

  • 1School of Pharmacy, Health Science Center, Xi'an Jiaotong University, No. 76, Yanta West Street, #54, Xi'an, Shaanxi Province, 710061, P. R. China.

Journal of Molecular Medicine (Berlin, Germany)
|October 17, 2024

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View abstract on PubMed

Summary
This summary is machine-generated.

Estrogen receptor beta (ERβ) promotes non-small cell lung cancer (NSCLC) progression by increasing cell proliferation and inhibiting apoptosis. Hypoxia-inducible factor-1α (HIF-1α) directly upregulates ERβ, making both targets promising for NSCLC therapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cellular Biology

Background:

  • Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related mortality.
  • Hypoxia is a common feature in solid tumors, driving cancer progression via hypoxia-inducible factors (HIF).
  • Estrogen receptor beta (ERβ) has been implicated in NSCLC, but its role and regulation under hypoxia are not fully understood.

Purpose of the Study:

  • To elucidate the role of ERβ in NSCLC progression under hypoxic conditions.
  • To investigate the regulatory relationship between HIF-1α and ERβ in NSCLC.
  • To evaluate the therapeutic potential of targeting HIF-1α and ERβ in NSCLC.

Main Methods:

  • Overexpression studies of ERβ in NSCLC cell lines and xenografts.
  • Tissue microarray analysis to correlate HIF-1α and ERβ expression.
Keywords:
Estrogen receptor βFulvestrantHypoxia-inducible factor 1αLW6

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  • Hypoxia induction using CoCl₂ and low oxygen (1% O₂) incubation.
  • Chromatin immunoprecipitation (ChIP) assay to identify HIF-1α binding sites.
  • In vitro and in vivo experiments to assess the effects of HIF-1α and ERβ suppression.

    • Main Results:

    • ERβ overexpression, but not ERα, enhanced NSCLC cell proliferation and inhibited apoptosis.
    • A significant positive correlation was observed between HIF-1α and ERβ protein expression in NSCLC tissues.
    • HIF-1α was found to directly induce ERβ gene transcription and protein expression by binding to a hypoxia response element in the ESR2 promoter.
    • Suppression of both HIF-1α and ERβ significantly reduced tumor growth in vitro and in vivo.

    Conclusions:

    • ERβ plays a critical role in promoting NSCLC progression, particularly under hypoxic conditions.
    • HIF-1α is a key regulator of ERβ expression in NSCLC, establishing a direct link between hypoxia and ERβ.
    • Targeting the HIF-1α/ERβ pathway represents a promising therapeutic strategy for NSCLC treatment.
    Non-small cell lung cancer