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Chronic psychological stress accelerates lung cancer growth. The lncRNA HIF1A-AS3/HIF-1α pathway, involving macrophages, drives this progression and presents a potential therapeutic target for stressed cancer patients.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Chronic psychological stress is linked to cancer development and progression.
  • Understanding the molecular mechanisms connecting stress and tumorigenesis is crucial for developing new therapies.
  • Lung cancer progression is notably influenced by external factors like stress.

Purpose of the Study:

  • To investigate the role of long non-coding RNAs (lncRNAs) in mediating the effects of chronic stress on lung cancer.
  • To elucidate the molecular mechanisms by which stress-induced factors promote lung cancer growth.
  • To identify potential diagnostic and therapeutic targets for lung cancer associated with psychological stress.

Main Methods:

  • Analysis of lncRNA expression profiles in chronic stress models and human lung cancer tissues.
  • In vitro and in vivo experiments to assess the functional role of lncRNA HIF1A-AS3 in lung cancer cell proliferation and invasion.
  • Mechanistic studies involving protein-RNA interactions (HIF1A-AS3, YBX1, HIF-1α) and transcriptional regulation.
  • Investigation of the tumor immune microenvironment, focusing on macrophage polarization and function.
  • Pharmacological targeting of the HIF1A-AS3/HIF-1α signaling axis in vivo.

Main Results:

  • Chronic stress significantly promoted lung cancer progression in vivo.
  • lncRNA HIF1A-AS3 was upregulated by chronic stress and in lung cancer tissues, promoting cancer cell proliferation and invasion.
  • HIF1A-AS3 activated HIF-1α translation via YBX1, and HIF-1α transcriptionally upregulated HIF1A-AS3, forming a positive feedback loop.
  • Chronic stress and HIF1A-AS3 induced M2-like macrophage polarization, enhancing tumor-promoting effects.
  • Targeting the HIF1A-AS3/HIF-1α axis counteracted stress-induced lung cancer progression.

Conclusions:

  • The HIF1A-AS3/HIF-1α positive feedback loop is a key mediator of chronic stress-induced lung cancer growth.
  • This axis promotes tumorigenesis through the reprogramming of tumor-associated macrophages.
  • The HIF1A-AS3/HIF-1α pathway represents a promising diagnostic and therapeutic target for lung cancer patients experiencing psychological stress.