M2 Macrophage exosomal HOXC13-AS in laryngeal cancer immunity via targeting miR-485-5p/IGF2BP2/PD-L1.

• This study uncovers a novel mechanism by which M2 macrophage-derived exosomes facilitate the progression of laryngeal squamous cell carcinoma (LSCC) through the transfer of HOXC13-AS to tumor microenvironment macrophages. • Utilizing a combination of advanced techniques, including transmission electron microscopy and western blot, the research provides evidence that M2- exo -mediated HOXC13-AS significantly enhances LSCC malignancy and immune evasion both in vitro and in vivo. • The findings reveal that silencing HOXC13-AS in M2-exo can effectively suppress LSCC's aggressive behavior and its ability to evade the immune system, offering a potential therapeutic target for LSCC treatment. • The study also demonstrates that M2- exo -mediated HOXC13-AS influences the expression of IGF2BP2, a key regulator of cellular functions and immune escape, highlighting the complexity of tumor-microenvironment interactions in LSCC. • By elucidating the role of exosomal HOXC13-AS in LSCC, this research contributes to the understanding of exosome-mediated intercellular communication in cancer progression and immune modulation. This study investigates the role of M2- exo -mediated HOXC13-AS in laryngeal squamous cell carcinoma (LSCC) by examining its transmission to tumor microenvironment (TME) macrophages. Exosomes from M2 macrophages were isolated and characterized using transmission electron microscopy, nanoparticle tracer analysis and western blot. Expression of HOXC13-AS, miR-485-5p, IGF2BP2, and PD-L1 was analyzed. Different interventions on LSCC cell function and immune escape were detected using molecular biological techniques. The study found that elevated HOXC13-AS were present in LSCC, and M2-exo expression was significantly increased in LSCC cells. Silencing HOXC13-AS in M2-exo inhibited LSCC malignant progression and immune escape in vivo and in vitro. M2- exo -mediated HOXC13-AS also regulated IGF2BP2 expression, impacting cellular biological function and immune escape process. The study concludes that M2- exo -mediated HOXC13-AS promotes LSCC malignancy and immune escape. [ABSTRACT FROM AUTHOR]