Macrophage M2 polarization induced by ANKRD22 in lung adenocarcinoma facilitates tumor angiogenesis.

Abstract

Introduction: Lung adenocarcinoma (LUAD), the most prevalent lung cancer type, poses a great threat to public health, with its incidence and mortality rates remaining alarmingly high. While ankyrin repeat domain-containing protein 22 (ANKRD22) is linked to the development of multiple cancers, the molecular mechanisms of its impact on the malignant progression of LUAD are not yet fully understood. This study seeks to elucidate the biological role of ANKRD22 in LUAD.

Material and methods: ANKRD22 expression in LUAD tissues and cells was assessed using the TCGA-LUAD database and quantitative reverse transcription polymerase chain reaction (qRT-PCR). The polarization of macrophages (derived from THP-1 cells) was examined through qRT-PCR, flow cytometry, and western blot to determine the influence of ANKRD22 on macrophage polarization. The effects of ANKRD22 knockdown on A549 cell proliferation and migration were measured using Cell Counting Kit-8 assay, colony formation, and Transwell assays. The impact of ANKRD22-induced macrophage M2 polarization on human umbilical vein endothelial cell (HUVEC) migration and angiogenesis was evaluated with Transwell and tube formation assays.

Results: The expression of ANKRD22 was elevated in LUAD tissue and cellular samples, and its overexpression promoted M2 polarization in macrophages. Blocking ANKRD22-mediated M2 polarization inhibited the migration and tube formation capacity of HUVEC cells.

Conclusions: Our findings showed that ANKRD22 mediates the malignant progression of LUAD by inducing M2 polarization of tumor-associated macrophages, thereby promoting angiogenesis.