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This research aims to explore the role of ANKRD1 derived from cancer-associated fibroblasts in lung cancer progression.

Impact of CAF-Derived ANKRD1 on Lung Cancer Tumor Microenvironment

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This research aims to explore the role of ANKRD1 derived from cancer-associated fibroblasts in lung cancer progression.
RNA sequencing was conducted to compare gene expression profiles between normal fibroblasts and CAFs.
Clinical databases analyzed for the prognostic significance of ANKRD1 in lung cancer.
Normal fibroblasts were stimulated with cancer cell-derived growth factors to assess ANKRD1 activation.
Effects of ANKRD1 on migration and treatment resistance were evaluated through migration and colony formation assays.
Angiogenesis effects were assessed by measuring VEGF secretion and conducting tube formation assays with HUVECs.
ANKRD1 was significantly overexpressed in CAFs and linked to poor prognosis in lung adenocarcinoma.
TGF-β stimulation increased ANKRD1 expression in normal fibroblasts.
ANKRD1-overexpressing fibroblasts demonstrated enhanced migratory ability and greater resistance to therapies.
Conditioned media from ANKRD1-overexpressing fibroblasts increased VEGF secretion in cancer cells and promoted angiogenesis in HUVECs.

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Research demonstrates ANKRD1 enhances tumor progression and treatment resistance in lung cancer, suggesting a potential therapeutic target.

Okada et al. (2026) studied this question.

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Research demonstrates ANKRD1 enhances tumor progression and treatment resistance in lung cancer, suggesting a potential therapeutic target.