Galectin-1 overexpression induces normal fibroblasts translate into cancer-associated fibroblasts and attenuates the sensitivity of anlotinib in lung cancer.
Lei ZhangWenbang ChenXiaojun LiGengming WangFubao XingXiao ZhuPublished in: Cell adhesion & migration (2024)
We aimed to investigate galectin-1 overexpression induces normal fibroblasts (NFs) translates into cancer-associated fibroblasts (CAFs). Galectin-1 overexpression was conducted in Human embryonic lung fibroblasts (HFL1) cell. The motilities of H1299 and A549 cells were measured. Human umbilical vein endothelial cell (HUVEC) proliferation and tube formation ability were assessed. Tumor volume and tumor weight was recorded. Cells motilities were increased, while apoptosis rates were decreased after CMs co-cultured. B-cell lymphoma-2 (Bcl-2) expression level was increased, while Bcl2-associatedX (Bax) and cleaved-caspase3 decreased. CMs treatment enhanced HUVEC proliferation and tube formation. Tumor volume and weight in CMs treated mice were increased, and the sensitivity of anlotinib in co-cultured cells was decreased. Our results revealed that galectin-1 overexpression induced NFs translated into CAFs.
Keyphrases
- induced apoptosis
- cell cycle arrest
- endothelial cells
- endoplasmic reticulum stress
- signaling pathway
- cell death
- cell proliferation
- extracellular matrix
- oxidative stress
- high glucose
- transcription factor
- body mass index
- physical activity
- single cell
- poor prognosis
- type diabetes
- bone marrow
- skeletal muscle
- metabolic syndrome
- stem cells
- drug induced
- adipose tissue
- cell therapy
- smoking cessation
- replacement therapy