Low molecular weight heparins (LMWH) are widely used to prevent or treat cancer- and thrombosis-related conditions. However, their direct effects on cancer cells remain unclear. Nine non-small cell lung cancer (NSCLC) cell lines (H1437, H2126, H661, H1299, H1563, H1975, H1573, 2106 T, 2427 T) were treated with tinzaparin (50 IU/ml, ~ 76.9 µM), cisplatin (15 µg/ml), or a combination. We assessed cell viability, proliferation, colony formation, and intracellular lipid droplet accumulation. RNA sequencing was performed on two adenocarcinoma (H1437, H1563) and two squamous cell carcinoma (2106 T, 2427 T) lines to explore transcriptomic changes. Tinzaparin increased proliferation in H1437, H2126, H1299, and H661 cells, but slightly reduced it in 2427 T cells. Colony formation was reduced only in 2427 T, with no effect in other lines despite some showing increased proliferation. Tinzaparin modestly increased viability in 2427 T cells and partially counteracted cisplatin-induced proliferation inhibition in H1573 and apoptosis in H1437 and H2126. Lipid droplet formation was unaffected. Transcriptomic analysis showed variable responses across cell lines, with only CTSL (Cathepsin L) and HMOX1 (Heme Oxygenase 1) consistently altered by tinzaparin. Tinzaparin affects proliferation, viability, colony formation, and drug sensitivity in NSCLC cells in a cell type–specific manner. These findings highlight the complex actions of LMWHs on lung cancer cells and underscore the need for further mechanistic studies to understand their potential impact on cancer progression and therapy.
Held et al. (2026) studied this question.