ArticleBiophotonics discovery2026
Sunitinib induces coordinated mitochondrial, lysosomal, and endoplasmic reticulum disruption, leading to cellular collapse.
Article in Biophotonics discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Significance: Understanding the subcellular mechanisms of sunitinib toxicity is critical for improving its therapeutic efficacy and minimizing adverse effects, as its intracellular mechanisms remain incompletely defined. Aim: We investigate the intracellular distribution and organelle-specific effects of sunitinib in HeLa cells using quantitative viability assays and structured illumination microscopy. Approach: Cell viability was assessed using CCK-8 assays. The intrinsic fluorescence of sunitinib allowed for live-cell imaging and colocalization analysis with organelle markers. Super-resolution imaging and quantitative morphometric analyses were used to evaluate mitochondrial, lysosomal, and endoplasmic reticulum integrity. Results: Sunitinib induced a dose-dependent reduction in cell viability. Imaging revealed preferential lysosomal accumulation. Mitochondria exhibited increased fragmentation and loss of hyperfused networks. Lysosomes appeared in reduced numbers while showing enlargement and decreased circularity, implying structural stress. ER networks displayed concentration-dependent fragmentation, as demonstrated by increased connectivity index values. Conclusions: Sunitinib induces coordinated structural and functional disruption across multiple organelles, highlighting organelle stress and loss of cellular homeostasis as key contributors to its cytotoxicity and intracellular pharmacodynamics.
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