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Updated: Jun 27, 2026

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity
Published on: October 17, 2025
Inhibitory effect of kinetin riboside in human heptamoa, HepG2
Jane Cheong1, David Goh, Jean Wan Hong Yong
1Applied Science School, Temasek Polytechnic, 21 Tampinese Avenue 1, Singapore, 529757, Republic of Singapore.
Abstract:
Cytokinins ribosides such as kinetin riboside are a class of plant hormone that were first identified as factors that promote cell division and have since been implicated in many other aspects of plant growth and development. From the data obtained from cell cycle analysis with flow cytometry, the in vitro growth inhibition of human heptamoa, HepG2 cells with kinetin riboside was mediated by causing G2/M cell cycle arrest and cell death. At the same time, treatment with various doses of kinetin riboside in HepG2 cells did not result in a population of cells positive for the active caspase 3. Differentially expressed proteins in the mitochondria of HepG2 cells with cell death induced by kinetin riboside were investigated. Without the use of stable isotope labeling, the proposed method using LC/MSMS provided a rapid approach to study the differentially expressed proteins in the mitochondria due to the cell death induced by kinetin riboside in HepG2 cells. The ability of kinetin riboside to induce cell death and attenuate G1 to S transition is probably a consequence of its ability to interfere with several components in the mitochondria. Hence, it was proposed that the cell death caused by kinetin riboside in HepG2 cells affected a network of proteins involved in cell death and electron transport.
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