ArticlePloS one2011
Lapatinib induces autophagy, apoptosis and megakaryocytic differentiation in chronic myelogenous leukemia K562 cells.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 63 citations in OpenAlex.
- Identification and functional characterization of splicing factors implicated in mantle cell lymphoma aggressiveness.Scientific reports · 2025Article
- Discovery of Potent IsoquinolinequinoneJournal of medicinal chemistry · 2024Article
- The Involvement of Canonical NFκB Pathway in Megakaryocyte Differentiation Induction by Nanocurcumin.International journal of hematology-oncology and stem cell research · 2023Article
- Involvement of autophagy in diosgenin‑induced megakaryocyte differentiation in human erythroleukemia cells.Molecular medicine reports · 2021Article
- Establishment of a novel mesenchymal stem cell-based regimen for chronic myeloid leukemia differentiation therapy.Cell death & disease · 2021Article
- Combination of carbon-ion beam and dual tyrosine kinase inhibitor, lapatinib, effectively destroys HER2 positive breast cancer stem-like cells.American journal of cancer research · 2020Article
- Glucose-6-phosphate dehydrogenase blockade potentiates tyrosine kinase inhibitor effect on breast cancer cells through autophagy perturbation.Journal of experimental & clinical cancer research : CR · 2019Article
- Low Autophagy (ATG) Gene Expression Is Associated with an Immature AML Blast Cell Phenotype and Can Be Restored during AML Differentiation Therapy.Oxidative medicine and cellular longevity · 2018Article
- Effects of lapatinib on cell proliferation and apoptosis in NB4 cells.Oncology letters · 2018Article
- 4-Nerolidylcatechol: apoptosis by mitochondrial mechanisms with reduction in cyclin D1 at G0/G1 stage of the chronic myelogenous K562 cell line.Pharmaceutical biology · 2017Article
- ERRF sensitizes ERBB2-positive breast cancer cells to lapatinib treatment likely by attenuating MCL1 and ERBB2 expression.Oncotarget · 2017Article
- 5-Aminoimidazole-4-carboxamide ribonucleoside-induced autophagy flux during differentiation of monocytic leukemia cells.Cell death discovery · 2017Article
- Radiosensitizing effect of lapatinib in human epidermal growth factor receptor 2-positive breast cancer cells.Oncotarget · 2016Article
- Inhibition of eEF-2 kinase sensitizes human nasopharyngeal carcinoma cells to lapatinib-induced apoptosis through the Src and Erk pathways.BMC cancer · 2016Article
- Photodynamic N-TiOScientific reports · 2016Article
- Armillaridin induces autophagy-associated cell death in human chronic myelogenous leukemia K562 cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Article
- Conserved molecular mechanisms underlying the effects of small molecule xenobiotic chemotherapeutics on cells.Molecular and clinical oncology · 2016Article
- EM23, a natural sesquiterpene lactone, targets thioredoxin reductase to activate JNK and cell death pathways in human cervical cancer cells.Oncotarget · 2016Article
- Lapatinib induces autophagic cell death and differentiation in acute myeloblastic leukemia.OncoTargets and therapy · 2016Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lapatinib is an oral, small-molecule, dual tyrosine kinase inhibitor of epidermal growth factor receptors (EGFR, or ErbB/Her) in solid tumors. Little is known about the effect of lapatinib on leukemia. Using human chronic myelogenous leukemia (CML) K562 cells as an experimental model, we found that lapatinib simultaneously induced morphological changes resembling apoptosis, autophagy, and megakaryocytic differentiation. Lapatinib-induced apoptosis was accompanied by a decrease in mitochondrial transmembrane potential and was attenuated by the pancaspase inhibitor z-VAD-fmk, indicating a mitochondria-mediated and caspase-dependent pathway. Lapatinib-induced autophagic cell death was verified by LC3-II conversion, and upregulation of Beclin-1. Further, autophagy inhibitor 3-methyladenine as well as autophagy-related proteins Beclin-1 (ATG6), ATG7, and ATG5 shRNA knockdown rescued the cells from lapatinib-induced growth inhibition. A moderate number of lapatinib-treated K562 cells exhibited features of megakaryocytic differentiation. In summary, lapatinib inhibited viability and induced multiple cellular events including apoptosis, autophagic cell death, and megakaryocytic differentiation in human CML K562 cells. This distinct activity of lapatinib against CML cells suggests potential for lapatinib as a therapeutic agent for treatment of CML. Further validation of lapatinib activity in vivo is warranted.
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