{
"@context": "http://schema.org",
"@type": "Dataset",
"@id": "https://doi.org/10.6084/m9.figshare.17694752",
"url": "https://tandf.figshare.com/articles/dataset/Downregulation_of_Smad4_expression_confers_chemoresistance_against_imatinib_mesylate_to_chronic_myeloid_leukemia_K562_cells/17694752",
"additionalType": "Dataset",
"name": "Downregulation of Smad4 expression confers chemoresistance against imatinib mesylate to chronic myeloid leukemia K562 cells",
"author": [
{
"name": "Jiangzhao Zhang",
"givenName": "Jiangzhao",
"familyName": "Zhang"
},
{
"name": "Min Zhang",
"givenName": "Min",
"familyName": "Zhang"
},
{
"name": "Yan Liang",
"givenName": "Yan",
"familyName": "Liang"
},
{
"name": "Min Liu",
"givenName": "Min",
"familyName": "Liu"
},
{
"name": "Zhiping Huang",
"givenName": "Zhiping",
"familyName": "Huang"
}
],
"description": "Objective: Imatinib mesylate (IM), a tyrosine kinase inhibitor, exhibits clinically prominent effects against chronic myeloid leukemia (CML); however, a few patients have shown resistance to IM treatment, resulting in disease progression. Smad4 is a tumor inhibitor that transduces TGF-β signaling and modulates genomic stability. Previous studies have indicated that decreased Smad4 expression played a bidirectional role in chemosensitivity in many types of cancers. Therefore, this study aims to evaluate the association between IM sensitivity and decreased Smad4 expression in human CML K562 cells. Methods: Bone marrow (BM) samples were acquired from the patients prior to treatment. qRT-PCR, Western Blotting (WB), colony formation assay (CFA), and apoptosis assay were used to detect relevant indices. Results: Smad4 expression was downregulated in the bone marrow and plasma of patients with multidrug-resistant CML as well as IM-resistant K562 (K562R) cells compared with samples collected from CML patients and K562 cells. Smad4 overexpression inhibited IM-treated K562R cell proliferation and augmented apoptosis, whereas Smad4 silencing promoted viability and inhibited apoptosis in IM-treated K562 cells. In addition, Smad4 expression was inversely correlated with laminin subunit gamma 1 (LAMC1) expression. The upregulation or downregulation of LAMC1 expression partially abolished the effect of Smad4 overexpression or silencing on the IM resistance of CML cells. Conclusion: The downregulation of Smad4 expression might induce drug resistance in CML cells and displayed a possible mechanism through which Smad4 modulates CML cell survival and apoptosis upon IM treatment.",
"license": "https://creativecommons.org/licenses/by/4.0/legalcode",
"keywords": "Biochemistry, Cell Biology, Molecular Biology, Pharmacology, Chemical Sciences not elsewhere classified, Cancer, Hematology",
"contentSize": "1277264 Bytes",
"dateCreated": "2021-12-27",
"datePublished": "2021",
"dateModified": "2023-05-30",
"@reverse": {
"isBasedOn": {
"@id": "https://doi.org/10.1080/16078454.2021.2010331",
"@type": "ScholarlyArticle"
}
},
"schemaVersion": "http://datacite.org/schema/kernel-4",
"publisher": {
"@type": "Organization",
"name": "Taylor & Francis"
},
"provider": {
"@type": "Organization",
"name": "datacite"
}
}