Academic Journal
View in EDS
Linked Full Text

Targeting SOS1 overcomes imatinib resistance with BCR-ABL independence through uptake transporter SLC22A4 in CML

Bibliographic Details
Title: Targeting SOS1 overcomes imatinib resistance with BCR-ABL independence through uptake transporter SLC22A4 in CML
Authors: Yanjun Liu, Chuting Li, Rui Su, Zhao Yin, Guiping Huang, Juhua Yang, Zhendong Li, Keda Zhang, Jia Fei
Source: Molecular Therapy: Oncolytics, Vol 23, Iss , Pp 560-570 (2021)
Publisher Information: Elsevier, 2021.
Publication Year: 2021
Collection: LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens
Subject Terms: SOS1, imatinib sensitivity, resistance with BCR-ABL independence, CML, SLC22A4, RNA-seq, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
More Details: Resistance to the BCR-ABL inhibitor imatinib mesylate poses a major problem for the treatment of chronic myeloid leukemia. Imatinib resistance often results from a secondary mutation in BCR-ABL that interferes with drug binding. However, sometimes there is no mutation in BCR-ABL, and the basis of such BCR-ABL-independent imatinib mesylate resistance remains to be elucidated. SOS1, a guanine nucleotide exchange factor for Ras protein, affects drug sensitivity and resistance to imatinib. The depletion of SOS1 markedly inhibits cell growth either in vitro or in vivo and significantly increases the sensitivity of chronic myeloid leukemia cells to imatinib. Furthermore, LC-MS/MS and RNA-seq assays reveal that SOS1 negatively regulates the expression of SLC22A4, a member of the carnitine/organic cation transporter family, which mediates the active uptake of imatinib into chronic myeloid leukemia cells. HPLC assay confirms that intracellular accumulation of imatinib is accompanied by upregulation of SLC22A4 through SOS1 inhibition in both sensitive and resistant chronic myeloid leukemia cells. BAY-293, an inhibitor of SOS1/Ras, was found to depress proliferation and colony formation in chronic myeloid leukemia cells with resistance and BCR-ABL independence. Altogether these findings indicate that targeting SOS1 inhibition promotes imatinib sensitivity and overcomes resistance with BCR-ABL independence by SLC22A4-mediated uptake transport.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2372-7705
Relation: http://www.sciencedirect.com/science/article/pii/S2372770521001595; https://doaj.org/toc/2372-7705
DOI: 10.1016/j.omto.2021.11.010
Access URL: https://doaj.org/article/bdf5d9c72c494d8ba975006ae84f5c9c
Accession Number: edsdoj.bdf5d9c72c494d8ba975006ae84f5c9c
Database: Directory of Open Access Journals
FullText Links:
  – Type: other
    Url: https://resolver.ebsco.com:443/public/rma-ftfapi/ejs/direct?AccessToken=488984892D89713905E4&Show=Object
Text:
  Availability: 0
CustomLinks:
  – Url: https://doaj.org/article/bdf5d9c72c494d8ba975006ae84f5c9c
    Name: EDS - DOAJ (s8985755)
    Category: fullText
    Text: View record from Directory of Open Access Journals
    MouseOverText: View record from Directory of Open Access Journals
  – Url: https://resolver.ebsco.com/c/xy5jbn/result?sid=EBSCO:edsdoj&genre=article&issn=23727705&ISBN=&volume=23&issue=560-570&date=20211201&spage=560&pages=560-570&title=Molecular Therapy: Oncolytics&atitle=Targeting%20SOS1%20overcomes%20imatinib%20resistance%20with%20BCR-ABL%20independence%20through%20uptake%20transporter%20SLC22A4%20in%20CML&aulast=Yanjun%20Liu&id=DOI:10.1016/j.omto.2021.11.010
    Name: Full Text Finder (for New FTF UI) (s8985755)
    Category: fullText
    Text: Find It @ SCU Libraries
    MouseOverText: Find It @ SCU Libraries
Header DbId: edsdoj
DbLabel: Directory of Open Access Journals
An: edsdoj.bdf5d9c72c494d8ba975006ae84f5c9c
RelevancyScore: 957
AccessLevel: 3
PubType: Academic Journal
PubTypeId: academicJournal
PreciseRelevancyScore: 956.691040039063
IllustrationInfo
Items – Name: Title
  Label: Title
  Group: Ti
  Data: Targeting SOS1 overcomes imatinib resistance with BCR-ABL independence through uptake transporter SLC22A4 in CML
– Name: Author
  Label: Authors
  Group: Au
  Data: <searchLink fieldCode="AR" term="%22Yanjun+Liu%22">Yanjun Liu</searchLink><br /><searchLink fieldCode="AR" term="%22Chuting+Li%22">Chuting Li</searchLink><br /><searchLink fieldCode="AR" term="%22Rui+Su%22">Rui Su</searchLink><br /><searchLink fieldCode="AR" term="%22Zhao+Yin%22">Zhao Yin</searchLink><br /><searchLink fieldCode="AR" term="%22Guiping+Huang%22">Guiping Huang</searchLink><br /><searchLink fieldCode="AR" term="%22Juhua+Yang%22">Juhua Yang</searchLink><br /><searchLink fieldCode="AR" term="%22Zhendong+Li%22">Zhendong Li</searchLink><br /><searchLink fieldCode="AR" term="%22Keda+Zhang%22">Keda Zhang</searchLink><br /><searchLink fieldCode="AR" term="%22Jia+Fei%22">Jia Fei</searchLink>
– Name: TitleSource
  Label: Source
  Group: Src
  Data: Molecular Therapy: Oncolytics, Vol 23, Iss , Pp 560-570 (2021)
– Name: Publisher
  Label: Publisher Information
  Group: PubInfo
  Data: Elsevier, 2021.
– Name: DatePubCY
  Label: Publication Year
  Group: Date
  Data: 2021
– Name: Subset
  Label: Collection
  Group: HoldingsInfo
  Data: LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens
– Name: Subject
  Label: Subject Terms
  Group: Su
  Data: <searchLink fieldCode="DE" term="%22SOS1%22">SOS1</searchLink><br /><searchLink fieldCode="DE" term="%22imatinib+sensitivity%22">imatinib sensitivity</searchLink><br /><searchLink fieldCode="DE" term="%22resistance+with+BCR-ABL+independence%22">resistance with BCR-ABL independence</searchLink><br /><searchLink fieldCode="DE" term="%22CML%22">CML</searchLink><br /><searchLink fieldCode="DE" term="%22SLC22A4%22">SLC22A4</searchLink><br /><searchLink fieldCode="DE" term="%22RNA-seq%22">RNA-seq</searchLink><br /><searchLink fieldCode="DE" term="%22Neoplasms%2E+Tumors%2E+Oncology%2E+Including+cancer+and+carcinogens%22">Neoplasms. Tumors. Oncology. Including cancer and carcinogens</searchLink><br /><searchLink fieldCode="DE" term="%22RC254-282%22">RC254-282</searchLink>
– Name: Abstract
  Label: Description
  Group: Ab
  Data: Resistance to the BCR-ABL inhibitor imatinib mesylate poses a major problem for the treatment of chronic myeloid leukemia. Imatinib resistance often results from a secondary mutation in BCR-ABL that interferes with drug binding. However, sometimes there is no mutation in BCR-ABL, and the basis of such BCR-ABL-independent imatinib mesylate resistance remains to be elucidated. SOS1, a guanine nucleotide exchange factor for Ras protein, affects drug sensitivity and resistance to imatinib. The depletion of SOS1 markedly inhibits cell growth either in vitro or in vivo and significantly increases the sensitivity of chronic myeloid leukemia cells to imatinib. Furthermore, LC-MS/MS and RNA-seq assays reveal that SOS1 negatively regulates the expression of SLC22A4, a member of the carnitine/organic cation transporter family, which mediates the active uptake of imatinib into chronic myeloid leukemia cells. HPLC assay confirms that intracellular accumulation of imatinib is accompanied by upregulation of SLC22A4 through SOS1 inhibition in both sensitive and resistant chronic myeloid leukemia cells. BAY-293, an inhibitor of SOS1/Ras, was found to depress proliferation and colony formation in chronic myeloid leukemia cells with resistance and BCR-ABL independence. Altogether these findings indicate that targeting SOS1 inhibition promotes imatinib sensitivity and overcomes resistance with BCR-ABL independence by SLC22A4-mediated uptake transport.
– Name: TypeDocument
  Label: Document Type
  Group: TypDoc
  Data: article
– Name: Format
  Label: File Description
  Group: SrcInfo
  Data: electronic resource
– Name: Language
  Label: Language
  Group: Lang
  Data: English
– Name: ISSN
  Label: ISSN
  Group: ISSN
  Data: 2372-7705
– Name: NoteTitleSource
  Label: Relation
  Group: SrcInfo
  Data: http://www.sciencedirect.com/science/article/pii/S2372770521001595; https://doaj.org/toc/2372-7705
– Name: DOI
  Label: DOI
  Group: ID
  Data: 10.1016/j.omto.2021.11.010
– Name: URL
  Label: Access URL
  Group: URL
  Data: <link linkTarget="URL" linkTerm="https://doaj.org/article/bdf5d9c72c494d8ba975006ae84f5c9c" linkWindow="_blank">https://doaj.org/article/bdf5d9c72c494d8ba975006ae84f5c9c</link>
– Name: AN
  Label: Accession Number
  Group: ID
  Data: edsdoj.bdf5d9c72c494d8ba975006ae84f5c9c
PLink https://login.libproxy.scu.edu/login?url=https://search.ebscohost.com/login.aspx?direct=true&site=eds-live&scope=site&db=edsdoj&AN=edsdoj.bdf5d9c72c494d8ba975006ae84f5c9c
RecordInfo BibRecord:
  BibEntity:
    Identifiers:
      – Type: doi
        Value: 10.1016/j.omto.2021.11.010
    Languages:
      – Text: English
    PhysicalDescription:
      Pagination:
        PageCount: 11
        StartPage: 560
    Subjects:
      – SubjectFull: SOS1
        Type: general
      – SubjectFull: imatinib sensitivity
        Type: general
      – SubjectFull: resistance with BCR-ABL independence
        Type: general
      – SubjectFull: CML
        Type: general
      – SubjectFull: SLC22A4
        Type: general
      – SubjectFull: RNA-seq
        Type: general
      – SubjectFull: Neoplasms. Tumors. Oncology. Including cancer and carcinogens
        Type: general
      – SubjectFull: RC254-282
        Type: general
    Titles:
      – TitleFull: Targeting SOS1 overcomes imatinib resistance with BCR-ABL independence through uptake transporter SLC22A4 in CML
        Type: main
  BibRelationships:
    HasContributorRelationships:
      – PersonEntity:
          Name:
            NameFull: Yanjun Liu
      – PersonEntity:
          Name:
            NameFull: Chuting Li
      – PersonEntity:
          Name:
            NameFull: Rui Su
      – PersonEntity:
          Name:
            NameFull: Zhao Yin
      – PersonEntity:
          Name:
            NameFull: Guiping Huang
      – PersonEntity:
          Name:
            NameFull: Juhua Yang
      – PersonEntity:
          Name:
            NameFull: Zhendong Li
      – PersonEntity:
          Name:
            NameFull: Keda Zhang
      – PersonEntity:
          Name:
            NameFull: Jia Fei
    IsPartOfRelationships:
      – BibEntity:
          Dates:
            – D: 01
              M: 12
              Type: published
              Y: 2021
          Identifiers:
            – Type: issn-print
              Value: 23727705
          Numbering:
            – Type: volume
              Value: 23
            – Type: issue
              Value: 560-570
          Titles:
            – TitleFull: Molecular Therapy: Oncolytics
              Type: main
ResultId 1