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  1. Article ; Online: Small-molecule inhibitors targeting FOXM1: Current challenges and future perspectives in cancer treatments.

    Raghuwanshi, Sanjeev / Gartel, Andrei L

    Biochimica et biophysica acta. Reviews on cancer

    2023  Volume 1878, Issue 6, Page(s) 189015

    Abstract: Forkhead box (FOX) protein M1 (FOXM1) is a critical proliferation-associated transcription factor (TF) that is aberrantly overexpressed in the majority of human cancers and has also been implicated in poor prognosis. A comprehensive understanding of ... ...

    Abstract Forkhead box (FOX) protein M1 (FOXM1) is a critical proliferation-associated transcription factor (TF) that is aberrantly overexpressed in the majority of human cancers and has also been implicated in poor prognosis. A comprehensive understanding of various aspects of this molecule has revealed its role in, cell proliferation, cell migration, invasion, angiogenesis and metastasis. The FOXM1 as a TF directly or indirectly regulates the expression of several target genes whose dysregulation is associated with almost all hallmarks of cancer. Moreover, FOXM1 expression is associated with chemoresistance to different anti-cancer drugs. Several studies have confirmed that suppression of FOXM1 enhanced the drug sensitivity of various types of cancer cells. Current data suggest that small molecule inhibitors targeting FOXM1 in combination with anticancer drugs may represent a novel therapeutic strategy for chemo-resistant cancers. In this review, we discuss the clinical utility of FOXM1, further, we summarize and discuss small-molecule inhibitors targeting FOXM1 and categorize them according to their mechanisms of targeting FOXM1. Despite great progress, small-molecule inhibitors targeting FOXM1 face many challenges, and we present here all small-molecule FOXM1 inhibitors in different stages of development. We discuss the current challenges and provide insights on the future application of FOXM1 inhibition to the clinic.
    MeSH term(s) Humans ; Forkhead Box Protein M1/genetics ; Forkhead Box Protein M1/metabolism ; Forkhead Box Protein M1/therapeutic use ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism
    Chemical Substances Forkhead Box Protein M1 ; Antineoplastic Agents ; FOXM1 protein, human
    Language English
    Publishing date 2023-10-31
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 2918802-7
    ISSN 1879-2561 ; 0304-419X
    ISSN (online) 1879-2561
    ISSN 0304-419X
    DOI 10.1016/j.bbcan.2023.189015
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 7162: Show issues Location:
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  2. Article ; Online: The antagonistic duality of NPM1 mutations in AML.

    Khan, Irum / Gartel, Andrei L

    Blood advances

    2022  Volume 6, Issue 13, Page(s) 4028–4030

    MeSH term(s) Humans ; Leukemia, Myeloid, Acute/genetics ; Mutation ; Nuclear Proteins/genetics ; Nucleophosmin/genetics
    Chemical Substances NPM1 protein, human ; Nuclear Proteins ; Nucleophosmin (117896-08-9)
    Language English
    Publishing date 2022-01-18
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2915908-8
    ISSN 2473-9537 ; 2473-9529
    ISSN (online) 2473-9537
    ISSN 2473-9529
    DOI 10.1182/bloodadvances.2022007420
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Regulation of HOX gene expression in AML.

    Khan, Irum / Amin, Mohammed A / Eklund, Elizabeth A / Gartel, Andrei L

    Blood cancer journal

    2024  Volume 14, Issue 1, Page(s) 42

    Abstract: As key developmental regulators, HOX cluster genes have varied and context-specific roles in normal and malignant hematopoiesis. A complex interaction of transcription factors, epigenetic regulators, long non-coding RNAs and chromatin structural changes ... ...

    Abstract As key developmental regulators, HOX cluster genes have varied and context-specific roles in normal and malignant hematopoiesis. A complex interaction of transcription factors, epigenetic regulators, long non-coding RNAs and chromatin structural changes orchestrate HOX expression in leukemia cells. In this review we summarize molecular mechanisms underlying HOX regulation in clinical subsets of AML, with a focus on NPM1 mutated (NPM1
    MeSH term(s) Humans ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Leukemia, Myeloid, Acute/pathology ; Nuclear Proteins/genetics ; Nucleophosmin ; Gene Expression Regulation, Leukemic ; Transcription Factors/genetics ; Chromatin ; Gene Expression
    Chemical Substances Homeodomain Proteins ; Nuclear Proteins ; Nucleophosmin (117896-08-9) ; Transcription Factors ; Chromatin
    Language English
    Publishing date 2024-03-07
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2600560-8
    ISSN 2044-5385 ; 2044-5385
    ISSN (online) 2044-5385
    ISSN 2044-5385
    DOI 10.1038/s41408-024-01004-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: FOXM1 in Cancer: Interactions and Vulnerabilities.

    Gartel, Andrei L

    Cancer research

    2017  Volume 77, Issue 12, Page(s) 3135–3139

    Abstract: FOXM1 is a transcription factor of the Forkhead family that is required for cell proliferation of normal cells. However, FOXM1 is repeatedly overexpressed in a variety of human cancers, and it has been implicated in all major hallmarks of cancer ... ...

    Abstract FOXM1 is a transcription factor of the Forkhead family that is required for cell proliferation of normal cells. However, FOXM1 is repeatedly overexpressed in a variety of human cancers, and it has been implicated in all major hallmarks of cancer delineated by Hanahan and Weinberg. It has been postulated that the oncogenic potential of FOXM1 is determined by its capacity to transactivate target genes that are implicated in different phases of cancer development. However, FOXM1 may also play an oncogenic role by interacting with other proteins, such as β-catenin or SMAD3 to induce oncogenic WNT and TGFβ signaling pathways, respectively. In this review, I will discuss the protein-protein interactions of FOXM1 that are critical for cancer development and may represent novel targets for anticancer drugs.
    MeSH term(s) Animals ; Forkhead Box Protein M1/physiology ; Gene Expression Regulation, Neoplastic/physiology ; Humans ; Neoplasms/genetics ; Neoplasms/metabolism ; Signal Transduction/physiology
    Chemical Substances Forkhead Box Protein M1
    Language English
    Publishing date 2017-06-15
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-16-3566
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: FOXM1: a potential therapeutic target in human solid cancers.

    Borhani, Soheila / Gartel, Andrei L

    Expert opinion on therapeutic targets

    2020  Volume 24, Issue 3, Page(s) 205–217

    Abstract: ... ...

    Abstract Introduction
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Drug Development ; Forkhead Box Protein M1/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Molecular Targeted Therapy ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/pathology ; Proto-Oncogene Proteins c-akt/metabolism
    Chemical Substances Antineoplastic Agents ; FOXM1 protein, human ; Forkhead Box Protein M1 ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2020-02-19
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2055208-7
    ISSN 1744-7631 ; 1472-8222
    ISSN (online) 1744-7631
    ISSN 1472-8222
    DOI 10.1080/14728222.2020.1727888
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5244: Show issues Location:
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  6. Article ; Online: Targeting FOXM1 auto-regulation in cancer.

    Gartel, Andrei L

    Cancer biology & therapy

    2015  Volume 16, Issue 2, Page(s) 185–186

    MeSH term(s) Animals ; Forkhead Box Protein M1 ; Forkhead Transcription Factors/antagonists & inhibitors ; Forkhead Transcription Factors/genetics ; Forkhead Transcription Factors/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Molecular Targeted Therapy ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism
    Chemical Substances FOXM1 protein, human ; Forkhead Box Protein M1 ; Forkhead Transcription Factors
    Language English
    Publishing date 2015-01-23
    Publishing country United States
    Document type Letter ; Research Support, N.I.H., Extramural
    ZDB-ID 2146305-0
    ISSN 1555-8576 ; 1538-4047
    ISSN (online) 1555-8576
    ISSN 1538-4047
    DOI 10.4161/15384047.2014.987566
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Thiazole Antibiotics Siomycin a and Thiostrepton Inhibit the Transcriptional Activity of FOXM1.

    Gartel, Andrei L

    Frontiers in oncology

    2013  Volume 3, Page(s) 150

    Language English
    Publishing date 2013-06-06
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2013.00150
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  8. Article: Suppression of the Oncogenic Transcription Factor FOXM1 by Proteasome Inhibitors.

    Gartel, Andrei L

    Scientifica

    2014  Volume 2014, Page(s) 596528

    Abstract: The oncogenic transcription factor FOXM1 is one of the key regulators of tumorigenesis. We found that FOXM1 upregulates its own transcription and its protein stability depends on its interaction with the chaperone nucleophosmin. We also determined that ... ...

    Abstract The oncogenic transcription factor FOXM1 is one of the key regulators of tumorigenesis. We found that FOXM1 upregulates its own transcription and its protein stability depends on its interaction with the chaperone nucleophosmin. We also determined that FOXM1 is negatively regulated by the tumor suppressor p53. We identified the thiazole antibiotics Siomycin A and thiostrepton as inhibitors of transcriptional activity and FOXM1 expression via proteasome inhibition. In addition, we found that all tested proteasome inhibitors target FOXM1. We showed synergy between thiostrepton and bortezomib in different human cancer cell lines and in vivo. We generated isogenic human cancer cell lines of different origin with wild-type p53 or p53 knockdown and we demonstrated that proteasome inhibitors induce p53-independent apoptosis in these cells. Using RNA-interference or proteasome inhibitors to inhibit FOXM1 we found that suppression of FOXM1 sensitized human cancer cells to apoptosis induced by DNA-damaging agents or oxidative stress. We encapsulated thiostrepton into micelle-nanoparticles and after injection we detected accumulation of nanoparticles in tumors and in the livers of treated mice. This treatment led to inhibition of human xenograft tumor growth in nude mice. Our data indicate that targeting FOXM1 increases apoptosis and inhibits tumor growth.
    Language English
    Publishing date 2014-06-24
    Publishing country Egypt
    Document type Journal Article ; Review
    ZDB-ID 2672321-9
    ISSN 2090-908X
    ISSN 2090-908X
    DOI 10.1155/2014/596528
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Found in transcription: FOXO1 upregulates miRNAs on chromosome X.

    Gartel, Andrei L

    Cell cycle (Georgetown, Tex.)

    2013  Volume 12, Issue 16, Page(s) 2523

    MeSH term(s) Chromosomes, Human, X/genetics ; Forkhead Transcription Factors/metabolism ; Humans ; MicroRNAs/metabolism
    Chemical Substances Forkhead Transcription Factors ; MicroRNAs
    Language English
    Publishing date 2013-07-29
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.4161/cc.25829
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5881: Show issues Location:
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  10. Article ; Online: Therapeutic Vulnerabilities of Transcription Factors in AML.

    Khan, Irum / Eklund, Elizabeth E / Gartel, Andrei L

    Molecular cancer therapeutics

    2020  Volume 20, Issue 2, Page(s) 229–237

    Abstract: Acute myeloid leukemia (AML) is characterized by impaired myeloid lineage differentiation, uncontrolled proliferation, and inhibition of proapoptotic pathways. In spite of a relatively homogeneous clinical disease presentation, risk of long-term survival ...

    Abstract Acute myeloid leukemia (AML) is characterized by impaired myeloid lineage differentiation, uncontrolled proliferation, and inhibition of proapoptotic pathways. In spite of a relatively homogeneous clinical disease presentation, risk of long-term survival in AML varies from 20% to 80% depending on molecular disease characteristics. In recognition of the molecular heterogeneity of AML, the European Leukemia Net (ELN) and WHO classification systems now incorporate cytogenetics and increasing numbers of gene mutations into AML prognostication. Several of the genomic AML subsets are characterized by unique transcription factor alterations that are highlighted in this review. There are many mechanisms of transcriptional deregulation in leukemia. We broadly classify transcription factors based on mechanisms of transcriptional deregulation including direct involvement of transcription factors in recurrent translocations, loss-of-function mutations, and intracellular relocalization. Transcription factors, due to their pleiotropic effects, have been attractive but elusive targets. Indirect targeting approaches include inhibition of upstream kinases such as TAK1 for suppression of NFκB signaling and downstream effectors such as FGF signaling in HOXA-upregulated leukemia. Other strategies include targeting scaffolding proteins like BrD4 in the case of MYC or coactivators such as menin to suppress HOX expression; disrupting critical protein interactions in the case of β-catenin:TCF/LEF, and preventing transcription factor binding to DNA as in the case of PU.1 or FOXM1. We comprehensively describe the mechanism of deregulation of transcription factors in genomic subsets of AML, consequent pathway addictions, and potential therapeutic strategies.
    MeSH term(s) Humans ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/pathology ; Transcription Factors/metabolism
    Chemical Substances Transcription Factors
    Language English
    Publishing date 2020-11-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 2063563-1
    ISSN 1538-8514 ; 1535-7163
    ISSN (online) 1538-8514
    ISSN 1535-7163
    DOI 10.1158/1535-7163.MCT-20-0115
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