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  1. AU="Van Baren, Megan"
  2. AU="Luce, Richard Ray"
  3. AU="Cheng, Shou-Ting"
  4. AU="Seyedmajidi, Seyed Ali"
  5. AU="Sawai, Katherine M"
  6. AU=Consolo Ugo
  7. AU="Emma Rabino Massa"
  8. AU="Florentino, Antonio Leite"
  9. AU="Savona, Steven"
  10. AU="Carabott, Romina"
  11. AU="Mastrodonato, Valeria"
  12. AU="Ocak, Süheyla"
  13. AU="Bain, Joseph"
  14. AU="Müller, Alina"
  15. AU="Moreno, Jessica L"
  16. AU="Guimaraes-Ferreira, Lucas"
  17. AU="Bhandari, Ruchi"
  18. AU="Fichtner, Maximilian"
  19. AU="Dina, Yemisi"

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  1. Artikel: Diclofenac Enhances Docosahexaenoic Acid-Induced Apoptosis in Vitro in Lung Cancer Cells.

    Poku, Rosemary A / Jones, Kylee J / Van Baren, Megan / Alan, Jamie K / Amissah, Felix

    Cancers

    2020  Band 12, Heft 9

    Abstract: Polyunsaturated fatty acids (PUFAs) and non-steroidal anti-inflammatory drugs (NSAIDs) show anticancer activities through diverse molecular mechanisms. However, the anticancer capacities of either PUFAs or NSAIDs alone is limited. We examined whether ... ...

    Abstract Polyunsaturated fatty acids (PUFAs) and non-steroidal anti-inflammatory drugs (NSAIDs) show anticancer activities through diverse molecular mechanisms. However, the anticancer capacities of either PUFAs or NSAIDs alone is limited. We examined whether combining NSAIDs with docosahexaenoic (DHA), commonly derived from fish oils, would possibly synergize their anticancer activity. We determined the viability of lung cancer cell lines (NCI-H1573, A549, NCI-H1299, and NCI-H1975) after exposure to DHA and various NSAIDs. We further conducted cell apoptosis assays and analyzed apoptosis-associated proteins and some key proteins in the RAS/MEK/ERK and PI3K/Akt pathways using western blot analysis. We also determined the impact of the treatment on the expression of inducible cancer-related genes using nCounter PanCancer Pathways gene expression analysis. The results showed that the combination of DHA and NSAIDs increased suppression of cell viability in all the lung cancer cell lines tested compared to each of the compounds used alone, with diclofenac being the most potent NSAID tested. This synergistic effect is especially significant in A549 and NCI-H1573 cells. The combination treatment was more effective at inhibiting clonogenic cell growth and anchorage-independent growth in soft agar, inducing caspase-dependent apoptosis, and altering expression of critical proteins in the RAS/MEK/ERK and PI3K/Akt pathways. The data from this study demonstrate that DHA combined with low dose diclofenac provides greater anticancer potential, which can be further developed for chemoprevention and adjunct therapy in lung cancer.
    Sprache Englisch
    Erscheinungsdatum 2020-09-20
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers12092683
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Chemical Biology Screening Identifies a Vulnerability to Checkpoint Kinase Inhibitors in TSC2-Deficient Renal Angiomyolipomas.

    Vaughan, Robert M / Kordich, Jennifer J / Chan, Chun-Yuan / Sasi, Nanda K / Celano, Stephanie L / Sisson, Kellie A / Van Baren, Megan / Kortus, Matthew G / Aguiar, Dean J / Martin, Katie R / MacKeigan, Jeffrey P

    Frontiers in oncology

    2022  Band 12, Seite(n) 852859

    Abstract: The tuberous sclerosis complex (TSC) is a rare genetic syndrome and multisystem disease resulting in tumor formation in major organs. A molecular hallmark of TSC is a dysregulation of the mammalian target of rapamycin (mTOR) through loss-of-function ... ...

    Abstract The tuberous sclerosis complex (TSC) is a rare genetic syndrome and multisystem disease resulting in tumor formation in major organs. A molecular hallmark of TSC is a dysregulation of the mammalian target of rapamycin (mTOR) through loss-of-function mutations in either tumor suppressor
    Sprache Englisch
    Erscheinungsdatum 2022-03-10
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2022.852859
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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