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  1. Article ; Online: Author Correction

    Caterina Bartolacci / Cristina Andreani / Gonçalo Vale / Stefano Berto / Margherita Melegari / Anna Colleen Crouch / Dodge L. Baluya / George Kemble / Kurt Hodges / Jacqueline Starrett / Katerina Politi / Sandra L. Starnes / Daniele Lorenzini / Maria Gabriela Raso / Luisa M. Solis Soto / Carmen Behrens / Humam Kadara / Boning Gao / Ignacio I. Wistuba /
    John D. Minna / Jeffrey G. McDonald / Pier Paolo Scaglioni

    Nature Communications, Vol 13, Iss 1, Pp 1-

    Targeting de novo lipogenesis and the Lands cycle induces ferroptosis in KRAS-mutant lung cancer

    2022  Volume 1

    Keywords Science ; Q
    Language English
    Publishing date 2022-08-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Targeting de novo lipogenesis and the Lands cycle induces ferroptosis in KRAS-mutant lung cancer

    Caterina Bartolacci / Cristina Andreani / Gonçalo Vale / Stefano Berto / Margherita Melegari / Anna Colleen Crouch / Dodge L. Baluya / George Kemble / Kurt Hodges / Jacqueline Starrett / Katerina Politi / Sandra L. Starnes / Daniele Lorenzini / Maria Gabriela Raso / Luisa M. Solis Soto / Carmen Behrens / Humam Kadara / Boning Gao / Ignacio I. Wistuba /
    John D. Minna / Jeffrey G. McDonald / Pier Paolo Scaglioni

    Nature Communications, Vol 13, Iss 1, Pp 1-

    2022  Volume 19

    Abstract: Mutant KRAS (KM) is associated with poor prognosis in lung cancer and reported to promote lipid metabolism. Here, the authors show that fatty acid synthesis, which provides lipids to repair oxidized phospholipids through the FASN-Lands cycle axis, is a ... ...

    Abstract Mutant KRAS (KM) is associated with poor prognosis in lung cancer and reported to promote lipid metabolism. Here, the authors show that fatty acid synthesis, which provides lipids to repair oxidized phospholipids through the FASN-Lands cycle axis, is a specific vulnerability for KM lung cancer.
    Keywords Science ; Q
    Language English
    Publishing date 2022-07-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: PIAS1-FAK Interaction Promotes the Survival and Progression of Non-Small Cell Lung Cancer

    Jerfiz D. Constanzo / Ke-jing Tang / Smita Rindhe / Margherita Melegari / Hui Liu / Ximing Tang / Jaime Rodriguez-Canales / Ignacio Wistuba / Pier Paolo Scaglioni

    Neoplasia : An International Journal for Oncology Research, Vol 18, Iss 5, Pp 282-

    2016  Volume 293

    Abstract: The sequence of genomic alterations acquired by cancer cells during tumor progression and metastasis is poorly understood. Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that integrates cytoskeleton remodeling, mitogenic signaling and cell ...

    Abstract The sequence of genomic alterations acquired by cancer cells during tumor progression and metastasis is poorly understood. Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that integrates cytoskeleton remodeling, mitogenic signaling and cell survival. FAK has previously been reported to undergo nuclear localization during cell migration, cell differentiation and apoptosis. However, the mechanism behind FAK nuclear accumulation and its contribution to tumor progression has remained elusive. We report that amplification of FAK and the SUMO E3 ligase PIAS1 gene loci frequently co-occur in non-small cell lung cancer (NSCLC) cells, and that both gene products are enriched in a subset of primary NSCLCs. We demonstrate that endogenous FAK and PIAS1 proteins interact in the cytoplasm and the cell nucleus of NSCLC cells. Ectopic expression of PIAS1 promotes proteolytic cleavage of the FAK C-terminus, focal adhesion maturation and FAK nuclear localization. Silencing of PIAS1 deregulates focal adhesion turnover, increases susceptibility to apoptosis in vitro and impairs tumor xenograft formation in vivo. Nuclear FAK in turn stimulates gene transcription favoring DNA repair, cell metabolism and cytoskeleton regulation. Consistently, ablation of FAK by CRISPR/Cas9 editing, results in basal DNA damage, susceptibility to ionizing radiation and impaired oxidative phosphorylation. Our findings provide insight into a mechanism regulating FAK cytoplasm-nuclear distribution and demonstrate that FAK activity in the nucleus promotes NSCLC survival and progression by increasing cell-ECM interaction and DNA repair regulation.
    Keywords Medicine ; R ; Internal medicine ; RC31-1245 ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282
    Subject code 570
    Publishing date 2016-05-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Corrigendum to “PIAS1-FAK Interaction Promotes the Survival and Progression of Non–Small Cell Lung Cancer” [Neoplasia 18 (2016) 282-293].

    Jerfiz D. Constanzo / Ke-jing Tang / Smita Rindhe / Margherita Melegari / Hui Liu / Ximing Tang / Jaime Rodriguez-Canales / Ignacio Wistuba / Pier Paolo Scaglioni

    Neoplasia: An International Journal for Oncology Research, Vol 18, Iss 7, p

    2016  Volume 457

    Keywords Medicine ; R ; Internal medicine ; RC31-1245 ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282
    Language English
    Publishing date 2016-07-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: PIAS1 Promotes Lymphomagenesis through MYC Upregulation

    Andrea Rabellino / Margherita Melegari / Van S. Tompkins / Weina Chen / Brian G. Van Ness / Julie Teruya-Feldstein / Maralice Conacci-Sorrell / Siegfried Janz / Pier Paolo Scaglioni

    Cell Reports, Vol 15, Iss 10, Pp 2266-

    2016  Volume 2278

    Abstract: The MYC proto-oncogene is a transcription factor implicated in a broad range of cancers. MYC is regulated by several post-translational modifications including SUMOylation, but the functional impact of this post-translational modification is still ... ...

    Abstract The MYC proto-oncogene is a transcription factor implicated in a broad range of cancers. MYC is regulated by several post-translational modifications including SUMOylation, but the functional impact of this post-translational modification is still unclear. Here, we report that the SUMO E3 ligase PIAS1 SUMOylates MYC. We demonstrate that PIAS1 promotes, in a SUMOylation-dependent manner, MYC phosphorylation at serine 62 and dephosphorylation at threonine 58. These events reduce the MYC turnover, leading to increased transcriptional activity. Furthermore, we find that MYC is SUMOylated in primary B cell lymphomas and that PIAS1 is required for the viability of MYC-dependent B cell lymphoma cells as well as several cancer cell lines of epithelial origin. Finally, Pias1-null mice display endothelial defects reminiscent of Myc-null mice. Taken together, these results indicate that PIAS1 is a positive regulator of MYC.
    Keywords Biology (General) ; QH301-705.5
    Subject code 500
    Language English
    Publishing date 2016-06-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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    Inter-library loan at ZB MED

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  6. Article ; Online: Multi-miRNA hairpin method that improves gene knockdown efficiency and provides linked multi-gene knockdown

    Daqian Sun / Margherita Melegari / Sunandini Sridhar / Charles E. Rogler / Liang Zhu

    BioTechniques, Vol 41, Iss 1, Pp 59-

    2006  Volume 63

    Abstract: A number of natural microRNA (miRNA) hairpins have been found in clusters of multiple identical or different copies, suggesting that effects of miRNAs can be enhanced and multiple genes can be regulated together by encoding multiple miRNA hairpins in a ... ...

    Abstract A number of natural microRNA (miRNA) hairpins have been found in clusters of multiple identical or different copies, suggesting that effects of miRNAs can be enhanced and multiple genes can be regulated together by encoding multiple miRNA hairpins in a single transcript. Here, we report a simple and effective artificial multi-hairpin method that stimulates production of mature 22-nucleotide small RNAs from modified miRNA hairpins, improves gene knockdown over single-hairpin constructs, and provides linked multi-gene knockdowns.
    Keywords Biology (General) ; QH301-705.5
    Language English
    Publishing date 2006-07-01T00:00:00Z
    Publisher Future Science Ltd
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Fatty Acid Oxidation Mediated by Acyl-CoA Synthetase Long Chain 3 Is Required for Mutant KRAS Lung Tumorigenesis

    Mahesh S. Padanad / Georgia Konstantinidou / Niranjan Venkateswaran / Margherita Melegari / Smita Rindhe / Matthew Mitsche / Chendong Yang / Kimberly Batten / Kenneth E. Huffman / Jingwen Liu / Ximing Tang / Jaime Rodriguez-Canales / Neda Kalhor / Jerry W. Shay / John D. Minna / Jeffrey McDonald / Ignacio I. Wistuba / Ralph J. DeBerardinis / Pier Paolo Scaglioni

    Cell Reports, Vol 16, Iss 6, Pp 1614-

    2016  Volume 1628

    Abstract: KRAS is one of the most commonly mutated oncogenes in human cancer. Mutant KRAS aberrantly regulates metabolic networks. However, the contribution of cellular metabolism to mutant KRAS tumorigenesis is not completely understood. We report that mutant ... ...

    Abstract KRAS is one of the most commonly mutated oncogenes in human cancer. Mutant KRAS aberrantly regulates metabolic networks. However, the contribution of cellular metabolism to mutant KRAS tumorigenesis is not completely understood. We report that mutant KRAS regulates intracellular fatty acid metabolism through Acyl-coenzyme A (CoA) synthetase long-chain family member 3 (ACSL3), which converts fatty acids into fatty Acyl-CoA esters, the substrates for lipid synthesis and β-oxidation. ACSL3 suppression is associated with depletion of cellular ATP and causes the death of lung cancer cells. Furthermore, mutant KRAS promotes the cellular uptake, retention, accumulation, and β-oxidation of fatty acids in lung cancer cells in an ACSL3-dependent manner. Finally, ACSL3 is essential for mutant KRAS lung cancer tumorigenesis in vivo and is highly expressed in human lung cancer. Our data demonstrate that mutant KRAS reprograms lipid homeostasis, establishing a metabolic requirement that could be exploited for therapeutic gain.
    Keywords ACSL3 ; mutant KRAS ; lung cancer ; cancer metabolism ; fatty acid oxidation ; lipid metabolism ; mouse cancer models ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2016-08-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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