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  1. Article: The Warburg Effect 97 Years after Its Discovery.

    Pascale, Rosa Maria / Calvisi, Diego Francesco / Simile, Maria Maddalena / Feo, Claudio Francesco / Feo, Francesco

    Cancers

    2020  Volume 12, Issue 10

    Abstract: The deregulation of the oxidative metabolism in cancer, as shown by the increased aerobic glycolysis and impaired oxidative phosphorylation (Warburg effect), is coordinated by genetic changes leading to the activation of oncogenes and the loss of ... ...

    Abstract The deregulation of the oxidative metabolism in cancer, as shown by the increased aerobic glycolysis and impaired oxidative phosphorylation (Warburg effect), is coordinated by genetic changes leading to the activation of oncogenes and the loss of oncosuppressor genes. The understanding of the metabolic deregulation of cancer cells is necessary to prevent and cure cancer. In this review, we illustrate and comment the principal metabolic and molecular variations of cancer cells, involved in their anomalous behavior, that include modifications of oxidative metabolism, the activation of oncogenes that promote glycolysis and a decrease of oxygen consumption in cancer cells, the genetic susceptibility to cancer, the molecular correlations involved in the metabolic deregulation in cancer, the defective cancer mitochondria, the relationships between the Warburg effect and tumor therapy, and recent studies that reevaluate the Warburg effect. Taken together, these observations indicate that the Warburg effect is an epiphenomenon of the transformation process essential for the development of malignancy.
    Language English
    Publishing date 2020-09-30
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers12102819
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: HCC in the Era of Direct-Acting Antiviral Agents (DAAs): Surgical and Other Curative or Palliative Strategies in the Elderly.

    Brozzetti, Stefania / Tancredi, Marsia / Bini, Simone / De Lucia, Chiara / Antimi, Jessica / D'Alterio, Chiara / De Sanctis, Giuseppe Maria / Furlan, Caterina / Malpassuti, Vittoria Carolina / Lucatelli, Pierleone / Di Martino, Michele / Bezzi, Mario / Ciardi, Antonio / Pascale, Rosa Maria

    Cancers

    2021  Volume 13, Issue 12

    Abstract: Hepatocellular carcinoma (HCC) accounts for 75-85% of primary liver malignancies, and elderlies have the highest incidence rates. Direct-acting antiviral agents (DAAs) have shown satisfying results in terms of HCV sustained viral response (SVR). However, ...

    Abstract Hepatocellular carcinoma (HCC) accounts for 75-85% of primary liver malignancies, and elderlies have the highest incidence rates. Direct-acting antiviral agents (DAAs) have shown satisfying results in terms of HCV sustained viral response (SVR). However, data regarding HCC risk post-DAA-SVR is still conflicting. This study aims to consider HCC onset in moderate underlying liver disease. We conducted a retrospective study on 227 chronically infected patients (cHCV), treated with DAAs. Patients were divided into three groups: "
    Language English
    Publishing date 2021-06-17
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers13123025
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Post-translational inhibition of YAP oncogene expression by 4-hydroxynonenal in bladder cancer cells.

    Cucci, Marie Angele / Compagnone, Alessandra / Daga, Martina / Grattarola, Margherita / Ullio, Chiara / Roetto, Antonella / Palmieri, Antonietta / Rosa, Arianna Carolina / Argenziano, Monica / Cavalli, Roberta / Simile, Maria Maddalena / Pascale, Rosa Maria / Dianzani, Chiara / Barrera, Giuseppina / Pizzimenti, Stefania

    Free radical biology & medicine

    2019  Volume 141, Page(s) 205–219

    Abstract: The transcriptional regulator YAP plays an important role in cancer progression and is negatively controlled by the Hippo pathway. YAP is frequently overexpressed in human cancers, including bladder cancer. Interestingly, YAP expression and activity can ... ...

    Abstract The transcriptional regulator YAP plays an important role in cancer progression and is negatively controlled by the Hippo pathway. YAP is frequently overexpressed in human cancers, including bladder cancer. Interestingly, YAP expression and activity can be inhibited by pro-oxidant conditions; moreover, YAP itself can also affect the cellular redox status through multiple mechanisms. 4-Hydroxynonenal (HNE), the most intensively studied end product of lipid peroxidation, is a pro-oxidant agent able to deplete GSH and has an anti-tumoral effect by affecting multiple signal pathways, including the down-regulation of oncogene expressions. These observations prompted us to investigate the effect of HNE on YAP expression and activity. We demonstrated that HNE inhibited YAP expression and its target genes in bladder cancer cells through a redox-dependent mechanism. Moreover, the YAP down-regulation was accompanied by an inhibition of proliferation, migration, invasion, and angiogenesis, as well as by an accumulation of cells in the G2/M phase of cell cycle and by an induction of apoptosis. We also established the YAP role in inhibiting cell viability and inducing apoptosis in HNE-treated cells by using an expression vector for YAP. Furthermore, we identified a post-translational mechanism for the HNE-induced YAP expression inhibition, involving an increase of YAP phosphorylation and ubiquitination, leading to proteasomal degradation. Our data established that HNE can post-translationally down-regulate YAP through a redox-dependent mechanism and that this modulation can contribute to determining the specific anti-cancer effects of HNE.
    MeSH term(s) Adaptor Proteins, Signal Transducing/metabolism ; Aldehydes/pharmacology ; Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; Down-Regulation ; Gene Expression Regulation, Neoplastic ; Human Umbilical Vein Endothelial Cells ; Humans ; Neoplasm Invasiveness ; Neovascularization, Pathologic ; Oncogenes ; Oxidation-Reduction ; Phosphoproteins/metabolism ; Protein Processing, Post-Translational ; Signal Transduction ; Transcription Factors/metabolism ; Urinary Bladder Neoplasms/drug therapy ; Urinary Bladder Neoplasms/genetics ; Urinary Bladder Neoplasms/metabolism
    Chemical Substances Adaptor Proteins, Signal Transducing ; Aldehydes ; Phosphoproteins ; Transcription Factors ; YAP1 protein, human ; 4-hydroxy-2-nonenal (K1CVM13F96)
    Language English
    Publishing date 2019-06-15
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 807032-5
    ISSN 1873-4596 ; 0891-5849
    ISSN (online) 1873-4596
    ISSN 0891-5849
    DOI 10.1016/j.freeradbiomed.2019.06.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2109: Show issues Location:
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  4. Article: Interaction of major genes predisposing to hepatocellular carcinoma with genes encoding signal transduction pathways influences tumor phenotype and prognosis.

    Feo, Francesco / Frau, Maddalena / Pascale, Rosa-Maria

    World journal of gastroenterology

    2008  Volume 14, Issue 43, Page(s) 6601–6615

    Abstract: Studies on rodents and humans demonstrate an inherited predisposition to hepatocellular carcinoma (HCC). Analysis of the molecular alterations involved in the acquisition of a phenotype resistant or susceptible to hepatocarcinogenesis showed a ... ...

    Abstract Studies on rodents and humans demonstrate an inherited predisposition to hepatocellular carcinoma (HCC). Analysis of the molecular alterations involved in the acquisition of a phenotype resistant or susceptible to hepatocarcinogenesis showed a deregulation of G1 and S phases in HCC of genetically susceptible F344 rats and a G1-S block in lesions of resistant Brown norway (BN) rats. Unrestrained extracellular signal-regulated kinase (ERK) activity linked to proteasomal degradation of dual-specificity phosphatase 1 (DUSP1), a specific ERK inhibitor, by the CKS1-SKP2 ubiquitin ligase complex occurs in more aggressive HCC of F344 rats and humans. This mechanism is less active in HCC of BN rats and human HCC with better prognosis. Upregulation of iNos cross-talk with IKK/NF-kappaB and RAS/ERK pathways occurs in rodent liver lesions at higher levels in the most aggressive models represented by HCC of F344 rats and c-Myc-TGF-alpha transgenic mice. iNOS, IKK/NF-kappaB, and RAS/ERK upregulation is highest in human HCC with a poorer prognosis and positively correlates with tumor proliferation, genomic instability and microvascularization, and negatively with apoptosis. Thus, cell cycle regulation and the activity of signal transduction pathways seem to be modulated by HCC modifier genes, and differences in their efficiency influence the susceptibility to hepatocarcinogenesis and probably the prognosis of human HCC.
    MeSH term(s) Animals ; Carcinoma, Hepatocellular/diagnosis ; Carcinoma, Hepatocellular/genetics ; Cell Cycle/genetics ; Disease Models, Animal ; Forkhead Box Protein M1 ; Forkhead Transcription Factors/genetics ; Genetic Predisposition to Disease/genetics ; Humans ; Liver Neoplasms/diagnosis ; Liver Neoplasms/genetics ; Mice ; Mice, Transgenic ; Mitogen-Activated Protein Kinase Kinases/genetics ; Nitric Oxide Synthase Type II/genetics ; Phenotype ; Prognosis ; Rats ; Rats, Inbred BN ; Rats, Inbred F344 ; Signal Transduction/genetics
    Chemical Substances FOXM1 protein, human ; Forkhead Box Protein M1 ; Forkhead Transcription Factors ; Foxm1 protein, mouse ; Foxm1 protein, rat ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2)
    Language English
    Publishing date 2008-11-25
    Publishing country United States
    Document type Editorial
    ZDB-ID 2185929-2
    ISSN 2219-2840 ; 1007-9327
    ISSN (online) 2219-2840
    ISSN 1007-9327
    DOI 10.3748/wjg.14.6601
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6039: Show issues Location:
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  5. Article ; Online: SNAI1 Promotes the Cholangiocellular Phenotype, but not Epithelial-Mesenchymal Transition, in a Murine Hepatocellular Carcinoma Model.

    Xu, Meng / Wang, Jingxiao / Xu, Zhong / Li, Rong / Wang, Pan / Shang, Runze / Cigliano, Antonio / Ribback, Silvia / Solinas, Antonio / Pes, Giovanni Mario / Evert, Katja / Wang, Haichuan / Song, Xinhua / Zhang, Shu / Che, Li / Pascale, Rosa Maria / Calvisi, Diego Francesco / Liu, Qingguang / Chen, Xin

    Cancer research

    2019  Volume 79, Issue 21, Page(s) 5563–5574

    Abstract: Hepatocellular carcinoma (HCC) is the most common type of liver cancer and has limited treatment options. Snail family transcriptional repressor 1 (SNAI1) is a master regulator of epithelial-mesenchymal transition (EMT) and has been implicated in HCC ... ...

    Abstract Hepatocellular carcinoma (HCC) is the most common type of liver cancer and has limited treatment options. Snail family transcriptional repressor 1 (SNAI1) is a master regulator of epithelial-mesenchymal transition (EMT) and has been implicated in HCC initiation and progression. However, the precise role of SNAI1 and the way it contributes to hepatocarcinogenesis have not been investigated in depth, especially
    MeSH term(s) Animals ; Cadherins/genetics ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/pathology ; Cell Movement/genetics ; Cholangiocarcinoma/genetics ; Cholangiocarcinoma/pathology ; Disease Models, Animal ; Epithelial-Mesenchymal Transition/genetics ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; Liver Neoplasms/genetics ; Liver Neoplasms/pathology ; Mice ; Phenotype ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-met/genetics ; Snail Family Transcription Factors/genetics ; Vimentin/genetics
    Chemical Substances Cadherins ; SNAI1 protein, human ; Snai1 protein, mouse ; Snail Family Transcription Factors ; Vimentin ; Proto-Oncogene Proteins c-met (EC 2.7.10.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2019-08-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-18-3750
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uh III Zs.135/5: Show issues Location:
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  6. Article ; Online: Cholesterol biosynthesis supports the growth of hepatocarcinoma lesions depleted of fatty acid synthase in mice and humans.

    Che, Li / Chi, Wenna / Qiao, Yu / Zhang, Jie / Song, Xinhua / Liu, Ye / Li, Lei / Jia, Jiaoyuan / Pilo, Maria G / Wang, Jingxiao / Cigliano, Antonio / Ma, Zhilong / Kuang, Wenhua / Tang, Zefang / Zhang, Zemin / Shui, Guanghou / Ribback, Silvia / Dombrowski, Frank / Evert, Matthias /
    Pascale, Rosa Maria / Cossu, Carla / Pes, Giovanni Mario / Osborne, Timothy F / Calvisi, Diego F / Chen, Xin / Chen, Ligong

    Gut

    2019  Volume 69, Issue 1, Page(s) 177–186

    Abstract: Objective: Increased de novo fatty acid (FA) synthesis and cholesterol biosynthesis have been independently described in many tumour types, including hepatocellular carcinoma (HCC).: Design: We investigated the functional contribution of fatty acid ... ...

    Abstract Objective: Increased de novo fatty acid (FA) synthesis and cholesterol biosynthesis have been independently described in many tumour types, including hepatocellular carcinoma (HCC).
    Design: We investigated the functional contribution of fatty acid synthase (Fasn)-mediated de novo FA synthesis in a murine HCC model induced by loss of Pten and overexpression of c-Met (sgPten/c-Met) using liver-specific
    Results: Ablation of
    Conclusion: Our study uncovers a novel functional crosstalk between aberrant lipogenesis and cholesterol biosynthesis pathways in hepatocarcinogenesis, whose concomitant inhibition might represent a therapeutic option for HCC.
    MeSH term(s) Animals ; Biosynthetic Pathways/drug effects ; Biosynthetic Pathways/genetics ; Carcinogenesis/genetics ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Cell Line, Tumor ; Cholesterol/biosynthesis ; Fatty Acid Synthase, Type I/genetics ; Fatty Acid Synthase, Type I/metabolism ; Fatty Acids/biosynthesis ; Female ; Gene Knockdown Techniques ; Gene Silencing ; Genomics ; Humans ; Hydroxymethylglutaryl CoA Reductases/genetics ; Hydroxymethylglutaryl CoA Reductases/metabolism ; Lipidomics ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Male ; Mice ; Mice, Knockout ; PTEN Phosphohydrolase/metabolism ; Proto-Oncogene Proteins c-met/metabolism ; Sterol Regulatory Element Binding Protein 2/genetics ; Sterol Regulatory Element Binding Protein 2/metabolism ; Transcriptome
    Chemical Substances Fatty Acids ; SREBF2 protein, human ; Srebf2 protein, mouse ; Sterol Regulatory Element Binding Protein 2 ; Cholesterol (97C5T2UQ7J) ; HMGCR protein, human (EC 1.1.1.-) ; Hydroxymethylglutaryl CoA Reductases (EC 1.1.1.-) ; FASN protein, human (EC 2.3.1.85) ; Fasn protein, mouse (EC 2.3.1.85) ; Fatty Acid Synthase, Type I (EC 2.3.1.85) ; Proto-Oncogene Proteins c-met (EC 2.7.10.1) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; Pten protein, mouse (EC 3.1.3.67)
    Language English
    Publishing date 2019-04-06
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80128-8
    ISSN 1468-3288 ; 0017-5749
    ISSN (online) 1468-3288
    ISSN 0017-5749
    DOI 10.1136/gutjnl-2018-317581
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 160: Show issues Location:
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  7. Article ; Online: S-adenosyl methionine regulates ubiquitin-conjugating enzyme 9 protein expression and sumoylation in murine liver and human cancers.

    Tomasi, Maria Lauda / Tomasi, Ivan / Ramani, Komal / Pascale, Rosa Maria / Xu, Jun / Giordano, Pasquale / Mato, José M / Lu, Shelly C

    Hepatology (Baltimore, Md.)

    2012  Volume 56, Issue 3, Page(s) 982–993

    Abstract: Unlabelled: Ubiquitin-conjugating enzyme 9 (Ubc9) is required for sumoylation and is overexpressed in several malignancies, but its expression in hepatocellular carcinoma (HCC) is unknown. Hepatic S-adenosyl methionine (SAMe) levels decrease in ... ...

    Abstract Unlabelled: Ubiquitin-conjugating enzyme 9 (Ubc9) is required for sumoylation and is overexpressed in several malignancies, but its expression in hepatocellular carcinoma (HCC) is unknown. Hepatic S-adenosyl methionine (SAMe) levels decrease in methionine adenosyltransferase 1A (Mat1a) knockout (KO) mice, which develop HCC, and in ethanol-fed mice. We examined the regulation of Ubc9 by SAMe in murine liver and human HCC, breast, and colon carcinoma cell lines and specimens. Real-time polymerase chain reaction and western blotting measured gene and protein expression, respectively. Immunoprecipitation followed by western blotting examined protein-protein interactions. Ubc9 expression increased in HCC and when hepatic SAMe levels decreased. SAMe treatment in Mat1a KO mice reduced Ubc9 protein, but not messenger RNA (mRNA) levels, and lowered sumoylation. Similarly, treatment of liver cancer cell lines HepG2 and Huh7, colon cancer cell line RKO, and breast cancer cell line MCF-7 with SAMe or its metabolite 5'-methylthioadenosine (MTA) reduced only Ubc9 protein level. Ubc9 posttranslational regulation is unknown. Ubc9 sequence predicted a possible phosphorylation site by cell division cycle 2 (Cdc2), which directly phosphorylated recombinant Ubc9. Mat1a KO mice had higher phosphorylated (phospho)-Ubc9 levels, which normalized after SAMe treatment. SAMe and MTA treatment lowered Cdc2 mRNA and protein levels, as well as phospho-Ubc9 and protein sumoylation in liver, colon, and breast cancer cells. Serine 71 of Ubc9 was required for phosphorylation, interaction with Cdc2, and protein stability. Cdc2, Ubc9, and phospho-Ubc9 levels increased in human liver, breast, and colon cancers.
    Conclusion: Cdc2 expression is increased and Ubc9 is hyperphosphorylated in several cancers, and this represents a novel mechanism to maintain high Ubc9 protein expression that can be inhibited by SAMe and MTA.
    MeSH term(s) Animals ; Cell Line, Tumor ; Humans ; Liver Neoplasms/metabolism ; Mice ; S-Adenosylmethionine/physiology ; Sumoylation ; Ubiquitin-Conjugating Enzymes/biosynthesis
    Chemical Substances S-Adenosylmethionine (7LP2MPO46S) ; Ubiquitin-Conjugating Enzymes (EC 2.3.2.23) ; ubiquitin-conjugating enzyme UBC9 (EC 6.3.2.-)
    Language English
    Publishing date 2012-07-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.25701
    Database MEDical Literature Analysis and Retrieval System OnLINE

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