Advances in biological regulation最新文献

{"title":"The potential of the nutraceutical berberine in the treatment of hepatocellular carcinoma and other liver diseases such as NAFLD and NASH","authors":"Melchiorre Cervello ,&nbsp;Giuseppa Augello ,&nbsp;Lucio Cocco ,&nbsp;Stefano Ratti ,&nbsp;Matilde Y. Follo ,&nbsp;Alberto M. Martelli ,&nbsp;Antonella Cusimano ,&nbsp;Giuseppe Montalto ,&nbsp;James A. McCubrey","doi":"10.1016/j.jbior.2024.101032","DOIUrl":"10.1016/j.jbior.2024.101032","url":null,"abstract":"<div><p>Hepatocellular carcinoma (HCC) is a common cancer which unfortunately has poor outcomes. Common anti-cancer treatments such as chemotherapy and targeted therapy have not increased patient survival significantly. A common treatment for HCC patients is transplantation, however, it has limitations and complications. Novel approaches are necessary to more effectively treat HCC patients. Berberine (BBR) is a nutraceutical derived from various fruits and trees, which has been used for centuries in traditional medicine to treat various diseases such as diabetes and inflammation. More recently, the anti-proliferation effects of BBR have been investigated in the treatment of patients with various cancers, especially colorectal cancer, and in non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). In this review, we will focus on studies with BBR in liver diseases.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"92 ","pages":"Article 101032"},"PeriodicalIF":0.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140781819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lysophosphatidic acid (LPA) receptor-mediated signaling and cellular responses to anticancer drugs and radiation of cancer cells","authors":"Hiroko Ikeda,&nbsp;Miwa Takai,&nbsp;Toshifumi Tsujiuchi","doi":"10.1016/j.jbior.2024.101029","DOIUrl":"10.1016/j.jbior.2024.101029","url":null,"abstract":"<div><p>Lysophosphatidic acid (LPA) is a simple physiological lipid and structurally consists of a fatty, a phosphate and a glycerol. LPA binds to G protein-coupled LPA receptors (LPA₁ to LPA₆). LPA receptor-mediated signaling mediates a variety of biological responses, such as cell growth, migration, morphogenesis, differentiation and protection from apoptosis. It is considered that LPA receptor-mediated signaling plays an important role in the pathogenesis of human malignancies. So far, genetic and epigenetic alterations of LPA receptors have been found in several cancer cells as well as abnormal LPA production. In addition, LPA receptor-mediated signaling regulates the promotion of malignant behaviors, including chemo- and/or radiation-resistance. Chemotherapy and radiotherapy are the common approaches to the treatments of cancers. However, resistance to anticancer drugs and irradiation is the most critical limitation for chemotherapy and radiotherapy. In this review, we provide the roles of LPA receptor-mediated signaling in the regulation of cellular responses induced by chemotherapeutic agents and irradiation and its biological utility as a possible molecular target for improving cancer cell responses to chemotherapy and radiotherapy.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"92 ","pages":"Article 101029"},"PeriodicalIF":0.0,"publicationDate":"2024-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139830187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A new method for quantifying the enzyme activity of DGKs","authors":"Millie Xin Barbernitz ,&nbsp;Daniel M. Raben","doi":"10.1016/j.jbior.2023.100998","DOIUrl":"10.1016/j.jbior.2023.100998","url":null,"abstract":"<div><p>Diacylglycerol kinases (DGKs) are a family of enzymes that catalyze the ATP-dependent conversion of diacylglycerol (DAG) to phosphatidic acid (PtdOH). A common approach to examine the activity of these enzymes relys on a radiometric assay (Epand and Topham, 2007; Tu-Sekine and Raben, 2017). This assay quantifies the DGK-catalyzed incorporation of ³²P into DAG from AT³²P to generate ³²PtdOH and is perhaps been the most widely used assay. While sensitive, its drawbacks are the expense and the potential negative impacts on health and the environment. In this report, we describe a new assay which utilizes fluorescent labeled NBD-DAG (1-Oleoyl-2-[12-[(7-nitro-2-1,3-benzoxadiazol-4-yl) amino] dodecanoyl]-sn-Glycero-3-diacylglycerol) to quantify the DGK-θ-catalyzed conversion of NBD-DAG to NBD-PtdOH. Furthermore, we show the assay is sufficiently sensitive as the measured specific activity was similar to that previously determined with AT³²P (Tu-Sekine and Raben, 2012) and was able to detect the activation of DGK-θ by synaptotagmin-1 (Barber et al., 2022). Overall, this assay is inexpensive, sensitive, and reproducible making it an attractive alternative to currently established assays.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"91 ","pages":"Article 100998"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135566034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biology of childhood hepatoblastoma and the search for novel treatments","authors":"Marjut Pihlajoki ,&nbsp;Katja Eloranta ,&nbsp;Ruth Nousiainen ,&nbsp;Ville Väyrynen ,&nbsp;Tea Soini ,&nbsp;Antti Kyrönlahti ,&nbsp;Seppo Parkkila ,&nbsp;Jukka Kanerva ,&nbsp;David B. Wilson ,&nbsp;Mikko P. Pakarinen ,&nbsp;Markku Heikinheimo","doi":"10.1016/j.jbior.2023.100997","DOIUrl":"10.1016/j.jbior.2023.100997","url":null,"abstract":"<div><p>Our research laboratory has a longstanding interest in developmental disorders and embryonic tumors, and recent efforts have focused on the pathogenesis of pediatric liver tumors. This review focuses on hepatoblastoma (HB), the most common pediatric liver malignancy. Despite advances in treatment, patients with metastatic HB have a poor prognosis, and survivors often have permanent side effects attributable to chemotherapy. In an effort to improve survival and lessen long-term complications of HB, we have searched for novel molecular vulnerabilities using a combination of patient derived cell lines, metabolomics, and RNA sequencing of human samples at diagnosis and follow-up. These studies have shed light on pathogenesis and identified putative targets for future therapies in children with advanced HB.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"91 ","pages":"Article 100997"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S221249262300043X/pdfft?md5=7d1cb69691b41ae0282774274077ed6c&pid=1-s2.0-S221249262300043X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136093654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent advances in the application of induced pluripotent stem cell technology to the study of myeloid malignancies","authors":"Dharamveer Tatwavedi,&nbsp;Andrea Pellagatti,&nbsp;Jacqueline Boultwood","doi":"10.1016/j.jbior.2023.100993","DOIUrl":"10.1016/j.jbior.2023.100993","url":null,"abstract":"<div><p>Acquired myeloid malignancies are a spectrum of clonal disorders known to be caused by sequential acquisition of genetic lesions in hematopoietic stem and progenitor cells, leading to their aberrant self-renewal and differentiation. The increasing use of induced pluripotent stem cell (iPSC) technology to study myeloid malignancies has helped usher a paradigm shift in approaches to disease modeling and drug discovery, especially when combined with gene-editing technology. The process of reprogramming allows for the capture of the diversity of genetic lesions and mutational burden found in primary patient samples into individual stable iPSC lines. Patient-derived iPSC lines, owing to their self-renewal and differentiation capacity, can thus be a homogenous source of disease relevant material that allow for the study of disease pathogenesis using various functional read-outs. Furthermore, genome editing technologies like CRISPR/Cas9 enable the study of the stepwise progression from normal to malignant hematopoiesis through the introduction of specific driver mutations, individually or in combination, to create isogenic lines for comparison. In this review, we survey the current use of iPSCs to model acquired myeloid malignancies including myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPN), acute myeloid leukemia and MDS/MPN overlap syndromes. The use of iPSCs has enabled the interrogation of the underlying mechanism of initiation and progression driving these diseases. It has also made drug testing, repurposing, and the discovery of novel therapies for these diseases possible in a high throughput setting.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"91 ","pages":"Article 100993"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2212492623000398/pdfft?md5=d8e09f7c3b671a2a8097f2350e2b7a5f&pid=1-s2.0-S2212492623000398-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41187961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ablation of diacylglycerol kinase ε promotes whitening of brown adipose tissue under high fat diet feeding","authors":"Tomoyuki Nakano,&nbsp;Ayako Suzuki,&nbsp;Kaoru Goto","doi":"10.1016/j.jbior.2023.100994","DOIUrl":"10.1016/j.jbior.2023.100994","url":null,"abstract":"<div><p>Adipose tissue (AT) comprises distinct fat depots such as white AT and brown AT. White and brown adipocytes exhibit different morphological and physiological properties. White adipocytes containing large single lipid droplet (LD) provide energy on demand whereas brown adipocytes loaded with multilocular LDs consume energy to generate heat or dissipate excess energy. Recent studies have shown that multilocular brown-like cells emerge in white AT under certain conditions. These cells termed beige adipocytes participate in energy expenditure and heat generation. In the process of lipolysis, TG is broken down into free fatty acid and diacylglycerol (DG). In this regard, DG also serves as a signaling molecule activating some proteins such as protein kinase C. Therefore, DG kinase (DGK), an enzyme which phosphorylates DG into phosphatidic acid (PA), plays a pivotal role in integrating energy homeostasis and intracellular signaling. Recently, we described that DGKε-KO mice exhibit increased adiposity in visceral white AT accompanied with impaired glucose tolerance early (40 days) in the course of high fat diet (HFD) feeding, although these mice exhibit “browning or beiging” in visceral white AT associated with improved glucose tolerance after longer term HFD feeding (180 days). This study was conducted to understand the overall features of adipose tissues and investigate changes in subcutaneous (inguinal) white AT and interscapular brown AT of DGKε-KO mice during the course of HFD feeding. Results demonstrated that fat accumulation is promoted in all fat depots under 40 days of HFD feeding conditions. Remarkably, “whitening” of brown adipocytes was identified in DGKε-deficient brown AT during the course of HFD feeding, suggesting brown adipocyte dysfunction. In addition, insulin levels were considerably elevated in DGKε-KO mice under 180 days of HFD feeding conditions. Collectively, these findings suggest that brown adipocytes are dysfunctional in DGKε-KO mice, which promotes browning or beiging in visceral white AT. Beige adipocytes may take over energy disposal and contribute to improving glucose tolerance with the aid of high levels of insulin in DGKε-KO mice upon excess feeding.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"91 ","pages":"Article 100994"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50156285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diacylglycerol kinases: A look into the future of immunotherapy","authors":"Miguel Martin-Salgado,&nbsp;Ane Ochoa-Echeverría,&nbsp;Isabel Mérida","doi":"10.1016/j.jbior.2023.100999","DOIUrl":"10.1016/j.jbior.2023.100999","url":null,"abstract":"<div><p>Cancer still represents the second leading cause of death right after cardiovascular diseases. According to the World Health Organization (WHO), cancer provoked around 10 million deaths in 2020, with lung and colon tumors accounting for the deadliest forms of cancer. As tumor cells become resistant to traditional therapeutic approaches, immunotherapy has emerged as a novel strategy for tumor control. T lymphocytes are key players in immune responses against tumors. Immunosurveillance allows identification, targeting and later killing of cancerous cells. Nevertheless, tumors evolve through different strategies to evade the immune response and spread in a process called metastasis. The ineffectiveness of traditional strategies to control tumor growth and expansion has led to novel approaches considering modulation of T cell activation and effector functions. Program death receptor 1 (PD-1) and cytotoxic T-lymphocyte antigen 4 (CTLA-4) showed promising results in the early 90s and nowadays are still being exploited together with other drugs for several cancer types. Other negative regulators of T cell activation are diacylglycerol kinases (DGKs) a family of enzymes that catalyze the conversion of diacylglycerol (DAG) into phosphatidic acid (PA). In T cells, DGKα and DGKζ limit the PLCγ/Ras/ERK axis thus attenuating DAG mediated signaling and T cell effector functions. Upregulation of either of both isoforms results in impaired Ras activation and anergy induction, whereas germline knockdown mice showed enhanced antitumor properties and more effective immune responses against pathogens. Here we review the mechanisms used by DGKs to ameliorate T cell activation and how inhibition could be used to reinvigorate T cell functions in cancer context. A better knowledge of the molecular mechanisms involved upon T cell activation will help to improve current therapies with DAG promoting agents.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"91 ","pages":"Article 100999"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2212492623000453/pdfft?md5=f6694ed8725f58691594eb04dca8f19b&pid=1-s2.0-S2212492623000453-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72207995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Key to photograph of participants","authors":"","doi":"10.1016/j.jbior.2024.101020","DOIUrl":"10.1016/j.jbior.2024.101020","url":null,"abstract":"","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"91 ","pages":"Article 101020"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2212492624000083/pdfft?md5=32aa151b49ce814c4560a89042d624ec&pid=1-s2.0-S2212492624000083-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139502126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Notch-3 affects chemoresistance in colorectal cancer via DNA base excision repair enzymes","authors":"Dennis C. George ,&nbsp;Fred E. Bertrand ,&nbsp;George Sigounas","doi":"10.1016/j.jbior.2024.101013","DOIUrl":"10.1016/j.jbior.2024.101013","url":null,"abstract":"<div><p>Colon cancer is the second leading cause of cancer death. With over 153,000 new CRC cases predicted, it is the third most commonly diagnosed cancer. Early detection can lead to curative surgical intervention, but recurrent and late metastatic disease is frequently treated with chemotherapeutic options based on induction of DNA damage. Understanding mechanism(s) that regulate DNA damage repair within colon tumor cells is essential to developing effective therapeutic strategies. The Notch signaling pathway<span> is known to participate in normal colon development and we have recently described a pathway by which Notch-1, Notch-3 and Smad may regulated EMT<span><span><span> and stem-like properties in colon tumor cells, promoting tumorigenesis. Little is known about how Notch may regulate drug resistance. In this study, we used shRNA<span> to generate colon tumor cells with loss of Notch-3 expression. These cells exhibited reduced expression of the base-excision repair proteins PARP1 and </span></span>APE1, along with increased sensitivity to ara-c and </span>cisplatin. These data point to a pathway in which Notch-3 signaling can regulate DNA repair within colon tumor cells and suggests that targeting Notch-3 may be an effective approach to rendering colon tumors sensitive to chemotherapeutic drugs.</span></span></p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"91 ","pages":"Article 101013"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139537329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Yusuf hannun photo","authors":"Lucio Ildebrando cocco","doi":"10.1016/j.jbior.2024.101021","DOIUrl":"10.1016/j.jbior.2024.101021","url":null,"abstract":"","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"91 ","pages":"Article 101021"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2212492624000095/pdfft?md5=4302333f928c687ad32edae663a9a29b&pid=1-s2.0-S2212492624000095-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139566357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}