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  • 1
    Online Resource
    Online Resource
    A Novel Polyhalogenated Monoterpene Induces Cell Cycle Arrest and Apoptosis in Breast Cancer Cells
    MDPI AG ; 2019
    In:  Marine Drugs Vol. 17, No. 8 ( 2019-07-25), p. 437-
    Details
    In: Marine Drugs, MDPI AG, Vol. 17, No. 8 ( 2019-07-25), p. 437-
    Abstract: Breast cancer is the most common cancer type and a primary cause of cancer mortality among females worldwide. Here, we analyzed the anticancer efficacy of a novel bromochlorinated monoterpene, PPM1, a synthetic analogue of polyhalogenated monoterpenes from Plocamium red algae and structurally similar non-brominated monoterpenes. PPM1, but not the non-brominated monoterpenes, decreased selectively the viability of several triple-negative as well as triple-positive breast cancer cells with different p53 status without significantly affecting normal breast epithelial cells. PPM1 induced accumulation of triple-negative MDA-MB-231 cells with 4N DNA content characterized by decreased histone H3-S10/T3 phosphorylation indicating cell cycle arrest in the G2 phase. Western immunoblot analysis revealed that PPM1 treatment triggered an initial rapid activation of Aurora kinases A/B/C and p21Waf1/Cip1 accumulation, which was followed by accumulation of polyploid 〉 4N cells. Flow cytometric analysis showed mitochondrial potential disruption, caspase 3/7 activation, phosphatidylserine externalization, reduction of the amount polyploid cells, and DNA fragmentation consistent with induction of apoptosis. Cell viability was partially restored by the pan-caspase inhibitor Z-VAD-FMK indicating caspase contribution. In vivo, PPM1 inhibited growth, proliferation, and induced apoptosis in MDA-MB-231 xenografted onto the chick chorioallantoic membrane. Hence, Plocamium polyhalogenated monoterpenes and synthetic analogues deserve further exploration as promising anticancer lead compounds.
    Type of Medium: Online Resource
    ISSN: 1660-3397
    URL: Article
    DOI: 10.3390/md17080437
    Language: English
    Publisher: MDPI AG
    Publication Date: 2019
    detail.hit.zdb_id: 2175190-0
    SSG: 15,3
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  • 2
    Online Resource
    Online Resource
    COVID-19 pandemic and therapy with ibuprofen or renin-angiotensin system blockers: no need for interruptions or changes in ongoing chronic treatments
    Springer Science and Business Media LLC ; 2020
    In:  Naunyn-Schmiedeberg's Archives of Pharmacology Vol. 393, No. 7 ( 2020-07), p. 1131-1135
    Details
    In: Naunyn-Schmiedeberg's Archives of Pharmacology, Springer Science and Business Media LLC, Vol. 393, No. 7 ( 2020-07), p. 1131-1135
    Abstract: Scientists hypothesized that drugs such as ibuprofen or renin-angiotensin system (RAS) blockers could exacerbate the novel coronavirus disease COVID-19 by upregulating the angiotensin-converting enzyme 2 (ACE2), which serves as an entry receptor for the coronavirus SARS-CoV-2. This hypothesis was taken up by the lay press and led to concerns among doctors and patients whether the use of these drugs was still safe and justified against the background of the pandemic spread of SARS-CoV-2 with an increasing number of cases and deaths. In this article, we summarize what is known about the effect of RAS blockers or non-steroidal anti-inflammatory drugs (NSAIDs) on the course of COVID-19 disease. In the case of RAS inhibition, we also find evidence for the opposite hypothesis, namely, that RAS inhibition in COVID-19 could be protective. In view of the inconsistent and limited evidence and after weighing up the benefits and risks, we would not currently recommend discontinuing or switching an effective treatment with RAS blockers. NSAIDs should be used at the lowest effective dose for the shortest possible period. The choice of drug to treat COVID-19-associated fever or pain should be based on a benefit-risk assessment for known side effects (e.g., kidney damage, gastrointestinal ulceration).
    Type of Medium: Online Resource
    ISSN: 0028-1298 , 1432-1912
    URL: Article
    DOI: 10.1007/s00210-020-01890-6
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2020
    detail.hit.zdb_id: 1462940-9
    SSG: 15,3
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  • 3
    Online Resource
    Online Resource
    COVID-19 pandemic–related adaptations of medical education in clinical pharmacology — impact on students and lecturers at a German university
    Springer Science and Business Media LLC ; 2022
    In:  Naunyn-Schmiedeberg's Archives of Pharmacology Vol. 395, No. 6 ( 2022-06), p. 681-690
    Details
    In: Naunyn-Schmiedeberg's Archives of Pharmacology, Springer Science and Business Media LLC, Vol. 395, No. 6 ( 2022-06), p. 681-690
    Abstract: In medical studies, pharmacology is a subject with a high teaching and study load. The COVID-19 pandemic–related switch to distance learning implies challenges for students and teachers. To identify changes of behavior, attitudes, and needs among students and teachers in clinical pharmacology during the pandemic, regular surveys were conducted at Ulm University, Germany. Overall, 884 students and 5 teachers answered the survey. Over time, students’ usage of learning materials in print form and further literature (textbooks, guidelines) constantly decreased. In turn, most students used digital materials provided via a learning management system. Attitudes and opinions of students and teachers significantly differed regarding (i) the benefit of certain teaching formats and learning materials, (ii) open-mindedness towards e-learning, and (iii) future visions. Most students and lecturers stated that they spent more time on study or teaching-related activities, respectively, and had less contact with fellow students or colleagues in comparison to pre-pandemic times. Furthermore, the subjective teaching load for most lecturers (80%) increased during the pandemic. To identify determinants of learning success, the survey data were correlated with students’ gradings in the written exams of clinical pharmacology. In the first online semester (summer term 2020), the use of paper-based learning scripts was correlated with better exam grades. No correlation with grade was found for any other learning materials. Age was inversely correlated with exam grading. Striking a balance between the future visions and needs of students and teachers implies a particular challenge for the educational system of the next years.
    Type of Medium: Online Resource
    ISSN: 0028-1298 , 1432-1912
    URL: Article
    DOI: 10.1007/s00210-022-02225-3
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 1462940-9
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  • 4
    Online Resource
    Online Resource
    Bardoxolone-Methyl (CDDO-Me) Impairs Tumor Growth and Induces Radiosensitization of Oral Squamous Cell Carcinoma Cells
    Frontiers Media SA ; 2021
    In:  Frontiers in Pharmacology Vol. 11 ( 2021-1-29)
    Details
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 11 ( 2021-1-29)
    Abstract: Radiotherapy represents a common treatment strategy for patients suffering from oral squamous cell carcinoma (OSCC). However, application of radiotherapy is immanently limited by radio-sensitivity of normal tissue surrounding the tumor sites. In this study, we used normal human epithelial keratinocytes (NHEK) and OSCC cells (Cal-27) as models to investigate radio-modulating and anti-tumor effects of the synthetic triterpenoid 2-cyano-3,12-dioxooleana-1,9,-dien-28-oic acid methyl ester (CDDO-Me). Nanomolar CDDO-Me significantly reduced OSCC tumor xenograft-growth in-ovo applying the chick chorioallantoic membrane (CAM) assay. In the presence of CDDO-Me reactive oxygen species (ROS) were found to be reduced in NHEK when applying radiation doses of 8 Gy, whereas ROS levels in OSCC cells rose significantly even without radiation. In parallel, CDDO-Me was shown to enhance metabolic activity in malignant cells only as indicated by significant accumulation of reducing equivalents NADPH/NADH. Furthermore, antioxidative heme oxygenase-1 (HO-1) levels were only enhanced in NHEK and not in the OSCC cell line, as shown by immunoblotting. Clonogenic survival was left unchanged by CDDO-Me treatment in NHEK but revealed to be abolished almost completely in OSCC cells. Our results indicate anti-cancer and radio-sensitizing effects of CDDO-Me treatment in OSCC cells, whereas nanomolar CDDO-Me failed to provoke clear detrimental consequences in non-malignant keratinocytes. We conclude, that the observed differential aftermath of CDDO-Me treatment in malignant OSCC and non-malignant skin cells may be utilized to broaden the therapeutic range of clinical radiotherapy.
    Type of Medium: Online Resource
    ISSN: 1663-9812
    URL: Article
    DOI: 10.3389/fphar.2020.607580
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
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  • 5
    Online Resource
    Online Resource
    Acovenoside A Induces Mitotic Catastrophe Followed by Apoptosis in Non-Small-Cell Lung Cancer Cells
    American Chemical Society (ACS) ; 2017
    In:  Journal of Natural Products Vol. 80, No. 12 ( 2017-12-22), p. 3203-3210
    Details
    In: Journal of Natural Products, American Chemical Society (ACS), Vol. 80, No. 12 ( 2017-12-22), p. 3203-3210
    Type of Medium: Online Resource
    ISSN: 0163-3864 , 1520-6025
    URL: Article
    DOI: 10.1021/acs.jnatprod.7b00546
    RVK:
    WA 15000
    Language: English
    Publisher: American Chemical Society (ACS)
    Publication Date: 2017
    detail.hit.zdb_id: 1491522-4
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Propensity of Fluoroquinolones with Different Moieties at Position 8 to Cause Resistance Development in Clinical Isolates of Streptococcus pneumoniae
    American Society for Microbiology ; 2001
    In:  Antimicrobial Agents and Chemotherapy Vol. 45, No. 9 ( 2001-09), p. 2666-2667
    Details
    In: Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Vol. 45, No. 9 ( 2001-09), p. 2666-2667
    Type of Medium: Online Resource
    ISSN: 0066-4804 , 1098-6596
    URL: Article
    DOI: 10.1128/AAC.45.9.2666-2667.2001
    RVK:
    XA 24552
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2001
    detail.hit.zdb_id: 1496156-8
    SSG: 12
    SSG: 15,3
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  • 7
    Online Resource
    Online Resource
    DataSheet1.DOCX
    Frontiers Media SA ; 2021
    In:  Frontiers in Pharmacology Vol. 12 ( 2021-5-5)
    Details
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 12 ( 2021-5-5)
    Abstract: Cardenolide glycosides are natural compounds known to inhibit the ion pumping function of the Na + /K + -ATPase in cellular systems. Interestingly, various cancer cell types are highly susceptible to cardenolide glycosides. Herein, we explore the cardenolide glycoside Acovenoside A (AcoA) with respect to its influences on human A549 non-small cell lung cancer (NSCLC) cells. We found that exposure to AcoA, digoxin and ouabain increases intracellular sodium and ATP levels indicating that the ion pumping function of the transmembrane Na + /K + -ATPase is effectively inhibited. Like digoxin and ouabain, AcoA inhibits transcription factor NF-κB activation and induces apoptotic cell death in NSCLC cells. This was confirmed by a preclinical in vivo model in which AcoA treatment of NSCLC xenografts grown on chick chorioallantoic membranes inhibited the expression of proliferation antigen Ki-67 and induced apoptotic DNA strand breaks. We aimed to elucidate the underlying mechanisms. The Na + /K + -ATPase transmembrane complex contains Src kinase and epidermal growth factor receptor (EGFR). Indeed, we found that AcoA activates Src kinase in A549 cells, but not in a cell-free assay using recombinant Src kinase. Src kinase is a downstream target of EGFR, and correlation analysis using the NCI60 database pointed to a role of EGFR in cardenolide glycoside-induced cancer cell death. Accordingly, NSCLC cells expressing hyperphosphorylated EGFR mut exhibited resistance to AcoA. To investigate the interaction between cardenolide glycosides and EGFR in detail, we performed immunoblotting studies: Whereas ligand binding and EGFR phosphorylation were not significantly affected, ubiquitinated EGFR accumulated after prolonged incubation with AcoA. To visualize EGFR trafficking we used A549 cells transfected with a fluorescent biosensor which binds to activated EGFR. Pretreatment with AcoA and digoxin induced accumulation of EGFR in endosomal compartments thus inhibiting EGF-induced EGFR degradation comparable to the Na + ionophore monensin, a known inducer of EGFR endosomal arrest. Intracellular Na + concentrations regulate EGFR trafficking and signaling. Na + homeostasis is maintained by the Na + /K + -ATPase, which might account for its close interaction with the EGFR. Cardenolide glycosides inhibit the ATP-dependent Na + /K + exchange through the Na + /K + -ATPase resulting in higher intracellular Na + levels. Our data provide first evidence that this impedes efficient EGFR trafficking at the endosomal compartment.
    Type of Medium: Online Resource
    ISSN: 1663-9812
    URL: Article
    URL: Article
    DOI: 10.3389/fphar.2021.611657
    DOI: 10.3389/fphar.2021.611657.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2587355-6
    SSG: 15,3
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