Der Beitrag von evangelischen Religionslehrerinnen und Religionslehrern zur Friedenserziehung

Friedensbildung steht im engen Zusammenhang mit Friedenserziehung und Friedenspädagogik. Die Vorteile der Einführung des Begriffs Friedensbildung in die pädagogische Diskussion werden dargestellt und in der Charakterisierung von fünf Dimensionen von Friedensbildung Subjektorientierung, Prozessorientierung, Dialogorientierung, Sachorientierung und Kompetenzorientierung – zusammengefasst. Die Internationalen Dekaden der Vereinten Nationen und des Ökumenischen Rates der Kirchen sollen eine Kultur des Friedens nachhaltig beeinflussen. Die Vorstellung der Intentionen und Materialien bieten Anknüpfungspunkte für friedensbildendes Lernen. Im Bereich der schulischen Bildung sind aktuell Bildungsstandards und Kompetenzen in Entwicklung, welche die Lernergebnisse und erworbenen Fähigkeiten, Fertigkeiten, von Schülerinnen und Schülern beschreiben. Auch die religiöse Kompetenz kommt dabei in den Blick und bietet bereits erste Forschungsergebnisse aus Deutschland. Der Erwerb von Friedenskompetenz wird als bedeutender Anteil religiöser Bildung herausgearbeitet. Der Beitrag des Evangelischen Religionsunterrichts zur Friedensbildung wird durch die Betrachtung und Erörterung von besonderen Organisationsmodellen im Religionsunterricht und von Rahmenbedingungen wie Lehrplan und Lehrerbildung dargestellt. Friedensbildungsstandards für den Evangelischen Religionsunterricht in Österreich werden für die 4., 8. und 12. Schulstufe erarbeitet und vorgelegt. Die fünf Dimensionen von Friedensbildung bilden die Grundlage dafür. Der Evangelische Religionsunterricht dient als Beispiel für demokratische Schulkultur ohne strukturelle Gewalt und fördert eine Kultur des Friedens.Peace-education distinguishes two different words in German; “Friedenserziehung” and “Friedenspädagogik”. Both don’t express the meaning. The advantages of the introduction of a new term “Friedensbildung” into the pedagogical discussion were exposed and comprised in characterizing five dimensions of peace-education: subject-orientation, process-orientation, dialog-orientation, content-orientation and competence-orientation. The international decades of the United Nations and the Ecumenical Council of the Churches should influence a culture of peace sustainable. The presentation of the intentions and the materials offer starting-points for peaceful education. Actually in the field of school-building are standards and competences in formation, which describe the outcomes and outputs of students. Also the religious competence comes into the view and offers already first results from research in Germany. Peace-competence is generated as important part of religious education. The contribution to peace-education of Protestant Religious Education is presented by the consideration and discussion of special models of Religious Education and structural conditions like curriculum and teacher education. Standards for peace-building for Protestant Religious Education in Austria at stage 4, 8 and 12 were elaborated and submitted. The five dimensions of peace-education are the basis therefore. The Protestant Religious Education serves as an example for democratic school-culture without structural violence and promotes a culture of peace

STAT3/LKB1 controls metastatic prostate cancer by regulating mTORC1/CREB pathway

Prostate cancer (PCa) is a common and fatal type of cancer in men. Metastatic PCa (mPCa) is a major factor contributing to its lethality, although the mechanisms remain poorly understood. PTEN is one of the most frequently deleted genes in mPCa. Here we show a frequent genomic co-deletion of PTEN and STAT3 in liquid biopsies of patients with mPCa. Loss of Stat3 in a Pten-null mouse prostate model leads to a reduction of LKB1/pAMPK with simultaneous activation of mTOR/CREB, resulting in metastatic disease. However, constitutive activation of Stat3 led to high LKB1/pAMPK levels and suppressed mTORC1/CREB pathway, preventing mPCa development. Metformin, one of the most widely prescribed therapeutics against type 2 diabetes, inhibits mTORC1 in liver and requires LKB1 to mediate glucose homeostasis. We find that metformin treatment of STAT3/AR-expressing PCa xenografts resulted in significantly reduced tumor growth accompanied by diminished mTORC1/CREB, AR and PSA levels. PCa xenografts with deletion of STAT3/AR nearly completely abrogated mTORC1/CREB inhibition mediated by metformin. Moreover, metformin treatment of PCa patients with high Gleason grade and type 2 diabetes resulted in undetectable mTORC1 levels and upregulated STAT3 expression. Furthermore, PCa patients with high CREB expression have worse clinical outcomes and a significantly increased risk of PCa relapse and metastatic recurrence. In summary, we have shown that STAT3 controls mPCa via LKB1/pAMPK/mTORC1/CREB signaling, which we have identified as a promising novel downstream target for the treatment of lethal mPCa

STAT3/LKB1 controls metastatic prostate cancer by regulating mTORC1/CREB pathway

Acknowledgements: The authors thank Stephanie Ponti, Anna Zacher and Victoria Weissenböck for their skilful help with animal handling as well as biolution GmbH for the support with the graphical abstract.Funder: Christian Doppler Research AssociationFunder: Austrian Federal Ministry of Science, Research and EconomyFunder: National Foundation for Research, Technology and DevelopmentFunder: Siemens HealthineersProstate cancer (PCa) is a common and fatal type of cancer in men. Metastatic PCa (mPCa) is a major factor contributing to its lethality, although the mechanisms remain poorly understood. PTEN is one of the most frequently deleted genes in mPCa. Here we show a frequent genomic co-deletion of PTEN and STAT3 in liquid biopsies of patients with mPCa. Loss of Stat3 in a Pten-null mouse prostate model leads to a reduction of LKB1/pAMPK with simultaneous activation of mTOR/CREB, resulting in metastatic disease. However, constitutive activation of Stat3 led to high LKB1/pAMPK levels and suppressed mTORC1/CREB pathway, preventing mPCa development. Metformin, one of the most widely prescribed therapeutics against type 2 diabetes, inhibits mTORC1 in liver and requires LKB1 to mediate glucose homeostasis. We find that metformin treatment of STAT3/AR-expressing PCa xenografts resulted in significantly reduced tumor growth accompanied by diminished mTORC1/CREB, AR and PSA levels. PCa xenografts with deletion of STAT3/AR nearly completely abrogated mTORC1/CREB inhibition mediated by metformin. Moreover, metformin treatment of PCa patients with high Gleason grade and type 2 diabetes resulted in undetectable mTORC1 levels and upregulated STAT3 expression. Furthermore, PCa patients with high CREB expression have worse clinical outcomes and a significantly increased risk of PCa relapse and metastatic recurrence. In summary, we have shown that STAT3 controls mPCa via LKB1/pAMPK/mTORC1/CREB signaling, which we have identified as a promising novel downstream target for the treatment of lethal mPCa

STAT3/LKB1 controls metastatic prostate cancer by regulating mTORC1/CREB pathway

Abstract Prostate cancer (PCa) is a common and fatal type of cancer in men. Metastatic PCa (mPCa) is a major factor contributing to its lethality, although the mechanisms remain poorly understood. PTEN is one of the most frequently deleted genes in mPCa. Here we show a frequent genomic co-deletion of PTEN and STAT3 in liquid biopsies of patients with mPCa. Loss of Stat3 in a Pten-null mouse prostate model leads to a reduction of LKB1/pAMPK with simultaneous activation of mTOR/CREB, resulting in metastatic disease. However, constitutive activation of Stat3 led to high LKB1/pAMPK levels and suppressed mTORC1/CREB pathway, preventing mPCa development. Metformin, one of the most widely prescribed therapeutics against type 2 diabetes, inhibits mTORC1 in liver and requires LKB1 to mediate glucose homeostasis. We find that metformin treatment of STAT3/AR-expressing PCa xenografts resulted in significantly reduced tumor growth accompanied by diminished mTORC1/CREB, AR and PSA levels. PCa xenografts with deletion of STAT3/AR nearly completely abrogated mTORC1/CREB inhibition mediated by metformin. Moreover, metformin treatment of PCa patients with high Gleason grade and type 2 diabetes resulted in undetectable mTORC1 levels and upregulated STAT3 expression. Furthermore, PCa patients with high CREB expression have worse clinical outcomes and a significantly increased risk of PCa relapse and metastatic recurrence. In summary, we have shown that STAT3 controls mPCa via LKB1/pAMPK/mTORC1/CREB signaling, which we have identified as a promising novel downstream target for the treatment of lethal mPCa

STAT3/LKB1 controls metastatic prostate cancer by regulating mTORC1/CREB pathway.

Acknowledgements: The authors thank Stephanie Ponti, Anna Zacher and Victoria Weissenböck for their skilful help with animal handling as well as biolution GmbH for the support with the graphical abstract.Funder: Christian Doppler Research AssociationFunder: Austrian Federal Ministry of Science, Research and EconomyFunder: National Foundation for Research, Technology and DevelopmentFunder: Siemens HealthineersProstate cancer (PCa) is a common and fatal type of cancer in men. Metastatic PCa (mPCa) is a major factor contributing to its lethality, although the mechanisms remain poorly understood. PTEN is one of the most frequently deleted genes in mPCa. Here we show a frequent genomic co-deletion of PTEN and STAT3 in liquid biopsies of patients with mPCa. Loss of Stat3 in a Pten-null mouse prostate model leads to a reduction of LKB1/pAMPK with simultaneous activation of mTOR/CREB, resulting in metastatic disease. However, constitutive activation of Stat3 led to high LKB1/pAMPK levels and suppressed mTORC1/CREB pathway, preventing mPCa development. Metformin, one of the most widely prescribed therapeutics against type 2 diabetes, inhibits mTORC1 in liver and requires LKB1 to mediate glucose homeostasis. We find that metformin treatment of STAT3/AR-expressing PCa xenografts resulted in significantly reduced tumor growth accompanied by diminished mTORC1/CREB, AR and PSA levels. PCa xenografts with deletion of STAT3/AR nearly completely abrogated mTORC1/CREB inhibition mediated by metformin. Moreover, metformin treatment of PCa patients with high Gleason grade and type 2 diabetes resulted in undetectable mTORC1 levels and upregulated STAT3 expression. Furthermore, PCa patients with high CREB expression have worse clinical outcomes and a significantly increased risk of PCa relapse and metastatic recurrence. In summary, we have shown that STAT3 controls mPCa via LKB1/pAMPK/mTORC1/CREB signaling, which we have identified as a promising novel downstream target for the treatment of lethal mPCa