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1. WO2013102878 - FAT1 GENE IN CANCER AND INFLAMMATION

Publication Number WO/2013/102878
Publication Date 11.07.2013
International Application No. PCT/IB2013/050086
International Filing Date 04.01.2013
Chapter 2 Demand Filed 03.10.2013
IPC
C12N 15/113 2010.1
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15Mutation or genetic engineering; DNA or RNA concerning genetic engineering, vectors, e.g. plasmids, or their isolation, preparation or purification; Use of hosts therefor
09Recombinant DNA-technology
11DNA or RNA fragments; Modified forms thereof
113Non-coding nucleic acids modulating the expression of genes, e.g. antisense oligonucleotides
A61K 31/713 2006.1
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61MEDICAL OR VETERINARY SCIENCE; HYGIENE
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35Antineoplastic agents
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AHUMAN NECESSITIES
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C12N 15/1135
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09Recombinant DNA-technology
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113Non-coding nucleic acids modulating the expression of genes, e.g. antisense oligonucleotides; Antisense DNA or RNA; Triplex- forming oligonucleotides; Catalytic nucleic acids, e.g. ribozymes; Nucleic acids used in co-suppression or gene silencing
1135against oncogenes or tumor suppressor genes
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09Recombinant DNA-technology
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113Non-coding nucleic acids modulating the expression of genes, e.g. antisense oligonucleotides; Antisense DNA or RNA; Triplex- forming oligonucleotides; Catalytic nucleic acids, e.g. ribozymes; Nucleic acids used in co-suppression or gene silencing
1136against growth factors, growth regulators, cytokines, lymphokines or hormones
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Applicants
  • DEPARTMENT OF BIOTECHNOLOGY (DBT) [IN]/[IN]
  • ALL INDIA INSTITUTE OF MEDICAL SCIENCES (AIIMS) [IN]/[IN]
  • NATIONAL BRAIN RESEARCH CENTRE (NBRC) [IN]/[IN]
Inventors
  • CHOSDOL, Kunzang
  • DIKSHIT, Bhawana
  • SINHA, Subrata
Agents
  • NIRANJAN, Samuel, C.J.
Priority Data
45/DEL/201205.01.2012IN
Publication Language English (en)
Filing Language English (EN)
Designated States
Title
(EN) FAT1 GENE IN CANCER AND INFLAMMATION
(FR) GÈNE FAT1 DANS LE CANCER ET L'INFLAMMATION
Abstract
(EN) The present invention demonstrates for the first time that FA Tl plays an important role in modulating PDCD4 expression, which in turn regulates AP-1 dependent transcription, controls processes crucial for migration and invasion in cancer cells, controls induction of a pro -inflammatory micro environment in cancer cells. The study illustrates a link between inflammation and cancer in cells or in a subject. This work highlights the importance of FAT 1 in the induction of the cellular pathways of migration and invasion, proteolysis of the ECM and the expression of pro- inflammatory molecules leading to a favorable micro environment for tumor and cancer progression. The present invention also provides the use of FAT1 in regulating neoplastic phenotypes and genotypes including invasiveness and inflammatory micro environment of the cancer cells by acting as a novel apical regulator of a signaling pathway by affecting the AP1 transcriptional activity, affecting the property of both cell migration and invasion and at the same time affecting the expression of inflammatory modulators. The present invention also identifies a novel regulatory pathway for inflammatory mediators and inflammatory cellular responses via PDCD4 and AP1. The invention describes a pathway for the upregulation of inflammatory processes as such, and hence a means of regulating inflammatory pathologies in general.
(FR) La présente invention démontre pour la première fois que FAT1 joue un rôle important dans la modulation de l'expression de PDCD4, qui à son tour régule la transcription dépendante d'AP-1, commande des procédés cruciaux pour la migration et l'invasion dans des cellules cancéreuses, commande l'induction d'un microenvironnement pro-inflammatoire dans des cellules cancéreuses. L'étude illustre une liaison entre l'inflammation et le cancer dans des cellules ou chez un sujet. Ce travail souligne l'importance de FAT1 dans l'induction des voies cellulaires de migration et d'invasion, la protéolyse de l'ECM et l'expression de molécules pro-inflammatoires conduisant à un microenvironnement favorable pour la progression d'une tumeur et du cancer. La présente invention concerne également l'utilisation de FAT1 dans la régulation de phénotypes néoplasiques et de génotypes néoplasiques, comprenant le pouvoir envahissant et un microenvironnement inflammatoire des cellules cancéreuses en agissant comme un nouveau régulateur apical d'une voie e signalisation en affectant l'activité transcriptionnelle d'AP-1, affectant la propriété à la fois de la migration cellulaire et de l'invasion cellulaire et, en même temps, en affectant l'expression de modulateurs inflammatoires. La présente invention concerne également une nouvelle voie régulatrice pour des médiateurs inflammatoires et des réponses cellulaires inflammatoires par l'intermédiaire de PDCD4 et AP1. L'invention concerne une voie pour la régulation à la hausse de procédés inflammatoires tels quels, et par conséquent un moyen de régulation de pathologies inflammatoires en général.
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