NORAD-regulated signaling pathways in breast cancer progression
Main Author: | |
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Publication Date: | 2024 |
Other Authors: | , , , |
Format: | Article |
Language: | eng |
Source: | Repositórios Científicos de Acesso Aberto de Portugal (RCAAP) |
Download full: | http://hdl.handle.net/10773/43455 |
Summary: | Long non-coding RNA activated by DNA damage (NORAD) has recently been associated with pathologic mechanisms underlying cancer progression. Due to NORAD's extended range of interacting partners, there has been contradictory data on its oncogenic or tumor suppressor roles in BC. This review will summarize the function of NORAD in different BC subtypes and how NORAD impacts crucial signaling pathways in this pathology. Through the preferential binding to pumilio (PUM) proteins PUM1 and PUM2, NORAD has been shown to be involved in the control of cell cycle, angiogenesis, mitosis, DNA replication and transcription and protein translation. More recently, NORAD has been associated with PUM-independent roles, accomplished by interacting with other ncRNAs, mRNAs and proteins. The intricate network of NORAD-mediated signaling pathways may provide insights into the potential design of novel unexplored strategies to overcome chemotherapy resistance in BC treatment. |
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NORAD-regulated signaling pathways in breast cancer progressionLncRNAsNORADPumilioBreast cancerChemotherapy resistanceLong non-coding RNA activated by DNA damage (NORAD) has recently been associated with pathologic mechanisms underlying cancer progression. Due to NORAD's extended range of interacting partners, there has been contradictory data on its oncogenic or tumor suppressor roles in BC. This review will summarize the function of NORAD in different BC subtypes and how NORAD impacts crucial signaling pathways in this pathology. Through the preferential binding to pumilio (PUM) proteins PUM1 and PUM2, NORAD has been shown to be involved in the control of cell cycle, angiogenesis, mitosis, DNA replication and transcription and protein translation. More recently, NORAD has been associated with PUM-independent roles, accomplished by interacting with other ncRNAs, mRNAs and proteins. The intricate network of NORAD-mediated signaling pathways may provide insights into the potential design of novel unexplored strategies to overcome chemotherapy resistance in BC treatment.MDPI2025-01-16T09:38:17Z2024-02-01T00:00:00Z2024-02-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/10773/43455eng2072-669410.3390/cancers16030636Capela, Ana MariaTavares-Marcos, CarlotaEstima-Arede, Hugo F.Nóbrega-Pereira, SandrinaJesus, Bruno Bernardes deinfo:eu-repo/semantics/openAccessreponame:Repositórios Científicos de Acesso Aberto de Portugal (RCAAP)instname:FCCN, serviços digitais da FCT – Fundação para a Ciência e a Tecnologiainstacron:RCAAP2025-01-20T01:48:13Zoai:ria.ua.pt:10773/43455Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireinfo@rcaap.ptopendoar:https://opendoar.ac.uk/repository/71602025-05-28T19:40:34.192405Repositórios Científicos de Acesso Aberto de Portugal (RCAAP) - FCCN, serviços digitais da FCT – Fundação para a Ciência e a Tecnologiafalse |
dc.title.none.fl_str_mv |
NORAD-regulated signaling pathways in breast cancer progression |
title |
NORAD-regulated signaling pathways in breast cancer progression |
spellingShingle |
NORAD-regulated signaling pathways in breast cancer progression Capela, Ana Maria LncRNAs NORAD Pumilio Breast cancer Chemotherapy resistance |
title_short |
NORAD-regulated signaling pathways in breast cancer progression |
title_full |
NORAD-regulated signaling pathways in breast cancer progression |
title_fullStr |
NORAD-regulated signaling pathways in breast cancer progression |
title_full_unstemmed |
NORAD-regulated signaling pathways in breast cancer progression |
title_sort |
NORAD-regulated signaling pathways in breast cancer progression |
author |
Capela, Ana Maria |
author_facet |
Capela, Ana Maria Tavares-Marcos, Carlota Estima-Arede, Hugo F. Nóbrega-Pereira, Sandrina Jesus, Bruno Bernardes de |
author_role |
author |
author2 |
Tavares-Marcos, Carlota Estima-Arede, Hugo F. Nóbrega-Pereira, Sandrina Jesus, Bruno Bernardes de |
author2_role |
author author author author |
dc.contributor.author.fl_str_mv |
Capela, Ana Maria Tavares-Marcos, Carlota Estima-Arede, Hugo F. Nóbrega-Pereira, Sandrina Jesus, Bruno Bernardes de |
dc.subject.por.fl_str_mv |
LncRNAs NORAD Pumilio Breast cancer Chemotherapy resistance |
topic |
LncRNAs NORAD Pumilio Breast cancer Chemotherapy resistance |
description |
Long non-coding RNA activated by DNA damage (NORAD) has recently been associated with pathologic mechanisms underlying cancer progression. Due to NORAD's extended range of interacting partners, there has been contradictory data on its oncogenic or tumor suppressor roles in BC. This review will summarize the function of NORAD in different BC subtypes and how NORAD impacts crucial signaling pathways in this pathology. Through the preferential binding to pumilio (PUM) proteins PUM1 and PUM2, NORAD has been shown to be involved in the control of cell cycle, angiogenesis, mitosis, DNA replication and transcription and protein translation. More recently, NORAD has been associated with PUM-independent roles, accomplished by interacting with other ncRNAs, mRNAs and proteins. The intricate network of NORAD-mediated signaling pathways may provide insights into the potential design of novel unexplored strategies to overcome chemotherapy resistance in BC treatment. |
publishDate |
2024 |
dc.date.none.fl_str_mv |
2024-02-01T00:00:00Z 2024-02-01 2025-01-16T09:38:17Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://hdl.handle.net/10773/43455 |
url |
http://hdl.handle.net/10773/43455 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
2072-6694 10.3390/cancers16030636 |
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info:eu-repo/semantics/openAccess |
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openAccess |
dc.format.none.fl_str_mv |
application/pdf |
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MDPI |
publisher.none.fl_str_mv |
MDPI |
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