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AuthorHamwi, Mahmoud N.
AuthorElsayed, Engy
AuthorDabash, Hanan
AuthorAbuawad, Amani
AuthorAweer, Noor A.
AuthorAl Zeir, Faissal
AuthorPedersen, Shona
AuthorAl-Mansoori, Layla
AuthorBurgon, Patrick G.
Available date2024-07-30T06:46:06Z
Publication Date2024-07-01
Publication NameCells
Identifierhttp://dx.doi.org/10.3390/cells13131109
CitationHamwi, M. N., Elsayed, E., Dabash, H., Abuawad, A., Aweer, N. A., Al Zeir, F., ... & Burgon, P. G. (2024). MLIP and Its Potential Influence on Key Oncogenic Pathways. Cells, 13(13), 1109.‏
URIhttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85198383709&origin=inward
URIhttp://hdl.handle.net/10576/57187
AbstractMuscle-enriched A-type lamin-interacting protein (MLIP) is an emerging protein involved in cellular homeostasis and stress adaptation. Eukaryotic cells regulate various cellular processes, including metabolism, DNA repair, and cell cycle progression, to maintain cellular homeostasis. Disruptions in this homeostasis can lead to diseases such as cancer, characterized by uncontrolled cell growth and division. This review aims to explore for the first time the unique role MLIP may play in cancer development and progression, given its interactions with the PI3K/Akt/mTOR pathway, p53, MAPK9, and FOXO transcription factors, all critical regulators of cellular homeostasis and tumor suppression. We discuss the current understanding of MLIP’s involvement in pro-survival pathways and its potential implications in cancer cells’ metabolic remodeling and dysregulated homeostasis. Additionally, we examine the potential of MLIP as a novel therapeutic target for cancer treatment. This review aims to shed light on MLIP’s potential impact on cancer biology and contribute to developing innovative therapeutic strategies.
Languageen
PublisherMultidisciplinary Digital Publishing Institute (MDPI)
SubjectAkt
cancer
MLIP
mTOR
PI3 kinase
tumorigenesis
TitleMLIP and Its Potential Influence on Key Oncogenic Pathways
TypeArticle Review
Issue Number13
Volume Number13
dc.accessType Open Access


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