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المؤلفHamwi, Mahmoud N.
المؤلفElsayed, Engy
المؤلفDabash, Hanan
المؤلفAbuawad, Amani
المؤلفAweer, Noor A.
المؤلفAl Zeir, Faissal
المؤلفPedersen, Shona
المؤلفAl-Mansoori, Layla
المؤلفBurgon, Patrick G.
تاريخ الإتاحة2024-07-30T06:46:06Z
تاريخ النشر2024-07-01
اسم المنشورCells
المعرّفhttp://dx.doi.org/10.3390/cells13131109
الاقتباسHamwi, 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.‏
معرّف المصادر الموحدhttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85198383709&origin=inward
معرّف المصادر الموحدhttp://hdl.handle.net/10576/57187
الملخصMuscle-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.
اللغةen
الناشرMultidisciplinary Digital Publishing Institute (MDPI)
الموضوعAkt
cancer
MLIP
mTOR
PI3 kinase
tumorigenesis
العنوانMLIP and Its Potential Influence on Key Oncogenic Pathways
النوعOther
رقم العدد13
رقم المجلد13
dc.accessType Open Access


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