NUAK2

Last update 08 May 2025

Basic Info

Synonyms

FLJ90349, NUAK family kinase 2, NUAK family SNF1-like kinase 2

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Introduction

Stress-activated kinase involved in tolerance to glucose starvation. Induces cell-cell detachment by increasing F-actin conversion to G-actin. Expression is induced by CD95 or TNF-alpha, via NF-kappa-B. Protects cells from CD95-mediated apoptosis and is required for the increased motility and invasiveness of CD95-activated tumor cells. Phosphorylates LATS1 and LATS2. Plays a key role in neural tube closure during embryonic development through LATS2 phosphorylation and regulation of the nuclear localization of YAP1 a critical downstream regulatory target in the Hippo signaling pathway (PubMed:32845958).

100 Clinical Results associated with NUAK2

100 Translational Medicine associated with NUAK2

0 Patents (Medical) associated with NUAK2

103

Literatures (Medical) associated with NUAK2

01 Mar 2025·Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

NUAKs facilitate mTOR-mediated NSCLC proliferation and metastasis by modulating glucose metabolism and inhibiting p53 activity

Article

Author: Yesupogu Moorthy Babu, Jaithanya ; Manoharan, Ravi

Non-small cell lung cancer (NSCLC) cells frequently exhibit aberrant glucose metabolism, characterized by elevated aerobic glycolysis, pentose phosphate pathway (PPP), and reduced oxidative phosphorylation. However, the specific mechanisms underlying the abnormal activation of glucose metabolism and its contribution to NSCLC tumorigenesis remain incompletely elucidated. In this study, we observed that both NUAK1 and NUAK2 mRNA expression levels were significantly elevated in NSCLC tissues compared to non-tumor tissues, and that high NUAK1/2 expression correlated with poor prognosis in NSCLC patients. Furthermore, NUAK1/2 promotes aerobic glycolysis and PPP in NSCLC cells and stimulates cellular proliferation and migration. Depletion or inhibition of NUAK1/2 results in decreased aerobic glycolysis, PPP activity, cell proliferation, and migration, leading to increased apoptosis of NSCLC cells. Mechanistically, NUAK1/2 enhances mTOR activity by suppressing the activity of p53, thereby promoting NSCLC cell growth and metastasis through the promotion of aerobic glycolysis and PPP. Our findings suggest that NUAK1/2 plays a crucial role in glucose reprogramming and tumorigenesis in NSCLC cells, indicating that targeting NUAK1/2 may represent a potential therapeutic strategy for NSCLC metabolism.

01 Jan 2025·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

NUAKs promote mTOR/c-Myc-induced glucose and glutamine reprogramming for cell growth and metastasis in breast cancer cells

Article

Author: Worral Wilfred Raj, Acily Skadon ; Raj, Acily Skadon Worral Wilfred ; Manoharan, Ravi

Breast cancer progression and metastasis are closely connected to changes in glucose and glutamine metabolism. While Novel (nua) kinase family 1 (NUAK1) and Novel (nua) kinase family 2 (NUAK2), which are two members of the AMPK-related kinases, have been associated with breast tumorigenesis, their role in the metabolic reprogramming that occurs during breast cancer progression remains unclear. Our research uncovers that NUAKs expression is significantly higher in breast cancer tissues and cell lines, and it is positively related to glycolysis, the pentose phosphate pathway (PPP), glutamine metabolism, and a poor prognosis for breast cancer patients. We show that NUAKs significantly increase metabolic reprogramming, including aerobic glycolysis, PPP, and glutamine metabolism in triple negative breast cancer subtypes but only induce aerobic glycolysis and PPP in luminal breast cancer subtypes to meet the anabolic demands of rapidly dividing breast cancer cells. In contrast, the depletion of NUAKs has the opposite effect. Mechanistic insights reveal that NUAKs activate mammalian target of rapamycin (mTOR) signaling, which in turn upregulates the c-Myc transcription factor, a crucial regulator of glucose and glutamine metabolic gene expression. Moreover, we demonstrate that NUAKs enhance mTOR/c-Myc signaling pathways, leading to increased glucose and glutamine reprogramming, which supports rapid cell proliferation and metastatic potential in breast cancer cells. Importantly, pretreating breast cancer cells with mTOR inhibitors blocked the metabolic reprogramming and tumor-promoting effect of NUAK1/2. Therefore, targeting NUAKs may represent a novel therapeutic strategy for the treatment of breast cancer.

18 Nov 2024·Essays in Biochemistry

NUAK: never underestimate a kinase

Review

Author: Lubawska, Dominika ; Murphy, Daniel J. ; Skalka, George L. ; Whyte, Declan

AbstractNUAK1 and NUAK2 belong to a family of kinases related to the catalytic α-subunits of the AMP-activated protein kinase (AMPK) complexes. Despite canonical activation by the tumour suppressor kinase LKB1, both NUAKs exhibit a spectrum of activities that favour tumour development and progression. Here, we review similarities in structure and function of the NUAKs, their regulation at gene, transcript and protein level, and discuss their phosphorylation of specific downstream targets in the context of the signal transduction pathways and biological activities regulated by each or both NUAKs.

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NUAK2

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