CNOT2, a central component of the CCR4-NOT transcription complex subunit 2, plays a pivotal role in the regulation of gene expression and metabolism. CNOT2 is involved in various cellular processes, including transcriptional regulation, mRNA deadenylation, and the modulation of mRNA stability. CNOT2 specifically contributes to the structural integrity and enzymatic activity of the CCR4-NOT complex with transcription factors and RNA-binding proteins. Recent studies have elucidated its involvement in cellular differentiation, immune response modulation, and the maintenance of genomic stability. Abnormal regulation of CNOT2 has been implicated in a spectrum of pathological conditions, including oncogenesis, neurodegenerative disorders, and metabolic dysfunctions. This review comprehensively examines the interplay between CNOT2 and p53, elucidating their collaborative and antagonistic interactions in various cellular contexts. CNOT2 is primarily involved in transcriptional regulation, mRNA deadenylation, and the modulation of mRNA stability, thereby influencing diverse biological processes such as cell proliferation, apoptosis, and differentiation. Conversely, p53 is renowned for its role in maintaining genomic integrity, inducing cell cycle arrest, apoptosis, and senescence in response to cellular stress and DNA damage. Emerging evidence suggests that CNOT2 can modulate p53 activity through multiple mechanisms, including the regulation of p53 mRNA stability and the modulation of p53 target gene expression. The dysregulation of CNOT2 and p53 interactions has been implicated in the pathogenesis and progression of various cancers, highlighting their potential as therapeutic targets. Additionally, CNOT2 regulates c-Myc, a well-known oncogene, in cancer cells. This review shows the essential roles of CNOT2 in maintaining cancer cellular homeostasis and explores its interactions within the CCR4-NOT complex that influence transcriptional and post-transcriptional regulation. Furthermore, we investigate the potential of CNOT2 as a biomarker and therapeutic target across various disease states, highlighting its significance in disease progression and treatment responsiveness.

Objectives: Hair loss is a prevalent condition influenced by genetic, hormonal, and environmental factors, and effective therapies with minimal side effects are highly desired. In this study, the hair growth-promoting potential of a biorenovated esculetin complex (BEC) was evaluated in a C57BL/6N mouse model. Methods: BEC was topically applied to the depilated dorsal skin of mice once daily for 24 days. Hair growth was evaluated by measuring hair length, thickness, and weight, together with histological assessment of hair follicle number, follicle depth, and dermal thickness. Protein expression associated with Wnt/β-catenin and AKT signaling was evaluated by Western blot analysis. Results: BEC treatment accelerated hair regrowth and increased hair length, thickness, and weight compared with the vehicle control under the present experimental conditions. Histological analysis of hematoxylin-and-eosin-stained skin sections showed increased hair follicle number and greater follicle depth in the BEC-treated group, whereas dermal thickness was not significantly altered. Western blot analysis showed changes in β-catenin, phospho-GSK-3β (Ser9), and PCNA levels following BEC treatment. The p-AKT/AKT ratio also showed an increasing trend, although the difference was not statistically significant. Conclusions: These findings demonstrate the hair growth-promoting activity of the BEC preparation in this short-term murine model and suggest that these effects are associated with changes in Wnt/β-catenin- and AKT-related signaling. Further studies are warranted to characterize the active components, dose dependence, mechanism of action, and safety profile of BEC.

RNA binding motif protein 23 (RBM23) is a member of the RNA binding motif gene family, functioning as a transcriptional cofactor and pre-mRNA splicing fact