LMNB2 (Lamin B2)

In conclusion, in the WHO/ISUP grading system, G1, G2 and G3 rely solely on nucleolar size as an indicator. However, in G4, both nuclear and cell morphology may be considered as indicators, since changes in nuclear envelope-associated proteins were only detected in this grade.

By analyzing global scientific research papers, we find that China leads in the "quantity" of research in this field, while the United States excels in "quality" and "impact" To foster better future development, scientists need to target emerging hotspots (such as "therapeutic targets") and collaborate with more outstanding teams. Administrators should not merely count the number of papers but focus on the quality of research outcomes and the depth of international collaboration.

LMNB2 also exhibited a regulatory role in tumor growth within the mouse xenograft model. This study proposed that LMNB2 could emerge as a novel therapeutic strategy for treating ESCA.

Lamins have also been shown to be dysregulated in a multitude of cancers, and research has uncovered a diabolical role of lamins in oncogenesis. The understanding of laminopathies and dysregulation of lamins resulting in disorders is critical in developing novel therapeutic strategies through drug repurposing and epigenetic modulation to curb the burden of the diseases.

LMNB1 and LMNB2 are prognostic factors for HCC. GSK461364 is a novel therapeutic candidate for HCC, with anti-HCC effects associated with LMNB1/2 suppression.

This compromised NE was more vulnerable to damage from farnesyltransferase inhibitors (FTIs), causing nuclear rupture in SPOP-mutant tumor cells. This study identified SPOP as a positive regulator of nuclear size; the findings suggest tumors with SPOP mutations may be vulnerable to FTI-based therapies.

Importantly, combinatorial targeting of LMNB2 with Atezolizumab (PD-L1 inhibitor) displayed a synergistic effect on suppressing tumor progression both in vitro and in vivo, particularly in HCC models with SPOP mutations or LMNB2 overexpression. These findings unveil a novel ubiquitination-dependent regulatory axis in HCC immune evasion and propose targeted co-inhibition strategies to overcome HCC immunotherapy resistance.

NOP2 catalyzes the m5C modification of LMNB2 mRNA to facilitate its stability, which contributes to the elevated LMNB2 protein level and CRC progression, suggesting the potential of NOP2 as a therapeutic target in the development of novel CRC treatment.

Collectively, our results revealed that exosomes exposed to ESCA cells induced greater drug resistance in DDP-resistant ESCA cells via HuR delivery. Targeting HuR or its positively related target LMNB2 may present new therapeutic opportunities for treating patients with DDP-resistant ESCA.

Further validation using RT-qPCR confirmed that the expression of all prognostic genes was significantly higher in HCC group compared to the control group. This study explored six prognostic genes (LMNB2, LMNB1, BAK1, CASP7, LMNA and AKT1) associated with MPT-DNRGs in HCC, which provides a reference for further research on HCC.

This chapter underscores the pivotal roles of lamins in nuclear architecture and cancer biology, emphasizing their impact on cellular functions and disease pathology. Understanding lamin behavior and regulation mechanisms holds promise for developing novel diagnostic tools and targeted therapies in cancer treatment.

Altogether, these data suggest that LMNB2 may serve as a tumor promoter and could be a possible target for cancer therapy.