LMNB1

Last update 23 Jan 2025

Basic Info

Synonyms

lamin B1, Lamin-B1, LMN2

+ [2]

Introduction

Lamins are components of the nuclear lamina, a fibrous layer on the nucleoplasmic side of the inner nuclear membrane, which is thought to provide a framework for the nuclear envelope and may also interact with chromatin.

100 Clinical Results associated with LMNB1

100 Translational Medicine associated with LMNB1

0 Patents (Medical) associated with LMNB1

804

Literatures (Medical) associated with LMNB1

01 Feb 2025·Neurochemical Research

Impact of Nuclear Peripheral Chromatin Lamin LMNB1 Gene in the Proliferation and Migration of Glioma Cells

Article

Author: Li, Cheng ; Feng, Yao ; Zhang, Ting ; Guo, Chen-Jia ; Yang, Qin ; Wang, Jie ; Shi, Xiang-Cheng ; Qu, Chong-Xiao

The goal of this study is to explore the role of the LMNB1 gene in glioma. A cohort of 160 patients who underwent glioma surgery were randomly selected of this study. The LMNB1 expression was assessed employing immunohistochemical and real-time quantitative polymerase chain reaction methods. Initially, RNA interference technology was applied to suppress gene expression, followed by the evaluation of tumor cell proliferation, apoptosis, cell cycle dynamics, and migration. The underlying molecular mechanisms of LMNB1 function were examined by a human phospho-kinase array and immunoblotting. And we established the xenograft models to determine the effect of tumor growth as well as the degree of invasion in shLMNB1 mice. Elevated LMNB1 expression correlated with unfavorable overall survival and disease-free survival. A substantial inhibition in cell growth was observed subsequent to LMNB1 knockdown in SHG-44 and U251 glioma cells. SHG-44-shLMNB1 cells exhibited a reduction in the S phase population, along with an increase in cells in G1 and G2 phases. Similarly, shLMNB1 U251 cells showed fewer cells in the S phase and an elevation in cells in G1 phase. Notably, increased apoptosis was observed in U251-shLMNB1 cells and SHG-44-shLMNB1 cells. Wound healing and Transwell migration assays demonstrated a significant decrease in the migration rate of both SHG-44-shLMNB1 and U251-shLMNB1 cells. The phosphorylation levels of Akt1/2/3, as well as the expressions of PI3K, AKT, and p-AKT proteins, were reduced in the shLMNB1 group. Downregulation of LMNB1 repressed tumor progress in vivo. The silencing of LMNB1 was found to significantly reduce the proliferation of human glioma cells, induce apoptosis in tumor cells, impede the progression of the cell cycle, and inhibit the migration of tumor cells. Consequently, we hypothesize that LMNB1 promotes glioma cell proliferation through mechanisms involving the inhibition of tumor cell apoptosis, acceleration of the cell cycle, and enhancement of tumor cell migration. We found that LMNB1 exert critical roles in glioma progression may via regulation of PI3K/Akt signaling pathway. These observations suggest that LMNB1 holds clinical potential for diagnostic and prognostic applications in glioma, presenting novel targets for drug development.

02 Jan 2025·Cancer Research

H4K20me3-Mediated Repression of Inflammatory Genes Is a Characteristic and Targetable Vulnerability of Persister Cancer Cells

Article

Author: Capellades, Jordi ; Serrano, Manuel ; Kovatcheva, Marta ; Yanes, Oscar ; Stephan-Otto Attolini, Camille ; Ramponi, Valentina ; Ficz, Gabriella ; Richart, Laia ; Lord, Alice E.

AbstractAnticancer therapies can induce cellular senescence or drug-tolerant persistence, two types of proliferative arrest that differ in their stability. While senescence is highly stable, persister cells efficiently resume proliferation upon therapy termination, resulting in tumor relapse. Here, we used an ATP-competitive mTOR inhibitor to induce and characterize persistence in human cancer cells of various origins. Using this model and previously described models of senescence, we compared the same cancer cell lines under the two types of proliferative arrest. Persister and senescent cancer cells shared an expanded lysosomal compartment and hypersensitivity to BCL-XL inhibition. However, persister cells lacked other features of senescence, such as loss of lamin B1, senescence-associated β-galactosidase activity, upregulation of MHC-I, and an inflammatory and secretory phenotype (senescence-associated secretory phenotype or SASP). A genome-wide CRISPR/Cas9 screening for genes required for the survival of persister cells revealed that they are hypersensitive to the inhibition of one-carbon (1C) metabolism, which was validated by the pharmacologic inhibition of serine hydroxymethyltransferase, a key enzyme that feeds methyl groups from serine into 1C metabolism. Investigation into the relationship between 1C metabolism and the epigenetic regulation of transcription uncovered the presence of the repressive heterochromatic mark H4K20me3 at the promoters of SASP and IFN response genes in persister cells, whereas it was absent in senescent cells. Moreover, persister cells overexpressed the H4K20 methyltransferases KMT5B/C, and their downregulation unleashed inflammatory programs and compromised the survival of persister cells. In summary, this study identifies distinctive features and actionable vulnerabilities of persister cancer cells and provides mechanistic insight into their low inflammatory activity.Significance: Cell persistence and senescence are distinct states of proliferative arrest induced by cancer therapy, with persister cells being characterized by the silencing of inflammatory genes through the heterochromatic mark H4K20me3.See related commentary by Schmitt, p. 7

01 Jan 2025·Applied Biochemistry and Biotechnology

Integrative Proteomics-Metabolomics of In Vitro Degeneration of Cardiovascular Cell Lines

Article

Author: Nan, Bingru ; Shen, Heqing ; Yang, Shijing

Long-term cell culture is an important biological approach but is also characterized by degeneration in cellular morphology, proliferation rate, and function. To explore this phenomenon in a systematic way, we conducted an integrative proteomics-metabolomics measurement of two cardiovascular cell lines of AC16 and HUVECs. The 18th culturing passages, i.e., G18, showed as the turning points by cell metabolism profiles, in which the metabolomic changes demonstrated the dysfunction of energy, amino acid, and ribonucleotide metabolism metabolic pathways. Although active protein networks showed mitochondria abundance AC16 and oxidative/nitrative sensitive HUVECs indicated the different degeneration patterns, the G18 and G30 proteomics evidenced the senescence by processes of signal transduction, signaling by interleukins, programmed cell death, cellular responses to stimuli, cell cycle, mRNA splicing, and translation. Some crucial proteins (RPS8, HNRNPR, SOD2, LMNB1, PSMA1, DECR1, GOT2, OGDH, PNP, CBS, ATIC, and IMPDH2) and metabolites (L-glutamic acid, guanine, citric acid, guanosine, guanosine diphosphate, glucose 6-phosphate, and adenosine) that contributed to the dysregulation of cellular homeostasis are identified by using the integrative proteomic-metabolomic analysis, which highlighted the increased cellular instability. These findings illuminate some vital molecular processes when culturing serial passages, which contribute holistic viewpoints of in vitro biology with emphasis on the replicative senescence of cardiovascular cells.

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LMNB1

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