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

Autor: Shi XC; The Pathology Department of Shanxi Provincial People's Hospital, Taiyuan, 030012, China., Zhang T; The Pathology Department of Shanxi Provincial People's Hospital, Taiyuan, 030012, China., Li C; The Pathology Department of Shanxi Provincial People's Hospital, Shanxi Medical University, Taiyuan, 030012, China., Guo CJ; The Pathology Department of Shanxi Provincial People's Hospital, Taiyuan, 030012, China., Yang Q; The Pathology Department of Shanxi Provincial People's Hospital, Taiyuan, 030012, China., Feng Y; The Pathology Department of Shanxi Provincial People's Hospital, Taiyuan, 030012, China., Wang J; The Pathology Department of Shanxi Provincial People's Hospital, Taiyuan, 030012, China., Qu CX; The Pathology Department of Shanxi Provincial People's Hospital, Taiyuan, 030012, China. quchongxiao_qcx@126.com.; Department of Pathology, Shanxi Provincial People's Hospital, No. 29 of Shuangtasi Road, Yingze District, Taiyuan, 030012, China. quchongxiao_qcx@126.com.
Jazyk: angličtina
Zdroj: Neurochemical research [Neurochem Res] 2024 Dec 05; Vol. 50 (1), pp. 46. Date of Electronic Publication: 2024 Dec 05.
DOI: 10.1007/s11064-024-04298-3
Abstrakt: 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.
Competing Interests: Declarations. Ethics Approval and Consent to Participate: Approval for this study was given by the medical ethics committee of Shanxi Provincial People’s Hospital (approval number 2022–163). This study was conducted in accordance with the declaration of Helsinki. Written informed consent was obtained from all participants. All applicable international, national, and/or institutional guidelines for the care and use of animals were followed. Consent for Publication: Not applicable. Competing Interests: The authors declare no competing interests.
(© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)
Databáze: MEDLINE
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