Lamin B2 promotes the progression of triple negative breast cancer via mediating cell proliferation and apoptosis

Zhao, Cuicui; Chen, Jing; Zhang, Liying; Liu, Hong; Zhang, Chuan-Gui; Liu, Yan

doi:10.1042/bsr20203874

Cited by 12 publications

(14 citation statements)

References 30 publications

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“…Furthermore, our study is the first to find significant upregulation of LMNB2 in EC. LMNB2 is a lamin protein known to regulate nuclear stability and gene expression [ 39 ], with noted upregulation in breast, colorectal and oesophageal cancers [ 40 , 41 , 42 ]. Our in silico study notes LMNB2 to be highly expressed in all EC subtypes, with unique upregulation in HGEC and G3 endometrioid cancer.…”

Section: Discussionmentioning

confidence: 99%

Role of Nucleolin in Endometrial Precancerous Hyperplasia and Carcinogenesis: Ex Vivo and In Silico Study

Barzilova

Drury

Rogers

et al. 2022

IJMS

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Endometrial cancer (EC) is the most common gynaecological malignancy. Nucleolin (NCL) is involved in rDNA transcription, cell proliferation, and apoptosis, with high expression associated with worse overall survival (OS) in other adenocarcinomas. Our aims were to assess NCL gene and protein expression and explore the differential expression of NCL-associated genes (NAGs) in endometrial carcinogenesis. Endometrial samples were obtained from 157 women to include healthy, hyperplastic (EH), EC, and metastatic groups. RT-qPCR and immunohistochemistry were employed to assess NCL gene and protein levels. In silico analysis of NAGs in TCGA and GEO datasets was performed, with the prognostic value determined via Human Protein Atlas. NCL mRNA level of EC was lower than in healthy post-menopausal endometrium (p < 0.01). EH samples had lower NCL immuno-expression scores than healthy pre-menopausal (p < 0.001), benign post-menopausal (p < 0.01), and EC (p < 0.0001) samples. Metastatic lesions demonstrated higher NCL quick scores than primary tissue (p = 0.04). Higher NCL Immuno quick scores carried a worse OS in high-grade EC (p = 0.01). Interrogating Uterine Corpus Endometrial Carcinoma (TCGA-UCEC) and Uterine Carcinosarcoma (TCGA-UCS) cohorts revealed NCL to be the most highly upregulated gene in carcinosarcoma, with S100A11, LMNB2, RERG, E2F1 and CCNA2 representing key dysregulated NAGs in EC. Since NCL is implicated in transforming hyperplastic glands into cancer, with further involvement in metastasis, it is suggested to be a promising target for better-informed diagnosis, risk stratification, and management of EC.

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Section: Discussionmentioning

confidence: 99%

Role of Nucleolin in Endometrial Precancerous Hyperplasia and Carcinogenesis: Ex Vivo and In Silico Study

Barzilova

Drury

Rogers

et al. 2022

IJMS

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“…In breast cancer, different studies have reported that both a decreased expression of lamin B1 [71] and an increase of lamin B2 [77] are related to bad outcome, confirming the importance to strictly maintain proper B-type lamin levels. (e) Neoplasms of the gastrointestinal tract Decrease of lamin B1 expression is linked to different type of gastrointestinal tumours, including colon carcinomas, adenomas and gastric cancers [70,78].…”

Section: (D) Breast Cancermentioning

confidence: 92%

Section: Cancermentioning

confidence: 99%

“…Furthermore, Zhang et al reported that the overexpression of lamin B2 promotes migration of non-small cell lung cancer by increasing H3K9me2 level, thus eliciting E-cadherin gene silencing [ 76 ]. Breast cancer In breast cancer, different studies have reported that both a decreased expression of lamin B1 [ 71 ] and an increase of lamin B2 [ 77 ] are related to bad outcome, confirming the importance to strictly maintain proper B-type lamin levels. Neoplasms of the gastrointestinal tract Decrease of lamin B1 expression is linked to different type of gastrointestinal tumours, including colon carcinomas, adenomas and gastric cancers [ 70 , 78 ].…”

Section: Cancermentioning

confidence: 99%

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The wide and growing range of lamin B-related diseases: from laminopathies to cancer

Evangelisti

Rusciano

Mongiorgi

et al. 2022

Cell. Mol. Life Sci.

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B-type lamins are fundamental components of the nuclear lamina, a complex structure that acts as a scaffold for organization and function of the nucleus. Lamin B1 and B2, the most represented isoforms, are encoded by LMNB1 and LMNB2 gene, respectively. All B-type lamins are synthesized as precursors and undergo sequential post-translational modifications to generate the mature protein. B-type lamins are involved in a wide range of nuclear functions, including DNA replication and repair, regulation of chromatin and nuclear stiffness. Moreover, lamins B1 and B2 regulate several cellular processes, such as tissue development, cell cycle, cellular proliferation, senescence, and DNA damage response. During embryogenesis, B-type lamins are essential for organogenesis, in particular for brain development. As expected from the numerous and pivotal functions of B-type lamins, mutations in their genes or fluctuations in their expression levels are critical for the onset of several diseases. Indeed, a growing range of human disorders have been linked to lamin B1 or B2, increasing the complexity of the group of diseases collectively known as laminopathies. This review highlights the recent findings on the biological role of B-type lamins under physiological or pathological conditions, with a particular emphasis on brain disorders and cancer. Graphical abstract

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“…The depletion of LMNB2 suppressed proliferation and induced apoptosis and inhibited tumor growth of TNBC cells in mice. The authors suggest that Lamin B2 may promote TNBC progression and could serve as a potential therapeutical target [276].…”

Section: Lamins and Cancermentioning

confidence: 99%

A Link between Replicative Stress, Lamin Proteins, and Inflammation

Willaume

Rass

Fontanilla-Ramirez

et al. 2021

Genes

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Double-stranded breaks (DSB), the most toxic DNA lesions, are either a consequence of cellular metabolism, programmed as in during V(D)J recombination, or induced by anti-tumoral therapies or accidental genotoxic exposure. One origin of DSB sources is replicative stress, a major source of genome instability, especially when the integrity of the replication forks is not properly guaranteed. To complete stalled replication, restarting the fork requires complex molecular mechanisms, such as protection, remodeling, and processing. Recently, a link has been made between DNA damage accumulation and inflammation. Indeed, defects in DNA repair or in replication can lead to the release of DNA fragments in the cytosol. The recognition of this self-DNA by DNA sensors leads to the production of inflammatory factors. This beneficial response activating an innate immune response and destruction of cells bearing DNA damage may be considered as a novel part of DNA damage response. However, upon accumulation of DNA damage, a chronic inflammatory cellular microenvironment may lead to inflammatory pathologies, aging, and progression of tumor cells. Progress in understanding the molecular mechanisms of DNA damage repair, replication stress, and cytosolic DNA production would allow to propose new therapeutical strategies against cancer or inflammatory diseases associated with aging. In this review, we describe the mechanisms involved in DSB repair, the replicative stress management, and its consequences. We also focus on new emerging links between key components of the nuclear envelope, the lamins, and DNA repair, management of replicative stress, and inflammation.

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Lamin B2 promotes the progression of triple negative breast cancer via mediating cell proliferation and apoptosis

Cited by 12 publications

References 30 publications

Role of Nucleolin in Endometrial Precancerous Hyperplasia and Carcinogenesis: Ex Vivo and In Silico Study

Role of Nucleolin in Endometrial Precancerous Hyperplasia and Carcinogenesis: Ex Vivo and In Silico Study

The wide and growing range of lamin B-related diseases: from laminopathies to cancer

A Link between Replicative Stress, Lamin Proteins, and Inflammation

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