Carbon Nanospheres Mediated Nuclear Delivery of SMAR1 Protein (DNA Binding domain) Controls Breast Tumor in Mice Model

Bhagat, Prasad; Jadhav, Sachin; Chattopadhyay, Samit; Paknikar, Kishore M.

doi:10.2217/nnm-2017-0298

Cited by 6 publications

(5 citation statements)

References 53 publications

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“…In embryonic development, BANP is essential for the DNA damage response and chromosome segregation during mitosis [35]. In oncological diseases, BANP overexpression inhibits tumor progression [36, 37]. In this study, overexpression of BANP in HUVECs resulted in the inhibition of proliferation, a blockage of the G1-S phase transition in the cell cycle, and an increase of SA-β-gal activity.…”

Section: Discussionmentioning

confidence: 68%

BANP Participates in the Chronic Intermittent Hypoxia-Induced Senescence of Vascular Endothelial Cells by Promoting P53 Phosphorylation and Nuclear Retention

Li,

Zhao,

Liu

et al. 2024

Gerontology

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Introduction The objective of this study is to examine the potential induction of senescence in vascular endothelial cells (VECs) by chronic intermittent hypoxia (CIH), a defining characteristic of obstructive sleep apnea (OSA). This investigation seeks to elucidate the underlying mechanisms that contribute to the development of cardiovascular diseases in patients with OSA, with a particular focus on CIH-induced vascular aging. Methods The BioSpherix-OxyCycler system was used to establish models of CIH in both rats and human umbilical vein endothelial cells (HUVECs). To assess VECs senescence, various methods were employed including EdU incorporation assay, cell cycle analysis, senescence-associated β-galactosidase (SA-β-gal) staining, and senescence protein testing. Vascular aging was evaluated through measurements of carotid-femoral pulse wave velocity, intima-media thickness, and Ki67 immunohistochemical staining. In order to identify the molecular mechanisms associated with CIH-induced senescence in VECs, a bioinformatics study was conducted utilizing the Gene Expression Omnibus database. Results Under conditions of CIH, HUVECs exhibited inhibited proliferation, arrested cell cycle, increased activity of SA-β-gal, and elevated expression levels of p53 and p21 compared to HUVECs under normoxic conditions. Similarly, rats exposed to CIH displayed increased carotid-femoral pulse wave velocity, intima-media thickness, vascular permeability, and SA-β-gal activity in VECs, along with decreased expression of arterial Ki67. BTG3-associated protein (BANP) was found to be highly expressed in CIH-induced VECs. Furthermore, the overexpression of BANP resulted in the senescence of VECs, along with elevated levels of p53 phosphorylation and nuclear localization. Conclusions These findings demonstrate that CIH can induce VECs senescence and contribute to vascular aging. Additionally, BANP can induce VECs senescence by promoting p53 phosphorylation and nuclear retention. These discoveries offer novel insights into the increased cardiovascular risk associated with OSA, thereby presenting new possibilities for therapeutic intervention.

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Section: Discussionmentioning

confidence: 68%

BANP Participates in the Chronic Intermittent Hypoxia-Induced Senescence of Vascular Endothelial Cells by Promoting P53 Phosphorylation and Nuclear Retention

Li,

Zhao,

Liu

et al. 2024

Gerontology

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“…Their properties are similar as that of graphene and have been designed for protein delivery. [219] Interestingly, this nanocomplex could internalize and localize in the nucleus of MCF-7 cells. [217] Furthermore, Zhang et al mixed C-dots with EGFP to prepare C-dots/EGFP nanocomplex with a size of around 200 nm.…”

Section: Wwwadvmatde Wwwadvancedsciencenewscommentioning

confidence: 99%

Rational Design of Nanocarriers for Intracellular Protein Delivery

et al. 2019

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Protein/antibody therapeutics have exhibited the advantages of high specificity and activity even at an extremely low concentration compared to small molecule drugs. However, they are accompanied by unfavorable physicochemical properties such as fragile tertiary structure, large molecular size, and poor penetration of the membrane, and thus the clinical use of protein drugs is hindered by inefficient delivery of proteins into the host cells. To overcome the challenges associated with protein therapeutics and enhance their biopharmaceutical applications, various protein‐loaded nanocarriers with desired functions, such as lipid nanocapsules, polymeric nanoparticles, inorganic nanoparticles, and peptides, are developed. In this review, the different strategies for intracellular delivery of proteins are comprehensively summarized. Their designed routes, mechanisms of action, and potential therapeutics in live cells or in vivo are discussed in detail. Furthermore, the perspective on the new generation of delivery systems toward the emerging area of protein‐based therapeutics is presented as well.

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“…BANP interacts with tumor suppressor tp53 to modulate its functions ( Kaul Ghanekar et al, 2003 ; Pavithra et al, 2009 ; Sinha et al, 2012 ; Sinha et al, 2010 ). Overexpression of BANP suppresses cancer growth ( Bhagat et al, 2018 ; Liu et al, 2014 ; Taye et al, 2018 ). However, these proposed cellular functions of BANP were based mostly on in vitro studies, and genetic deletion of Banp was reportedly unsuccessful ( Grand et al, 2021 ), whereas Banp knockout mice show embryonic lethality ( Chemmannur et al, 2015 ), which makes in vivo analysis difficult.…”

Section: Introductionmentioning

confidence: 99%

Banp regulates DNA damage response and chromosome segregation during the cell cycle in zebrafish retina

Babu

Takeuchi

Masai

2022

eLife

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Btg3-associated nuclear protein (Banp) was originally identified as a nuclear matrix-associated region (MAR)-binding protein and it functions as a tumor suppressor. At the molecular level, Banp regulates transcription of metabolic genes via a CGCG-containing motif called the Banp motif. However, its physiological roles in embryonic development are unknown. Here, we report that Banp is indispensable for the DNA damage response and chromosome segregation during mitosis. Zebrafish banp mutants show mitotic cell accumulation and apoptosis in developing retina. We found that DNA replication stress and tp53-dependent DNA damage responses were activated to induce apoptosis in banp mutants, suggesting that Banp is required for regulation of DNA replication and DNA damage repair. Furthermore, consistent with mitotic cell accumulation, chromosome segregation was not smoothly processed from prometaphase to anaphase in banp morphants, leading to a prolonged M-phase. Our RNA- and ATAC-sequencing identified 31 candidates for direct Banp target genes that carry the Banp motif. Interestingly, a DNA replication fork regulator, wrnip1, and two chromosome segregation regulators, cenpt and ncapg, are included in this list. Thus, Banp directly regulates transcription of wrnip1 for recovery from DNA replication stress, and cenpt and ncapg for chromosome segregation during mitosis. Our findings provide the first in vivo evidence that Banp is required for cell-cycle progression and cell survival by regulating DNA damage responses and chromosome segregation during mitosis.

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Carbon Nanospheres Mediated Nuclear Delivery of SMAR1 Protein (DNA Binding domain) Controls Breast Tumor in Mice Model

Abstract: DNA binding domain of the SMAR1 protein (His 5) has potent anticancer activity and its CNs mediated delivery could control breast tumor in mice model.

Cited by 6 publications

References 53 publications

BANP Participates in the Chronic Intermittent Hypoxia-Induced Senescence of Vascular Endothelial Cells by Promoting P53 Phosphorylation and Nuclear Retention

BANP Participates in the Chronic Intermittent Hypoxia-Induced Senescence of Vascular Endothelial Cells by Promoting P53 Phosphorylation and Nuclear Retention

Rational Design of Nanocarriers for Intracellular Protein Delivery

Banp regulates DNA damage response and chromosome segregation during the cell cycle in zebrafish retina

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