Nuclear Actin Dynamics in Gene Expression, DNA Repair, and Cancer

Huang, Yuesheng; Zhang, Shengzhe; Park, Jae-Il

doi:10.1007/978-3-031-06573-6_23

Cited by 8 publications

(3 citation statements)

References 271 publications

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“…Meanwhile, they participate in signal transduction events, influencing cellular processes such as proliferation, differentiation, and survival. Together, they control the development of lamellipodia, cytoskeletal remodelling, and cellular protrusion, all of which are necessary for cell mobility [83]. In addition, they are involved in the force for cell motility and the stimulation of DNA repair by promoting nuclear actin polymerization.…”

Section: Resultsmentioning

confidence: 99%

Analysis and Review of Downregulated Actin Cytoskeletal Proteins in Non-Small Cell Lung Cancer

Mageed,

Sahu,

Sundararajan

2024

JBM

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Actin, a highly conserved protein, plays a dominant role in Non-small cell lung cancer (NSCLC). Late diagnosis and the aggressive nature of NSCLC pose a significant threat. Studying the clinic pathological properties of NSCLC proteins is a potential alternative for developing treatment strategies. Towards this, 35 downregulated actin cytoskeletal proteins on NSCLC prognosis and treatment were studied by examining their protein-protein interactions, gene ontology enrichment terms, and signaling pathways. Using PubMed, various proteins in NSCLC were identified. The protein-protein interactions and functional associations of these proteins were examined using the STRING database. The focal adhesion signaling pathway was selected from all available KEGG and Wiki pathways because of its role in regulating gene expression, facilitating cell movement and reproduction, and significantly impacting NSCLC. The protein-protein interaction network of the 35 downregulated actin cytoskeleton proteins revealed that ACTG1, ACTR2,

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Section: Resultsmentioning

confidence: 99%

Analysis and Review of Downregulated Actin Cytoskeletal Proteins in Non-Small Cell Lung Cancer

Mageed,

Sahu,

Sundararajan

2024

JBM

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“…Additionally, nuclear actin is engaged in transcriptional regulation 42,43 . Thus, it is possible that upon CRACD inactivation, NOTCH signaling dysregulation or epigenetic reprogramming might trigger NE cell plasticity, which needs to be addressed in future studies.…”

Section: Discussionmentioning

confidence: 99%

CRACD suppresses neuroendocrinal plasticity of lung adenocarcinoma

Kim

Zhang

Huang

et al. 2023

Preprint

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Tumor cell plasticity contributes to intratumoral heterogeneity and therapy resistance. Through cell plasticity, lung adenocarcinoma (LUAD) cells transform into neuroendocrinal (NE) tumor cells. However, the mechanisms of NE cell plasticity remain unclear. CRACD, a capping protein inhibitor, is frequently inactivated in cancers. CRACD knock-out (KO) de-represses NE-related gene expression in the pulmonary epithelium and LUAD cells. In LUAD mouse models, Cracd KO increases intratumoral heterogeneity with NE gene expression. Single-cell transcriptomic analysis showed that Cracd KO-induced NE plasticity is associated with cell de-differentiation and activated stemness-related pathways. The single-cell transcriptomes of LUAD patient tumors recapitulate that the distinct LUAD NE cell cluster expressing NE genes is co-enriched with SOX2, OCT4, and NANOG pathway activation, and impaired actin remodeling. This study reveals an unexpected role of CRACD in restricting NE cell plasticity that induces cell de-differentiation, providing new insights into cell plasticity of LUAD.

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“…For instance, research by Irianto et al revealed that the disruption of lamin-A in cancer cells results in more pliable nuclei, increasing the invasiveness and migration of cancer cells [ 93 ]. Additionally, it is known that physical stimuli applied to the nucleus can change the translocation of several growth regulators associated with cancer, such as Yes-associated protein (YAP) [ 5 , 94 ], nuclear actin [ 95 ], and transcription factors linked to the retinoic acid receptor (RAR) [ 96 ], establishing a connection between aberrant nuclear mechanotransduction and cancer. Nuclear mechanotransduction regulation is a complex process due to the vast array of proteins involved, and the diverse ways forces can deform nuclear components with expression consequences.…”

Section: Nuclear Mechanotransductionmentioning

confidence: 99%