Unconventional roles of chromatin remodelers and long non-coding RNAs in cell division

Prozzillo, Yuri; Santopietro, Maria Virginia; Messina, Giovanni; Dimitri, Patrizio

doi:10.1007/s00018-023-04949-8

Cited by 3 publications

(1 citation statement)

References 118 publications

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“…These results indicate that their regulatory network plasticity, potentially involving the altered expression of both canonical and noncanonical cellular components -from moonlighting proteins to transient translatomes ( 58 – 62 ), allows cells to adapt to various environments and even compensate for the loss of some gene functions ( 63 ). In turn, this adaptation allows nonlethal deleterious mutations to persist within the population for an extended time.…”

Section: Discussionmentioning

confidence: 99%

Nonlethal deleterious mutation–induced stress accelerates bacterial aging

Kohram,

Sanderson,

Loui

et al. 2024

Proc. Natl. Acad. Sci. U.S.A.

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Random mutagenesis, including when it leads to loss of gene function, is a key mechanism enabling microorganisms’ long-term adaptation to new environments. However, loss-of-function mutations are often deleterious, triggering, in turn, cellular stress and complex homeostatic stress responses, called “allostasis,” to promote cell survival. Here, we characterize the differential impacts of 65 nonlethal, deleterious single-gene deletions on Escherichia coli growth in three different growth environments. Further assessments of select mutants, namely, those bearing single adenosine triphosphate (ATP) synthase subunit deletions, reveal that mutants display reorganized transcriptome profiles that reflect both the environment and the specific gene deletion. We also find that ATP synthase α-subunit deleted ( ΔatpA ) cells exhibit elevated metabolic rates while having slower growth compared to wild-type (wt) E. coli cells. At the single-cell level, compared to wt cells, individual ΔatpA cells display near normal proliferation profiles but enter a postreplicative state earlier and exhibit a distinct senescence phenotype. These results highlight the complex interplay between genomic diversity, adaptation, and stress response and uncover an “aging cost” to individual bacterial cells for maintaining population-level resilience to environmental and genetic stress; they also suggest potential bacteriostatic antibiotic targets and -as select human genetic diseases display highly similar phenotypes, - a bacterial origin of some human diseases.

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Section: Discussionmentioning

confidence: 99%

Nonlethal deleterious mutation–induced stress accelerates bacterial aging

Kohram,

Sanderson,

Loui

et al. 2024

Proc. Natl. Acad. Sci. U.S.A.

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The pathogenesis mechanism and potential clinical value of lncRNA in gliomas

Liu,

Yuan,

Fan

et al. 2024

Discov Onc

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Glioma is the most common malignant tumor in the central nervous system, and its unique pathogenesis often leads to poor treatment outcomes and prognosis. In 2021, the World Health Organization (WHO) divided gliomas into five categories based on their histological characteristics and molecular changes. Non-coding RNA is a type of RNA that does not encode proteins but can exert biological functions at the RNA level, and long non-coding RNA (lncRNA) is a type of non-coding RNA with a length exceeding 200 nt. It is controlled by various transcription factors and plays an indispensable role in the regulatory processes in various cells. Numerous studies have confirmed that the dysregulation of lncRNA is critical in the pathogenesis, progression, and malignancy of gliomas. Therefore, this article reviews the proliferation, apoptosis, invasion, migration, angiogenesis, immune regulation, glycolysis, stemness, and drug resistance changes caused by the dysregulation of lncRNA in gliomas, and summarizes their potential clinical significance in gliomas.

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LINC01614 Promotes Oral Squamous Cell Carcinoma by Regulating FOXC1

Che,

Zhang,

Cao

et al. 2024

Genes

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Background: Long non-coding RNAs (lncRNAs) are pivotal mediators during the development of carcinomas; however, it remains to be investigated whether lncRNAs are implicated in oral squamous cell carcinoma (OSCC). Methods: In this study, quantitative real-time PCR was conducted for detecting the expression of LINC01614 in OSCC cell lines. The biological functions of LINC01614 were assessed by loss- and gain-of-function experiments conducted both in vivo and in vitro. Cellular proliferation, migration, and invasion were investigated herein, and dual luciferase reporter assays were additionally performed to explore the relationships among LINC01614, miR-138-5p, and Forkhead box C1 (FOXC1). Results: The research presented herein revealed that OSCC cells express high levels of LINC01614. Functional experiments employing cellular and animal models demonstrated that LINC01614 knockdown repressed the malignant phenotypes of OSCC cells, including their growth, invasiveness, and migration. Further investigation revealed that LINC01614 absorbs miR-138-5p miRNA by functioning as a competing endogenous RNA to downregulate the abundance of FOXC1. Conclusions: The findings revealed that LINC01614 contributes to the progression of OSCC by targeting the FOXC1 signaling pathway. The study provides insights into a novel mechanistic process to regulate the development of OSCC, and established a possible target for the therapeutic management of OSCC.

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Unconventional roles of chromatin remodelers and long non-coding RNAs in cell division

Cited by 3 publications

References 118 publications

Nonlethal deleterious mutation–induced stress accelerates bacterial aging

Nonlethal deleterious mutation–induced stress accelerates bacterial aging

The pathogenesis mechanism and potential clinical value of lncRNA in gliomas

LINC01614 Promotes Oral Squamous Cell Carcinoma by Regulating FOXC1

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