The second half of mitosis and its implications in cancer biology

Moreno-Andrés, Daniel; Holl, Kristin; Antonin, Wolfram

doi:10.1016/j.semcancer.2022.11.013

Cited by 7 publications

(5 citation statements)

References 259 publications

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“…In contrast, in cells that undergo open mitosis, such as mammalian cells, the NE fully disassembles (in a process called nuclear envelope breakdown, NEBD) during mitotic entry, detaches from the chromatin, and disperses into the mitotic ER network [ 4 ]. NEBD allows cytoplasmic spindle microtubules to access chromosomes, which is crucial for chromosome alignment on the metaphase spindle and subsequent segregation during mitosis [ 14 , 15 ]. In this section, we describe the molecular regulation of NE disassembly during open mitosis and discuss whether the NE identity is completely lost.…”

Section: Ne Breakdown and Its Absorption Into The Mitotic Er: Is Ne I...mentioning

confidence: 99%

“…What mediates the attachment of ER membranes to the chromosome surface during mitotic exit at the molecular level? After anaphase onset, the phosphorylation events that induce NEBD at prophase are reversed by the inactivation of mitotic kinases such as CDK1 and the reactivation of phosphatases such as protein phosphatase 1 (PP1) and 2A (PP2A) [ 15 , 24 ]. This makes lamins, INM proteins, and nucleoporins competent for rebinding to chromatin and to each other.…”

Section: Ne Reformation From Mitotic Er: When Is the Ne Identity Re-e...mentioning

confidence: 99%

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Sculpting nuclear envelope identity from the endoplasmic reticulum during the cell cycle

Deolal,

Scholz,

Ren

et al. 2024

Nucleus

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The nuclear envelope (NE) regulates nuclear functions, including transcription, nucleocytoplasmic transport, and protein quality control. While the outer membrane of the NE is directly continuous with the endoplasmic reticulum (ER), the NE has an overall distinct protein composition from the ER, which is crucial for its functions. During open mitosis in higher eukaryotes, the NE disassembles during mitotic entry and then reforms as a functional territory at the end of mitosis to reestablish nucleocytoplasmic compartmentalization. In this review, we examine the known mechanisms by which the functional NE reconstitutes from the mitotic ER in the continuous ER–NE endomembrane system during open mitosis. Furthermore, based on recent findings indicating that the NE possesses unique lipid metabolism and quality control mechanisms distinct from those of the ER, we explore the maintenance of NE identity and homeostasis during interphase. We also highlight the potential significance of membrane junctions between the ER and NE.

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Section: Ne Breakdown and Its Absorption Into The Mitotic Er: Is Ne I...mentioning

confidence: 99%

Section: Ne Reformation From Mitotic Er: When Is the Ne Identity Re-e...mentioning

confidence: 99%

Sculpting nuclear envelope identity from the endoplasmic reticulum during the cell cycle

Deolal,

Scholz,

Ren

et al. 2024

Nucleus

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“…203 Meanwhile, cyclin B degradation inactivates cyclin-dependent kinase 1 (Cdk1), allowing the cells to proceed to mitotic exit and complete cell division. 185,186,214,215 In eukaryotic cells, SAC plays a crucial role in genomic integrity and its abnormality leads to chromosome segregation errors. 10,101 Defects in SAC result in the failure of proper monitoring and controlling the timing of sister chromatid segregation.…”

Section: Causes Of Cinmentioning

confidence: 99%

The two sides of chromosomal instability: drivers and brakes in cancer

Hosea,

Hillary,

Naqvi

et al. 2024

Sig Transduct Target Ther

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Chromosomal instability (CIN) is a hallmark of cancer and is associated with tumor cell malignancy. CIN triggers a chain reaction in cells leading to chromosomal abnormalities, including deviations from the normal chromosome number or structural changes in chromosomes. CIN arises from errors in DNA replication and chromosome segregation during cell division, leading to the formation of cells with abnormal number and/or structure of chromosomes. Errors in DNA replication result from abnormal replication licensing as well as replication stress, such as double-strand breaks and stalled replication forks; meanwhile, errors in chromosome segregation stem from defects in chromosome segregation machinery, including centrosome amplification, erroneous microtubule–kinetochore attachments, spindle assembly checkpoint, or defective sister chromatids cohesion. In normal cells, CIN is deleterious and is associated with DNA damage, proteotoxic stress, metabolic alteration, cell cycle arrest, and senescence. Paradoxically, despite these negative consequences, CIN is one of the hallmarks of cancer found in over 90% of solid tumors and in blood cancers. Furthermore, CIN could endow tumors with enhanced adaptation capabilities due to increased intratumor heterogeneity, thereby facilitating adaptive resistance to therapies; however, excessive CIN could induce tumor cells death, leading to the “just-right” model for CIN in tumors. Elucidating the complex nature of CIN is crucial for understanding the dynamics of tumorigenesis and for developing effective anti-tumor treatments. This review provides an overview of causes and consequences of CIN, as well as the paradox of CIN, a phenomenon that continues to perplex researchers. Finally, this review explores the potential of CIN-based anti-tumor therapy.

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“…This event takes place in three phases: gap 1 (G 1 ), DNA synthesis (S-phase), and gap 2 (G 2 ) [ 1 ]. The mitotic phase (M), on the other hand, is divided into five well-defined phases: prophase, prometaphase, metaphase, anaphase, and telophase [ 2 ] ( Figure 1 ). During these phases, the cell separates its DNA into two sets.…”

Section: Introductionmentioning

confidence: 99%

“…Ts = It × all BrdU positive cells − labeled cells all IdU stained cells − labeled cells (2) where "T S " is the length of the S-phase and "It" is the time period between BrdU and IdD labeling. From Equation (1), the Tc can be estimated.…”

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confidence: 99%

Methods for Inferring Cell Cycle Parameters Using Thymidine Analogues

Martí-Clúa

2023

Biology

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Tritiated thymidine autoradiography, 5-bromo-2′-deoxyuridine (BrdU) 5-chloro-2′-deoxyuridine (CldU), 5-iodo-2′-deoxyuridine (IdU), and 5-ethynyl-2′-deoxyiridine (EdU) labeling have been used for identifying the fraction of cells undergoing the S-phase of the cell cycle and to follow the fate of these cells during the embryonic, perinatal, and adult life in several species of vertebrate. In this current review, I will discuss the dosage and times of exposition to the aforementioned thymidine analogues to label most of the cells undergoing the S-phase of the cell cycle. I will also show how to infer, in an asynchronous cell population, the duration of the G1, S, and G2 phases, as well as the growth fraction and the span of the whole cell cycle on the base of some labeling schemes involving a single administration, continuous nucleotide analogue delivery, and double labeling with two thymidine analogues. In this context, the choice of the optimal dose of BrdU, CldU, IdU, and EdU to label S-phase cells is a pivotal aspect to produce neither cytotoxic effects nor alter cell cycle progression. I hope that the information presented in this review can be of use as a reference for researchers involved in the genesis of tissues and organs.

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The second half of mitosis and its implications in cancer biology

Cited by 7 publications

References 259 publications

Sculpting nuclear envelope identity from the endoplasmic reticulum during the cell cycle

Sculpting nuclear envelope identity from the endoplasmic reticulum during the cell cycle

The two sides of chromosomal instability: drivers and brakes in cancer

Methods for Inferring Cell Cycle Parameters Using Thymidine Analogues

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