Stathmin and microtubules regulate mitotic entry in HeLa cells by controlling activation of both Aurora kinase A and Plk1

Silva, Victoria C.; Cassimeris, Lynne

doi:10.1091/mbc.e13-02-0108

Cited by 24 publications

(24 citation statements)

References 76 publications

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“…For this dynamic instability, the abrupt switching behavior between microtubule growth and shrinkage, may provide some clues. Silva and Cassimeris proposed that stathmin may stand as a gatekeeper at the G 2 /M checkpoint via regulation of Plk1 and Aurora A activities which act upstream of Cdc25a phosphatase to facilitate cell cycle progression by withdrawing inhibitory phosphrylations from CDK1 partially through microtubule-dependent mechanisms in Hela cells43. This is in accord with our findings that Cdc25a could rescue the precocious differentiation phenotypes in stmn4 morphants.…”

Section: Discussionsupporting

confidence: 92%

Stathmin-like 4 is critical for the maintenance of neural progenitor cells in dorsal midbrain of zebrafish larvae

Lin

Lee

2016

Sci Rep

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A delicate balance between proliferating and differentiating signals is necessary to ensure proper growth and neuronal specification. By studying the developing zebrafish brain, we observed a specific and dynamic expression of a microtubule destabilizer gene, stathmin-like 4 (stmn4), in the dorsal midbrain region. The expression of stmn4 was mutually exclusive to a pan-neuronal marker, elavl3 that indicates its role in regulating neurogenesis. We showed the knockdown or overexpression of stmn4 resulted in premature neuronal differentiation in dorsal midbrain. We also generated stmn4 maternal-zygotic knockout zebrafish by the CRISPR/Cas9 system. Unexpectedly, only less than 10% of stmn4 mutants showed similar phenotypes observed in that of stmn4 morphants. It might be due to the complementation of the increased stmn1b expression observed in stmn4 mutants. In addition, time-lapse recordings revealed the changes in cellular proliferation and differentiation in stmn4 morphants. Stmn4 morphants displayed a longer G2 phase that could be rescued by Cdc25a. Furthermore, the inhibition of Wnt could reduce stmn4 transcripts. These results suggest that the Wnt-mediated Stmn4 homeostasis is crucial for preventing dorsal midbrain from premature differentiation via the G2 phase control during the neural keel stage.

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Section: Discussionsupporting

confidence: 92%

Stathmin-like 4 is critical for the maintenance of neural progenitor cells in dorsal midbrain of zebrafish larvae

Lin

Lee

2016

Sci Rep

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“…The Aurora kinases belong to the serine/threonine family and regulate many steps in the mitotic phase, including the formation of the mitotic spindle, chromosome organization and alignment, and the exit from mitosis. [42][43][44][45] A large body of literature has proven that the overexpression of Aurora kinases causes the override of mitotic checkpoints in human cancers. 12,[46][47][48][49] Given the Aurora kinases' pivotal roles in the mitotic process during cell cycle, their over-expressions in malignancies and their crosstalk with tumor suppressors and oncogenic signaling pathways, small molecules targeting the Aurora kinases have attracted intense attention in the field of tumor therapy.…”

Section: Discussionmentioning

confidence: 99%

The p38 MAPK inhibitor BIRB796 enhances the antitumor effects of VX680 in cervical cancer

Jin

Zhang

et al. 2016

Cancer Biology & Therapy

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VX680 is a potent and selective inhibitor that targets the Aurora kinase family. The p38 mitogen-activated protein kinase (MAPK) regulates a large number of cellular pathways and plays an important role in the regulation of cell survival and apoptosis. This study aimed to evaluate the effect of VX680 on cervical cancer cells and investigate whether the effects on apoptosis are enhanced by the ablation of p38 MAPK activation. The results suggested that VX680 inhibited the proliferation of cervical cancer cells by causing G2/M phase arrest and endoreduplication and that the apoptotic effect was attenuated by the activation of p38 MAPK. However, the addition of BIRB796, which is an important p38 MAPK inhibitor, effectively eliminated the expression of p-p38 and hence significantly enhanced the cell death induced by VX680 in vitro. Further study demonstrated that BIRB796 cooperated with VX680 to suppress cervical cancer cell growth in a mouse xenograft model. Taken together, our results demonstrated that VX680 induced cell cycle arrest and endoreduplication in human cervical cancer cells. Combined treatment with VX680 and BIRB796 synergistically inhibited tumor growth both in vitro and in vivo. Dual blockade of Aurora kinases and p38 MAPK is therefore a promising strategy for cervical cancer treatment.

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“…The physiological 'raison d'être' of microtubule stabilization in quiescent cell remains a mystery. An appealing hypothesis might be that stable microtubules sequester critical cell-cycle-regulating factors (Zhang et al, 2015;Ruiz-Miró et al, 2011;Silva and Cassimeris, 2013), thereby maintaining cells in a quiescent state.…”

Section: Microtubulesmentioning

confidence: 99%

The cell biology of quiescent yeast – a diversity of individual scenarios

Sagot

Laporte

2019

Journal of Cell Science

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Most cells, from unicellular to complex organisms, spend part of their life in quiescence, a temporary non-proliferating state. Although central for a variety of essential processes including tissue homeostasis, development and aging, quiescence is poorly understood. In fact, quiescence encompasses various cellular situations depending on the cell type and the environmental niche. Quiescent cell properties also evolve with time, adding another layer of complexity. Studying quiescence is, above all, limited by the fact that a quiescent cell can be recognized as such only after having proved that it is capable of re-proliferating. Recent cellular biology studies in yeast have reported the relocalization of hundreds of proteins and the reorganization of several cellular machineries upon proliferation cessation. These works have revealed that quiescent cells can display various properties, shedding light on a plethora of individual behaviors. The deciphering of the molecular mechanisms beyond these reorganizations, together with the understanding of their cellular functions, have begun to provide insights into the physiology of quiescent cells. In this Review, we discuss recent findings and emerging concepts in Saccharomyces cerevisiae quiescent cell biology.

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Stathmin and microtubules regulate mitotic entry in HeLa cells by controlling activation of both Aurora kinase A and Plk1

Abstract: Stathmin depletion, acting partially via microtubules, delays cells during G2 of the cell cycle through reduced activation of both Aurora kinase A and Polo-like kinase 1.

Cited by 24 publications

References 76 publications

Stathmin-like 4 is critical for the maintenance of neural progenitor cells in dorsal midbrain of zebrafish larvae

Stathmin-like 4 is critical for the maintenance of neural progenitor cells in dorsal midbrain of zebrafish larvae

The p38 MAPK inhibitor BIRB796 enhances the antitumor effects of VX680 in cervical cancer

The cell biology of quiescent yeast – a diversity of individual scenarios

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