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Data · dataset · 2015

Gamma-actin is involved in regulating centrosome function and mitotic progression in cancer cells

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Reorganization of the actin cytoskeleton during mitosis is crucial for regulating cell division.

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A functional role for γ-actin in mitotic arrest induced by the microtubule-targeted agent, paclitaxel, has recently been demonstrated. We hypothesized that γ-actin plays a role in mitosis.

Herein, we investigated the effect of γ-actin in mitosis and demonstrated that γ-actin is important in the distribution of β-actin and formation of actin-rich retraction fibers during mitosis. The reduced ability of paclitaxel to induce mitotic arrest as a result of γ-actin depletion was replicated with a range of mitotic inhibitors, suggesting that γ-actin loss reduces the ability of broad classes of anti-mitotic agents to induce mitotic arrest.

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In addition, partial depletion of γ-actin enhanced centrosome amplification in cancer cells and caused a significant delay in prometaphase/metaphase. This prolonged prometaphase/metaphase arrest was due to mitotic defects such as uncongressed and missegregated chromosomes, and correlated with an increased presence of mitotic spindle abnormalities in the γ-actin depleted cells. Collectively, these results demonstrate a previously unknown role for γ-actin in regulating centrosome function, chromosome alignment and maintenance of mitotic spindle integrity.

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Cancer · Cancer
Provenance · 2 source records, 14 field assertions
SourceKeyLast seenRaw
DataCite10.6084/m9.figshare.162797314 d agoJSON v1
DataCite10.6084/m9.figshare.1627973.v114 d agoJSON v1
FieldAssertionExtractorEvidence
access_levelsource · DataCiteconnector:datacite@1.0.0/data/attributes/rightsList
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concepts[disease].local:disease:cancermapping · DataCitevocabulary-mapper@1.0.0keywords['Cancer']
concepts[disease].local:disease:cancermapping · DataCitevocabulary-mapper@1.0.0keywords['Cancer']
concepts[field].fos:biological-sciencessource · DataCiteconnector:datacite@1.0.0
concepts[field].fos:biological-sciencessource · DataCiteconnector:datacite@1.0.0
concepts[field].fos:physical-sciencessource · DataCiteconnector:datacite@1.0.0
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