<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Roy A</submitter><funding>NCI NIH HHS</funding><funding>Department of Defense</funding><pagination>1785-1797</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9923726</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(11)</volume><pubmed_abstract>Aurora A kinase (AURKA) is a master cell-cycle regulator that is often dysregulated in human cancers. Its overexpression has been associated with genome instability and oncogenic transformation. The protein kinase D (PKD) family is an emerging therapeutic target of cancer. Aberrant PKD activation has been implicated in tumor growth and survival, yet the underlying mechanisms remain to be elucidated. This study identified, for the first time, a functional crosstalk between PKD2 and Aurora A kinase in cancer cells. The data demonstrate that PKD2 is catalytically active during the G&lt;sub>2&lt;/sub>-M phases of the cell cycle, and inactivation or depletion of PKD2 causes delay in mitotic entry due to downregulation of Aurora A, an effect that can be rescued by overexpression of Aurora A. Moreover,</pubmed_abstract><journal>Molecular cancer research : MCR</journal><pubmed_title>Protein Kinase D2 Modulates Cell Cycle By Stabilizing Aurora A Kinase at Centrosomes.</pubmed_title><pmcid>PMC9923726</pmcid><funding_grant_id>PC150190</funding_grant_id><funding_grant_id>R01 CA229431</funding_grant_id><funding_grant_id>R01 CA142580</funding_grant_id><funding_grant_id>R01 CA129127</funding_grant_id><pubmed_authors>Veroli MV</pubmed_authors><pubmed_authors>Prasad S</pubmed_authors><pubmed_authors>Wang QJ</pubmed_authors><pubmed_authors>Roy A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Protein Kinase D2 Modulates Cell Cycle By Stabilizing Aurora A Kinase at Centrosomes.</name><description>Aurora A kinase (AURKA) is a master cell-cycle regulator that is often dysregulated in human cancers. Its overexpression has been associated with genome instability and oncogenic transformation. The protein kinase D (PKD) family is an emerging therapeutic target of cancer. Aberrant PKD activation has been implicated in tumor growth and survival, yet the underlying mechanisms remain to be elucidated. This study identified, for the first time, a functional crosstalk between PKD2 and Aurora A kinase in cancer cells. The data demonstrate that PKD2 is catalytically active during the G&lt;sub>2&lt;/sub>-M phases of the cell cycle, and inactivation or depletion of PKD2 causes delay in mitotic entry due to downregulation of Aurora A, an effect that can be rescued by overexpression of Aurora A. Moreover,</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Nov</publication><modification>2026-03-31T10:53:54.942Z</modification><creation>2025-04-04T00:34:53.544Z</creation></dates><accession>S-EPMC9923726</accession><cross_references><pubmed>30018032</pubmed><doi>10.1158/1541-7786.mcr-18-0641</doi><doi>10.1158/1541-7786.MCR-18-0641</doi></cross_references></HashMap>