Last update 01 Nov 2024

CDK11B

Last update 01 Nov 2024

Basic Info

Synonyms

CDC2L1, CDK11, CDK11-p110

+ [14]

Introduction

Plays multiple roles in cell cycle progression, cytokinesis and apoptosis. Involved in pre-mRNA splicing in a kinase activity-dependent manner. Isoform 7 may act as a negative regulator of normal cell cycle progression.

100 Clinical Results associated with CDK11B

100 Translational Medicine associated with CDK11B

0 Patents (Medical) associated with CDK11B

Literatures (Medical) associated with CDK11B

02 Dec 2022·Molecular Cancer Research

Molecular Profile Changes in Patients with Castrate-Resistant Prostate Cancer Pre- and Post-Abiraterone/Prednisone Treatment

Article

Author: Kohli, Manish ; Bhargava, Vipul ; Vedell, Peter T. ; Gormley, Michael ; Bryce, Alan H. ; Kalari, Krishna R. ; Tan, Winston ; Sinnwell, Jason P. ; Jimenez, Raphael E. ; Li, Ying ; Qin, Sisi ; Dehm, Scott M. ; Hillman, David W. ; Carlson, Rachel E. ; Weinshilboum, Richard M. ; Sicotte, Hugues ; Wang, Liewei

AbstractWe identified resistance mechanisms to abiraterone acetate/prednisone (AA/P) in patients with metastatic castration-resistant prostate cancer (mCRPC) in the Prostate Cancer Medically Optimized Genome-Enhanced Therapy (PROMOTE) study.We analyzed whole-exome sequencing (WES) and RNA-sequencing data from 83 patients with metastatic biopsies before (V1) and after 12 weeks of AA/P treatment (V2). Resistance was determined by time to treatment change (TTTC).At V2, 18 and 11 of 58 patients had either short-term (median 3.6 months; range 1.4–4.5) or long-term (median 29 months; range 23.5–41.7) responses, respectively. Nonresponders had low expression of TGFBR3 and increased activation of the Wnt pathway, cell cycle, upregulation of AR variants, both pre- and posttreatment, with further deletion of AR inhibitor CDK11B posttreatment. Deletion of androgen processing genes, HSD17B11, CYP19A1 were observed in nonresponders posttreatment. Genes involved in cell cycle, DNA repair, Wnt-signaling, and Aurora kinase pathways were differentially expressed between the responder and non-responder at V2. Activation of Wnt signaling in nonresponder and deactivation of MYC or its target genes in responders was detected via SCN loss, somatic mutations, and transcriptomics. Upregulation of genes in the AURKA pathway are consistent with the activation of MYC regulated genes in nonresponders. Several genes in the AKT1 axis had increased mutation rate in nonresponders. We also found evidence of resistance via PDCD1 overexpression in responders.Implications:Finally, we identified candidates drugs to reverse AA/P resistance: topoisomerase inhibitors and drugs targeting the cell cycle via the MYC/AURKA/AURKB/TOP2A and/or PI3K_AKT_MTOR pathways.

01 Nov 2021·Cancer Gene TherapyQ2 · MEDICINE

Involvement of CDK11B-mediated SPDEF ubiquitination and SPDEF-mediated microRNA-448 activation in the oncogenicity and self-renewal of hepatocellular carcinoma stem cells

Q2 · MEDICINE

Article

Author: Guo, Min ; Zheng, Jin-Fang ; Liu, Zhuo ; Yang, Yi-Jun ; Zhang, Jian-Quan ; Guo, Jun-Cheng

Increasing evidence has suggested the crucial role cyclin-dependent kinases (CDKs) in the biology of hepatocellular carcinoma (HCC), a lethal malignancy with high morbidity and mortality. Hence, this study explored the modulatory effect of the putative cyclin-dependent kinase 11B (CDK11B)-mediated ubiquitination on HCC stem cells. The expression of CDK11B, SAM pointed domain-containing ETS transcription factor (SPDEF) and DOT1-like histone lysine methyltransferase (DOT1L) was determined by RT-qPCR and western blot analysis in HCC tissues and cells. The interaction among CDK11B, SPDEF, miR-448, and DOT1L was analyzed by Co-IP, ubiquitination-IP and ChIP assays, whereas their effects on the biological characteristics of HCC stem cells were assessed by sphere formation and colony formation assays. An in vivo xenograft tumor model was developed for validating the regulation of CDK11B in oncogenicity of HCC stem cells. We characterized the aberrant upregulation of CDK11B and downregulation SPDEF in HCC tissues and cells. CDK11B degraded SPDEF through ubiquitin-proteasome pathway, whereas SPDEF could bind to the miR-448 promoter and inhibit the expression of DOT1L by activating miR-448, whereby promoting self-renewal of HCC stem cells. Knockdown of CDK11B attenuated the self-renewal capability of HCC stem cells and their oncogenicity in vivo. These findings highlighted that blocking the CDK11B-induced degradation of SPDEF and enhancing miR-448-dependent inhibition of DOT1L may delay the progression of HCC by restraining self-renewal capability of HCC stem cells, representing novel targets for HCC management.

01 Nov 2020·Anticancer ResearchQ4 · MEDICINE

Sequencing of Sclerosing Microcystic Adenocarcinoma Identifies Mutational Burden and Somatic Variants Associated With Tumorigenesis

Q4 · MEDICINE

Article

Author: Judson, Benjamin L ; Jiang, Roy ; Tower, Jacob I ; Marquez, Jonathan ; Jacobs, Daniel ; Chen, Wenqian ; Prasad, Manju Lata ; Mehra, Saral

BACKGROUND/AIMSclerosing microcystic adenocarcinoma (SMA) is a rare oral cavity neoplasia, histologically resembling microcystic adnexal carcinoma (MAC) of the skin. Only nine SMA cases have been reported in the literature, frequently in the context of immunosuppression; SMA has not been recognized in the most recent WHO tumor classification. We sought to identify potential molecular mechanisms of tumorigenesis in a case of SMA relative to those known for MAC.CASE REPORTA 41-year-old female with psoriatic arthritis undergoing immunosuppression therapy presented with a tongue mass. Biopsy revealed a diagnosis of SMA. Partial glossectomy and neck dissection showed no residual tumor or nodal disease.RESULTSwhole exome sequencing revealed moderate mutational burden and putative loss of function mutations in CDK11B but no overlap with known MAC mutations.CONCLUSIONWe characterized the genomic profile of SMA for the first time, identifying both mutational burden and unique somatic variants associated with tumorigenesis.

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CDK11B

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