ZDHHC11 and ZDHHC11B are critical novel components of the oncogenic MYC-miR-150-MYB network in Burkitt lymphoma

Dzikiewicz‐Krawczyk, Agnieszka; Kok, Klaartje; Ślęzak-Prochazka, Izabella; Robertus, J-L; Bruining, Jan; Tayari, Mina M.; Rutgers, Bea; Jong, Debora de; Koerts, Jasper; Seitz, Annika; Li, Jun; Tillema, B; Guikema, Jeroen E. J.; Nolte, Ilja M.; Diepstra, Arjan; Visser, Lydia; Kluiver, Joost; Berg, Anke van den

doi:10.1038/leu.2017.94

Cited by 45 publications

(66 citation statements)

References 16 publications

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“…Dzikiewicz-Krawczyk et al (2017) reported that ZDHHC11B promotes the proliferation of lymphoma cells through a coordinated action with MYC and MYB. 30 Moreover, TARP is overexpressed in several types of cancer and promotes proliferation and invasion of cancer cells. 23,44,45 Importantly, IHC of the primary EACSCC tissues showed that the overexpression of ZDHHC11B and the copy number amplification are positively correlated, and that TARP is expressed in all of the cases.…”

Section: Discussionmentioning

confidence: 99%

Genetic landscape of external auditory canal squamous cell carcinoma

et al. 2020

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External auditory canal squamous cell carcinoma (EACSCC) is an extremely rare and aggressive malignancy. Due to its rarity, the molecular and genetic characteristics of EACSCC have not yet been elucidated. To reveal the genetic alterations of EACSCC, we performed whole exome sequencing (WES) on 11 primary tumors, 1 relapsed tumor and 10 noncancerous tissues from 10 patients with EACSCC, including 1 with a rare case of synchronous bilateral EACSCC of both ears. WES of the primary tumor samples showed that the most frequently mutated gene is TP53 (63.6%). In addition, recurrent mutations in CDKN2A, NOTCH1, NOTCH2, FAT1 and FAT3 were detected in multiple samples. The mutational signature analysis of primary tumors indicated that the mutational processes associated with the activation of apolipoprotein B mRNA‐editing enzyme catalytic polypeptide‐like (APOBEC) deaminases are the most common in EACSCC, suggesting its similarity to SCC from other primary sites. Analysis of arm‐level copy number alterations detected notable amplification of chromosomes 3q, 5p and 8q as well as deletion of 3p across multiple samples. Focal chromosomal aberrations included amplifications of 5p15.33 (ZDHHC11B) and 7p14.1 (TARP) as well as deletion of 9p21.3 (CDKN2A/B). The protein expression levels of ZDHHC11B and TARP in EACSCC tissues were validated by immunohistochemistry. Moreover, WES of the primary and relapsed tumors from a case of synchronous bilateral EACSCC showed the intrapatient genetic heterogeneity of EACSCC. In summary, this study provides the first evidence for genetic alterations of EACSCC. Our findings suggest that EACSCC mostly resembles other SCC.

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Section: Discussionmentioning

confidence: 99%

Genetic landscape of external auditory canal squamous cell carcinoma

et al. 2020

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“…Cancer links is defined broadly as any literature link between a ZDHHC-family member and a particular cancer, including large-scale and small-scale experimental studies, animal and cell culture studies, and clinical studies, whether functional or correlative. References: ZDHHC2[70,129,130], ZDHHC3[131][132][133], ZDHHC5[87], ZDHHC7[47,134], ZDHHC9[89,92,135,136], ZDHHC11[77,78,137,138], ZDHHC13[49,73], ZDHHC14[82][83][84][85], ZDHHC20[81], ZDHHC23[139]. HPA, Human Protein Atlas (www.proteinatlas.org/).…”

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confidence: 99%

Protein palmitoylation and cancer

2018

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Protein S-palmitoylation is a reversible post-translational modification that alters the localization, stability, and function of hundreds of proteins in the cell. S-palmitoylation is essential for the function of both oncogenes (e.g., NRAS and EGFR) and tumor suppressors (e.g., SCRIB, melanocortin 1 receptor). In mammalian cells, the thioesterification of palmitate to internal cysteine residues is catalyzed by 23 Asp-His-His-Cys (DHHC)-family palmitoyl S-acyltransferases while the removal of palmitate is catalyzed by serine hydrolases, including acyl-protein thioesterases (APTs). These enzymes modulate the function of important oncogenes and tumor suppressors and often display altered expression patterns in cancer. Targeting S-palmitoylation or the enzymes responsible for palmitoylation dynamics may therefore represent a candidate therapeutic strategy for certain cancers.

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“…As a further validation, the overlap between the AGO2-IPe enriched probes of the two primary BL cases and two BL cell lines that was published previously was determined. 12 Of 2025 probes enriched in at least one of the BL cases, 996 (49%) also were AGO2-IPeenriched in at least one of the BL cell lines. On the other hand, of 2450 probes enriched in at least one BL cell line, 1454 (59%) were not AGO2-IPeenriched in any of the BL cases ( Figure 1E).…”

Section: Primary Bl Cases and Normal B Cells Have Distinct Mirna Targmentioning

confidence: 96%

“…E: Overlap of AGO2-IPeenriched probes in two primary BL cases with two BL cell lines from our previous study. 12 Sixty-two percent of probes identified in BL cases also were AGO2-IPeenriched in at least one BL cell line. F and G: Percentage of TargetScan-predicted target genes of selected miRNAs known to be down-regulated (F) or up-regulated (G) in BL, among all expressed genes and among genes enriched in the AGO2-IP fraction of both BL cases or two of three CD19 þ samples.…”

Section: Primary Bl Cases and Normal B Cells Have Distinct Mirna Targmentioning

confidence: 99%

“…Next, enrichment in the AGO2-IP fraction of genes predicted to be targeted by miRNAs known to be deregulated in BL was checked. Members of the miR-17w92 cluster known to be upregulated in BL, 27,28 and miR-15/16, 29 miR-26, 30 miR-28, 8,11 miR-29, 9 miR-150, 12,31 and miR-155 32 known to be downregulated in BL compared with normal B cells, were studied. TargetScan-predicted conserved targets (TargetScan Release 7.1 33 ) of miR-29-3p and miR-150-5p were significantly more enriched in the AGO2-IP fraction of CD19 þ B cells compared with BL cases.…”

Section: Primary Bl Cases and Normal B Cells Have Distinct Mirna Targmentioning

confidence: 99%

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Argonaute 2 RNA Immunoprecipitation Reveals Distinct miRNA Targetomes of Primary Burkitt Lymphoma Tumors and Normal B Cells

Dzikiewicz‐Krawczyk

Diepstra

Rutgers

et al. 2018

The American Journal of Pathology

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miRNAs are small noncoding RNAs involved in the posttranscriptional regulation of gene expression. Deregulated miRNA levels have been linked to Burkitt lymphoma (BL) pathogenesis. To date, the number of known pathogenesis-related miRNA-target gene interactions is limited. Here, we determined for the first time the miRNA targetomes of primary BL tumors and normal B cells. AGO2-RNA immunoprecipitation of two frozen diagnostic BL tissue samples and three CD19 B-cell samples isolated from routinely removed tonsils showed distinct miRNA targetomes of BL and normal B cells. In contrast to normal B cells, miRNA target genes in BL were enriched for targets of the oncogenic miR-17 to 92 cluster, and were involved mainly in cell cycle and cell death. Immunohistochemistry on BL and tonsil tissues confirmed altered protein levels for two of six selected miRNA targets, in line with the differential AGO2-IP enrichment between BL and normal B cells. A comparison of AGO2-IP-enriched genes in primary BL cases with BL cell lines indicated that despite a considerable overlap, the miRNA targetomes of BL cell lines show substantial differences with the targetomes of primary BL tumors. In summary, we identified distinct miRNA targetomes of BL and normal B cells, and showed both the necessity and feasibility of studying miRNA-target gene interactions in primary tumors.

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ZDHHC11 and ZDHHC11B are critical novel components of the oncogenic MYC-miR-150-MYB network in Burkitt lymphoma

Cited by 45 publications

References 16 publications

Genetic landscape of external auditory canal squamous cell carcinoma

Genetic landscape of external auditory canal squamous cell carcinoma

Protein palmitoylation and cancer

Argonaute 2 RNA Immunoprecipitation Reveals Distinct miRNA Targetomes of Primary Burkitt Lymphoma Tumors and Normal B Cells

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