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Article ; Online: CCAR-1 works together with the U2AF large subunit UAF-1 to regulate alternative splicing.

Lugano, Doreen I / Barrett, Lindsey N / Chaput, Dale / Park, Margaret A / Westerheide, Sandy D

2023 Volume 21, Issue 1, Page(s) 1–11

Abstract: The Cell Division Cycle and Apoptosis Regulator (CCAR) protein family members have recently emerged as regulators of alternative splicing and transcription, as well as having other key physiological functions. For example, mammalian CCAR2/DBC1 forms a ... ...

Abstract	The Cell Division Cycle and Apoptosis Regulator (CCAR) protein family members have recently emerged as regulators of alternative splicing and transcription, as well as having other key physiological functions. For example, mammalian CCAR2/DBC1 forms a complex with the zinc factor protein ZNF326 to integrate alternative splicing with RNA polymerase II transcriptional elongation in AT-rich regions of the DNA. Additionally,
MeSH term(s)	Animals ; Alternative Splicing ; Base Sequence ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/metabolism ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; Ribonucleoproteins/genetics ; Ribonucleoproteins/metabolism ; RNA Splicing ; Splicing Factor U2AF/genetics ; Splicing Factor U2AF/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism
Chemical Substances	Caenorhabditis elegans Proteins ; Ribonucleoproteins ; Splicing Factor U2AF ; ccar-1 protein, C elegans ; Membrane Proteins ; UAF-1 protein, C elegans
Language	English
Publishing date	2023-12-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	2159587-2
ISSN	1555-8584 ; 1555-8584
ISSN (online)	1555-8584
ISSN	1555-8584
DOI	10.1080/15476286.2023.2289707
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The relationship between multidrug resistance and glucosylceramide levels: an opportunity for combined therapies.

Park, Margaret A

Cancer biology & therapy

2009 Volume 8, Issue 12, Page(s) 1122–1124

MeSH term(s)	Breast Neoplasms/drug therapy ; Breast Neoplasms/metabolism ; Drug Resistance, Multiple ; Drug Resistance, Neoplasm ; Female ; Glucosylceramides/metabolism ; Humans
Chemical Substances	Glucosylceramides
Language	English
Publishing date	2009-06-09
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	2146305-0
ISSN	1555-8576 ; 1538-4047
ISSN (online)	1555-8576
ISSN	1538-4047
DOI	10.4161/cbt.8.12.8706
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Article: Deregulated expression of the 14q32 miRNA cluster in clear cell renal cancer cells.

Chhabra, Ravneet / Guergues, Jennifer / Wohlfahrt, Jessica / Rockfield, Stephanie / Espinoza Gonzalez, Pamela / Rego, Shanon / Park, Margaret A / Berglund, Anders E / Stevens, Stanley M / Nanjundan, Meera

Frontiers in oncology

2023 Volume 13, Page(s) 1048419

Abstract: Clear cell renal cell carcinomas (ccRCC) are characterized by arm-wide chromosomal alterations. Loss at 14q is associated with disease aggressiveness in ccRCC, which responds poorly to chemotherapeutics. The 14q locus contains one of the largest miRNA ... ...

Abstract	Clear cell renal cell carcinomas (ccRCC) are characterized by arm-wide chromosomal alterations. Loss at 14q is associated with disease aggressiveness in ccRCC, which responds poorly to chemotherapeutics. The 14q locus contains one of the largest miRNA clusters in the human genome; however, little is known about the contribution of these miRNAs to ccRCC pathogenesis. In this regard, we investigated the expression pattern of selected miRNAs at the 14q32 locus in TCGA kidney tumors and in ccRCC cell lines. We demonstrated that the miRNA cluster is downregulated in ccRCC (and cell lines) as well as in papillary kidney tumors relative to normal kidney tissues (and primary renal proximal tubule epithelial (RPTEC) cells). We demonstrated that agents modulating expression of DNMT1 (e.g., 5-Aza-deoxycytidine) could modulate 14q32 miRNA expression in ccRCC cell lines. Lysophosphatidic acid (LPA, a lysophospholipid mediator elevated in ccRCC) not only increased labile iron content but also modulated expression of a 14q32 miRNA. Through an overexpression approach targeting a subset of 14q32 miRNAs (specifically at subcluster A: miR-431-5p, miR-432-5p, miR-127-3p, and miR-433-3p) in 769-P cells, we uncovered changes in cellular viability and claudin-1, a tight junction marker. A global proteomic approach was implemented using these miRNA overexpressing cell lines which uncovered ATXN2 as a highly downregulated target. Collectively, these findings support a contribution of miRNAs at 14q32 in ccRCC pathogenesis.
Language	English
Publishing date	2023-04-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2023.1048419
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Article ; Online: Translational relevance of SOS1 targeting for KRAS-mutant colorectal cancer.

Alem, Diego / Yang, Xinrui / Beato, Francisca / Sarcar, Bhaswati / Tassielli, Alexandra F / Dai, Ruifan / Hogenson, Tara L / Park, Margaret A / Jiang, Kun / Cai, Jianfeng / Yuan, Yu / Fernandez-Zapico, Martin E / Tan, Aik Choon / Fleming, Jason B / Xie, Hao

Molecular carcinogenesis

2023 Volume 62, Issue 7, Page(s) 1025–1037

Abstract: It has been challenging to target mutant KRAS (mKRAS) in colorectal cancer (CRC) and other malignancies. Recent efforts have focused on developing inhibitors blocking molecules essential for KRAS activity. In this regard, SOS1 inhibition has arisen as an ...

Abstract	It has been challenging to target mutant KRAS (mKRAS) in colorectal cancer (CRC) and other malignancies. Recent efforts have focused on developing inhibitors blocking molecules essential for KRAS activity. In this regard, SOS1 inhibition has arisen as an attractive approach for mKRAS CRC given its essential role as a guanine nucleotide exchange factor for this GTPase. Here, we demonstrated the translational value of SOS1 blockade in mKRAS CRC. We used CRC patient-derived organoids (PDOs) as preclinical models to evaluate their sensitivity to SOS1 inhibitor BI3406. A combination of in silico analyses and wet lab techniques was utilized to define potential predictive markers for SOS1 sensitivity and potential mechanisms of resistance in CRC. RNA-seq analysis of CRC PDOs revealed two groups of CRC PDOs with differential sensitivities to SOS1 inhibitor BI3406. The resistant group was enriched in gene sets involving cholesterol homeostasis, epithelial-mesenchymal transition, and TNF-α/NFκB signaling. Expression analysis identified a significant correlation between SOS1 and SOS2 mRNA levels (Spearman's ρ 0.56, p < 0.001). SOS1/2 protein expression was universally present with heterogeneous patterns in CRC cells but only minimal to none in surrounding nonmalignant cells. Only SOS1 protein expression was associated with worse survival in patients with RAS/RAF mutant CRC (p = 0.04). We also found that SOS1/SOS2 protein expression ratio >1 by immunohistochemistry (p = 0.03) instead of KRAS mutation (p = 1) was a better predictive marker to BI3406 sensitivity of CRC PDOs, concordant with the significant positive correlation between SOS1/SOS2 protein expression ratio and SOS1 dependency. Finally, we showed that GTP-bound RAS level underwent rebound even in BI3406-sensitive PDOs with no change of KRAS downstream effector genes, thus suggesting upregulation of guanine nucleotide exchange factor as potential cellular adaptation mechanisms to SOS1 inhibition. Taken together, our results show that high SOS1/SOS2 protein expression ratio predicts sensitivity to SOS1 inhibition and support further clinical development of SOS1-targeting agents in CRC.
MeSH term(s)	Humans ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism ; Signal Transduction ; SOS1 Protein/genetics ; SOS1 Protein/metabolism ; Guanine Nucleotide Exchange Factors/genetics ; Mutation ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics
Chemical Substances	Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; SOS1 Protein ; Guanine Nucleotide Exchange Factors ; KRAS protein, human
Language	English
Publishing date	2023-04-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1004029-8
ISSN	1098-2744 ; 0899-1987
ISSN (online)	1098-2744
ISSN	0899-1987
DOI	10.1002/mc.23543
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Article: Challenges in the Treatment of Triple Negative and HER2-Overexpressing Breast Cancer.

Hoeferlin, L Alexis / E Chalfant, Charles / Park, Margaret A

Journal of surgery and science

2014 Volume 1, Issue 1, Page(s) 3–7

Abstract: While the 5-year survival rate of breast cancer is at an all-time high of 90%, this disease remains the second most common cause of cancer-related death, surpassed only by lung cancer in the US. The reasons for this discrepancy stem from cancer subtypes ... ...

Abstract	While the 5-year survival rate of breast cancer is at an all-time high of 90%, this disease remains the second most common cause of cancer-related death, surpassed only by lung cancer in the US. The reasons for this discrepancy stem from cancer subtypes which become resistant to current therapies. These subtypes: "Triple negative" and ErbB2-overexpressing, are discussed in this review.
Language	English
Publishing date	2014-04-09
Publishing country	United States
Document type	Journal Article
ISSN	2333-4703
ISSN	2333-4703
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Article ; Online: Splice variants of cytosolic polyadenylation element-binding protein 2 (CPEB2) differentially regulate pathways linked to cancer metastasis.

DeLigio, James T / Lin, Grace / Chalfant, Charles E / Park, Margaret A

The Journal of biological chemistry

2017 Volume 292, Issue 43, Page(s) 17909–17918

Abstract: The translational regulator cytosolic polyadenylation element-binding protein 2 (CPEB2) has two isoforms, CPEB2A and CPEB2B, derived by alternative splicing of RNA into a mature form that either includes or excludes exon 4. Previously, we reported that ... ...

Abstract	The translational regulator cytosolic polyadenylation element-binding protein 2 (CPEB2) has two isoforms, CPEB2A and CPEB2B, derived by alternative splicing of RNA into a mature form that either includes or excludes exon 4. Previously, we reported that this splicing event is highly dysregulated in aggressive forms of breast cancers, which overexpress CPEB2B. The loss of CPEB2A with a concomitant increase in CPEB2B was also required for breast cancer cells to resist cell death because of detachment (anoikis resistance) and metastasize
MeSH term(s)	Alternative Splicing ; Anoikis ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Cyclic AMP Response Element-Binding Protein/genetics ; Cyclic AMP Response Element-Binding Protein/metabolism ; Female ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Neoplasm Metastasis ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Twist-Related Protein 1/genetics ; Twist-Related Protein 1/metabolism
Chemical Substances	Cyclic AMP Response Element-Binding Protein ; HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; Neoplasm Proteins ; Nuclear Proteins ; TWIST1 protein, human ; Twist-Related Protein 1
Language	English
Publishing date	2017-09-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M117.810127
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Article: A rapid and adaptable lipidomics method for quantitative UPLC-mass spectrometric analysis of phosphatidylethanolamine and phosphatidylcholine in vitro, and in cells

Stephenson, Daniel J / MacKnight, H. Patrick / Hoeferlin, L. Alexis / Park, Margaret A / Allegood, Jeremy C / Cardona, Christopher L / Chalfant, Charles E

Analytical methods. 2019 Mar. 28, v. 11, no. 13

2019

Abstract: Phosphatidylethanolamine (PE) and phosphatidylcholine (PC) are highly prevalent phospholipids in mammalian membranes. There are currently no methods for detection of minute levels of these phospholipids or simultaneously with products of the utilization ... ...

Abstract	Phosphatidylethanolamine (PE) and phosphatidylcholine (PC) are highly prevalent phospholipids in mammalian membranes. There are currently no methods for detection of minute levels of these phospholipids or simultaneously with products of the utilization of these phospholipid substrates by phospholipase A2 (PLA2) enzymes. To examine the substrate utilization of PE and PC by PLA2, we developed a method to accurately detect and measure specific forms of PE and PC as low as 50 femtomoles. Validation of this method consisted of an enzymatic assay to monitor docosahexaenoic acid and arachidonic acid release from the hydrolysis of PE and PC by group IV phospholipase A2 (cPLA2α) coupled to the generation of Lyso-PE (LPE) and Lyso-PC (LPC). In addition, the PE and PC profiles of RAW 264.7 macrophages were monitored with zymosan/lipopolysaccharide-treatment. Finally, genetic validation for the specificity of the method consisted of the downregulation of two biosynthetic enzymes responsible for the production of PE and PC, choline kinase A (CHKA) and ethanolamine kinase 1 (ETNK1). This new UPLC ESI-MS/MS method provides accurate and highly sensitive detection of PE and PC species containing AA and DHA allowing for the specific examination of the substrate utilization of these phospholipids by PLA2in vitro and in cells.
Keywords	arachidonic acid ; biosynthesis ; choline kinase ; docosahexaenoic acid ; ethanolamine ; gene expression regulation ; hydrolysis ; macrophages ; mammals ; phosphatidylcholines ; phosphatidylethanolamines ; phospholipase A2 ; phospholipases ; tandem mass spectrometry
Language	English
Dates of publication	2019-0328
Size	p. 1765-1776.
Publishing place	The Royal Society of Chemistry
Document type	Article
ZDB-ID	2515210-5
ISSN	1759-9679 ; 1759-9660
ISSN (online)	1759-9679
ISSN	1759-9660
DOI	10.1039/c9ay00052f
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: A pilot study to evaluate tissue- and plasma-based DNA driver mutations in a cohort of patients with pancreatic intraductal papillary mucinous neoplasms.

G3 (Bethesda, Md.)

2022 Volume 13, Issue 2

Abstract: Intraductal papillary mucinous neoplasms (IPMNs) are precursor lesions to pancreatic ductal adenocarcinoma that are challenging to manage due to limited imaging, cytologic, and molecular markers that accurately classify lesions, grade of dysplasia, or ... ...

Abstract	Intraductal papillary mucinous neoplasms (IPMNs) are precursor lesions to pancreatic ductal adenocarcinoma that are challenging to manage due to limited imaging, cytologic, and molecular markers that accurately classify lesions, grade of dysplasia, or focus of invasion preoperatively. The objective of this pilot study was to determine the frequency and type of DNA mutations in a cohort of surgically resected, pathologically confirmed IPMN, and to determine if concordant mutations are detectable in paired pretreatment plasma samples. Formalin-fixed paraffin-embedded (FFPE) tissue from 46 surgically resected IPMNs (31 low-grade, 15 high-grade) and paired plasma from a subset of 15 IPMN cases (10 low-grade, 5 high-grade) were subjected to targeted mutation analysis using a QIAseq Targeted DNA Custom Panel. Common driver mutations were detected in FFPE from 44 of 46 (95.6%) IPMN cases spanning all grades; the most common DNA mutations included: KRAS (80%), RNF43 (24%), and GNAS (43%). Of note, we observed a significant increase in the frequency of RNF43 mutations from low-grade to high-grade IPMNs associated or concomitant with invasive carcinoma (trend test, P = 0.01). Among the subset of cases with paired plasma, driver mutations identified in the IPMNs were not detected in circulation. Overall, our results indicate that mutational burden for IPMNs is a common occurrence, even in low-grade IPMNs. Furthermore, although blood-based biopsies are an attractive, noninvasive method for detecting somatic DNA mutations, the QIAseq panel was not sensitive enough to detect driver mutations that existed in IPMN tissue using paired plasma in the volume we were able to retrieve for this retrospective study.
MeSH term(s)	Humans ; Pancreatic Intraductal Neoplasms/genetics ; Pancreatic Intraductal Neoplasms/pathology ; Pilot Projects ; Retrospective Studies ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; Pancreatic Neoplasms/surgery ; Mutation ; Neoplasms, Cystic, Mucinous, and Serous
Language	English
Publishing date	2022-12-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2629978-1
ISSN	2160-1836 ; 2160-1836
ISSN (online)	2160-1836
ISSN	2160-1836
DOI	10.1093/g3journal/jkac314
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Article: Potential role of apoptosis in development of the cystinotic phenotype.

Park, Margaret A / Thoene, Jess G

Pediatric nephrology (Berlin, Germany)

2005 Volume 20, Issue 4, Page(s) 441–446

Abstract: Much still remains unclear about the proximal biochemical effects of mutations on development of the phenotype in inborn errors of metabolism. Cystinosis is an example of this phenomenon. We have recently shown that cystinotic cells undergo apoptosis at ... ...

Abstract	Much still remains unclear about the proximal biochemical effects of mutations on development of the phenotype in inborn errors of metabolism. Cystinosis is an example of this phenomenon. We have recently shown that cystinotic cells undergo apoptosis at a two- to fourfold higher rate than controls. Cystinotic cells pre-treated with cysteamine, normalizing cystine content, display a four- to fivefold decrease in apoptosis, while normal cells pre-treated with cystine dimethylester, increasing lysosomal cystine, exhibit a fivefold increase in apoptosis. We speculate that cystine exits the lysosomal compartment during early apoptosis and affects apoptotic proteins in the cytosol, causing an inappropriate commitment to proceed to cell death. The resulting chronic hypocellularity could account for all the characteristics of the nephropathic cystinotic phenotype. The milder variants of cystinosis may result from modifying mutations within an apoptotic protein, ablating the proapoptotic effects of cystine. Failure of the mouse knockout for cystinosis to show renal involvement may be the result of differences in apoptotic processes between man and mouse. Apoptosis is a major final common pathway for many disease states. Therefore, a better understanding of the effect of lysosomal cystine on apoptosis may help to clarify development of other diseases.
MeSH term(s)	Animals ; Apoptosis ; Cystinosis/etiology ; Cystinosis/genetics ; Humans ; Lysosomes ; Phenotype
Language	English
Publishing date	2005-04
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-004-1712-9
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Article ; Online: PRMT2 interacts with splicing factors and regulates the alternative splicing of BCL-X.

Vhuiyan, Mynol I / Pak, Magnolia L / Park, Margaret A / Thomas, Dylan / Lakowski, Ted M / Chalfant, Charles E / Frankel, Adam

Journal of biochemistry

2017 Volume 162, Issue 1, Page(s) 17–25

Abstract: Protein arginine N-methyltransferase 2 (PRMT2) functions in JAK-STAT and Wnt/β-catenin signalling pathways, serves as a nuclear receptor-dependent transcriptional co-activator, and represses NF-κB and E2F1 transcription factor activities to promote ... ...

Abstract	Protein arginine N-methyltransferase 2 (PRMT2) functions in JAK-STAT and Wnt/β-catenin signalling pathways, serves as a nuclear receptor-dependent transcriptional co-activator, and represses NF-κB and E2F1 transcription factor activities to promote apoptosis. We have previously demonstrated that PRMT2 interacts with PRMT1 and increases its activity. Here, we reveal associations using proteomics between the PRMT2 SH3 domain and splicing factors including Src-associated in mitosis 68 kDa protein (SAM68), a PRMT1 substrate and trans-acting factor that mediates BCL-X alternative splicing. We determined that PRMT2 interacts with SAM68 in cells and regulates its subcellular localization via the SH3 domain of PRMT2, prompting us to investigate the potential role of PRMT2 in BCL-X alternative splicing. We found that the expression of the full-length, wildtype form of PRMT2 promotes an increase in the BCL-X(L)/BCL-X(s) ratio in TNF-α or LPS stimulated cells. These results indicate that active PRMT2 may play a role during inflammation in alternative splicing regulation.
MeSH term(s)	Adaptor Proteins, Signal Transducing/chemistry ; Adaptor Proteins, Signal Transducing/metabolism ; Alternative Splicing/genetics ; DNA-Binding Proteins/chemistry ; DNA-Binding Proteins/metabolism ; HEK293 Cells ; HeLa Cells ; Humans ; Intracellular Signaling Peptides and Proteins/chemistry ; Intracellular Signaling Peptides and Proteins/metabolism ; Protein-Arginine N-Methyltransferases/chemistry ; Protein-Arginine N-Methyltransferases/metabolism ; Proteomics ; RNA Splicing Factors/metabolism ; RNA-Binding Proteins/chemistry ; RNA-Binding Proteins/metabolism ; Tumor Cells, Cultured ; bcl-X Protein/genetics ; bcl-X Protein/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; DNA-Binding Proteins ; Intracellular Signaling Peptides and Proteins ; KHDRBS1 protein, human ; RNA Splicing Factors ; RNA-Binding Proteins ; bcl-X Protein ; PRMT2 protein, human (EC 2.1.1.319) ; Protein-Arginine N-Methyltransferases (EC 2.1.1.319)
Language	English
Publishing date	2017-07-01
Publishing country	England
Document type	Journal Article
ZDB-ID	218073-x
ISSN	1756-2651 ; 0021-924X
ISSN (online)	1756-2651
ISSN	0021-924X
DOI	10.1093/jb/mvw102
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