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Book ; Online ; Thesis: Unraveling metabolic mechanisms underlying the folate pathway and targeting antifolate resistance via synthetic lethality

Pirona, Anna Chiara [Verfasser] / Mayer, Matthias P. [Akademischer Betreuer]

2022

Author's details	Anna Chiara Pirona ; Betreuer: Matthias Mayer
Keywords	Biowissenschaften, Biologie ; Life Science, Biology
Subject code	sg570
Language	English
Publisher	Universitätsbibliothek Heidelberg
Publishing place	Heidelberg
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article ; Online: Process for an efficient lentiviral cell transduction.

Pirona, Anna Chiara / Oktriani, Risky / Boettcher, Michael / Hoheisel, Jörg D

Biology methods & protocols

2020 Volume 5, Issue 1, Page(s) bpaa005

Abstract: The combination of lentiviruses with techniques such as CRISPR-Cas9 has resulted in efficient and precise processes for targeted genome modification. An often-limiting aspect, however, is the efficiency of cell transduction. Low efficiencies with ... ...

Abstract	The combination of lentiviruses with techniques such as CRISPR-Cas9 has resulted in efficient and precise processes for targeted genome modification. An often-limiting aspect, however, is the efficiency of cell transduction. Low efficiencies with particular cell types and/or the high complexity of lentiviral libraries can cause insufficient representation. Here, we present a protocol that yielded substantial increases in transduction efficiency in various cell lines in comparison to several other procedures.
Language	English
Publishing date	2020-02-10
Publishing country	England
Document type	Journal Article
ISSN	2396-8923
ISSN (online)	2396-8923
DOI	10.1093/biomethods/bpaa005
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Article ; Online: TAZ facilitates breast tumor growth by promoting an immune-suppressive tumor microenvironment.

Gershoni, Anat / Hassin, Ori / Nataraj, Nishanth Belugali / Baruch, Sivan / Avioz-Seligman, Adi / Pirona, Anna Chiara / Fellus-Alyagor, Liat / Meir Salame, Tomer / Mukherjee, Saptaparna / Mallel, Giuseppe / Yarden, Yosef / Aylon, Yael / Oren, Moshe

Molecular oncology

2023 Volume 17, Issue 12, Page(s) 2675–2693

Abstract: The core Hippo pathway module consists of a tumour-suppressive kinase cascade that inhibits the transcriptional coactivators Yes-associated protein (YAP) and WW domain-containing transcription regulator protein 1 (WWTR1; also known as TAZ). When the ... ...

Abstract	The core Hippo pathway module consists of a tumour-suppressive kinase cascade that inhibits the transcriptional coactivators Yes-associated protein (YAP) and WW domain-containing transcription regulator protein 1 (WWTR1; also known as TAZ). When the Hippo pathway is downregulated, as often occurs in breast cancer, YAP/TAZ activity is induced. To elaborate the roles of TAZ in triple-negative breast cancer (TNBC), we depleted Taz in murine TNBC 4T1 cells, using either CRISPR/Cas9 or small hairpin RNA (shRNA). TAZ-depleted cells and their controls, harbouring wild-type levels of TAZ, were orthotopically injected into the mammary fat pads of syngeneic BALB/c female mice, and mice were monitored for tumour growth. TAZ depletion resulted in smaller tumours compared to the tumours generated by control cells, in line with the notion that TAZ functions as an oncogene in breast cancer. Tumours, as well as their corresponding in vitro cultured cells, were then subjected to gene expression profiling by RNA sequencing (RNA-seq). Interestingly, pathway analysis of the RNA-seq data indicated a TAZ-dependent enrichment of 'Inflammatory Response', a pathway correlated with TAZ expression levels also in human breast cancer tumours. Specifically, the RNA-seq analysis predicted a significant depletion of regulatory T cells (Tregs) in TAZ-deficient tumours, which was experimentally validated by the staining of tumour sections and by quantitative cytometry by time of flight (CyTOF). Strikingly, the differences in tumour size were completely abolished in immune-deficient mice, demonstrating that the immune-modulatory capacity of TAZ is critical for its oncogenic activity in this setting. Cytokine array analysis of conditioned medium from cultured cells revealed that TAZ increased the abundance of a small group of cytokines, including plasminogen activator inhibitor 1 (Serpin E1; also known as PAI-1), CCN family member 4 (CCN4; also known as WISP-1) and interleukin-23 (IL-23), suggesting a potential mechanistic explanation for its in vivo immunomodulatory effect. Together, our results imply that TAZ functions in a non-cell-autonomous manner to modify the tumour immune microenvironment and dampen the anti-tumour immune response, thereby facilitating tumour growth.
MeSH term(s)	Animals ; Female ; Humans ; Mice ; Hippo Signaling Pathway ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Transcription Factors/metabolism ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/pathology ; Tumor Microenvironment ; Transcriptional Coactivator with PDZ-Binding Motif Proteins/metabolism
Chemical Substances	Intracellular Signaling Peptides and Proteins ; Transcription Factors ; WWTR1 protein, human ; Transcriptional Coactivator with PDZ-Binding Motif Proteins
Language	English
Publishing date	2023-10-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	2415106-3
ISSN	1878-0261 ; 1574-7891
ISSN (online)	1878-0261
ISSN	1574-7891
DOI	10.1002/1878-0261.13525
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Article ; Online: Preparation of highly multiplexed small RNA sequencing libraries.

Persson, Helena / Søkilde, Rolf / Pirona, Anna Chiara / Rovira, Carlos

BioTechniques

2017 Volume 63, Issue 2, Page(s) 57–64

Abstract: MicroRNAs (miRNAs) are ~22-nucleotide-long small non-coding RNAs that regulate the expression of protein-coding genes by base pairing to partially complementary target sites, preferentially located in the 3´ untranslated region (UTR) of target mRNAs. The ...

Abstract	MicroRNAs (miRNAs) are ~22-nucleotide-long small non-coding RNAs that regulate the expression of protein-coding genes by base pairing to partially complementary target sites, preferentially located in the 3´ untranslated region (UTR) of target mRNAs. The expression and function of miRNAs have been extensively studied in human disease, as well as the possibility of using these molecules as biomarkers for prognostication and treatment guidance. To identify and validate miRNAs as biomarkers, their expression must be screened in large collections of patient samples. Here, we develop a scalable protocol for the rapid and economical preparation of a large number of small RNA sequencing libraries using dual indexing for multiplexing. Combined with the use of off-the-shelf reagents, more samples can be sequenced simultaneously on large-scale sequencing platforms at a considerably lower cost per sample. Sample preparation is simplified by pooling libraries prior to gel purification, which allows for the selection of a narrow size range while minimizing sample variation. A comparison with publicly available data from benchmarking of miRNA analysis platforms showed that this method captures absolute and differential expression as effectively as commercially available alternatives.
MeSH term(s)	Cell Line, Tumor ; Gene Expression Profiling/economics ; Gene Expression Profiling/methods ; Gene Library ; High-Throughput Nucleotide Sequencing/economics ; High-Throughput Nucleotide Sequencing/methods ; Humans ; MicroRNAs/genetics ; Sequence Analysis, RNA/economics ; Sequence Analysis, RNA/methods ; Transcriptome
Chemical Substances	MicroRNAs
Language	English
Publishing date	2017-08-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	48453-2
ISSN	1940-9818 ; 0736-6205
ISSN (online)	1940-9818
ISSN	0736-6205
DOI	10.2144/000114574
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Article ; Online: p53 deficient breast cancer cells reprogram preadipocytes toward tumor-protective immunomodulatory cells.

Hassin, Ori / Sernik, Miriam / Seligman, Adi / Vogel, Felix C E / Wellenstein, Max D / Smollich, Joachim / Halperin, Coral / Pirona, Anna Chiara / Toledano, Liron Nomi / Caballero, Carolina Dehesa / Schlicker, Lisa / Salame, Tomer-Meir / Sarusi Portuguez, Avital / Aylon, Yael / Scherz-Shouval, Ruth / Geiger, Tamar / de Visser, Karin E / Schulze, Almut / Oren, Moshe

Proceedings of the National Academy of Sciences of the United States of America

2023 Volume 120, Issue 52, Page(s) e2311460120

Abstract: ... ...

Abstract	The
MeSH term(s)	Humans ; Female ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Breast Neoplasms/pathology ; Genes, p53 ; Adipose Tissue/metabolism ; Adipocytes/metabolism ; Tumor Microenvironment/genetics
Chemical Substances	Tumor Suppressor Protein p53
Language	English
Publishing date	2023-12-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2311460120
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Article ; Online: Detailed Functional Characterization of a Waist-Hip Ratio Locus in 7p15.2 Defines an Enhancer Controlling Adipocyte Differentiation.

Castillejo-Lopez, Casimiro / Pjanic, Milos / Pirona, Anna Chiara / Hetty, Susanne / Wabitsch, Martin / Wadelius, Claes / Quertermous, Thomas / Arner, Erik / Ingelsson, Erik

iScience

2019 Volume 20, Page(s) 42–59

Abstract: We combined CAGE sequencing in human adipocytes during differentiation with data from genome-wide association studies to identify an enhancer in the SNX10 locus on chromosome 7, presumably involved in body fat distribution. Using reporter assays and ... ...

Abstract	We combined CAGE sequencing in human adipocytes during differentiation with data from genome-wide association studies to identify an enhancer in the SNX10 locus on chromosome 7, presumably involved in body fat distribution. Using reporter assays and CRISPR-Cas9 gene editing in human cell lines, we characterized the role of the enhancer in adipogenesis. The enhancer was active during adipogenesis and responded strongly to insulin and isoprenaline. The allele associated with increased waist-hip ratio in human genetic studies was associated with higher enhancer activity. Mutations of the enhancer resulted in less adipocyte differentiation. RNA sequencing of cells with disrupted enhancer showed reduced expression of established adipocyte markers, such as ADIPOQ and LPL, and identified CHI3L1 on chromosome 1 as a potential gene involved in adipocyte differentiation. In conclusion, we identified and characterized an enhancer in the SNX10 locus and outlined its plausible mechanisms of action and downstream targets.
Language	English
Publishing date	2019-09-10
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2019.09.006
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Article ; Online: Tumor Reliance on Cytosolic versus Mitochondrial One-Carbon Flux Depends on Folate Availability.

Lee, Won Dong / Pirona, Anna Chiara / Sarvin, Boris / Stern, Alon / Nevo-Dinur, Keren / Besser, Elazar / Sarvin, Nikita / Lagziel, Shoval / Mukha, Dzmitry / Raz, Shachar / Aizenshtein, Elina / Shlomi, Tomer

Cell metabolism

2020 Volume 33, Issue 1, Page(s) 190–198.e6

Abstract: Folate metabolism supplies one-carbon (1C) units for biosynthesis and methylation and has long been a target for cancer chemotherapy. Mitochondrial serine catabolism is considered the sole contributor of folate-mediated 1C units in proliferating cancer ... ...

Abstract	Folate metabolism supplies one-carbon (1C) units for biosynthesis and methylation and has long been a target for cancer chemotherapy. Mitochondrial serine catabolism is considered the sole contributor of folate-mediated 1C units in proliferating cancer cells. Here, we show that under physiological folate levels in the cell environment, cytosolic serine-hydroxymethyltransferase (SHMT1) is the predominant source of 1C units in a variety of cancers, while mitochondrial 1C flux is overly repressed. Tumor-specific reliance on cytosolic 1C flux is associated with poor capacity to retain intracellular folates, which is determined by the expression of SLC19A1, which encodes the reduced folate carrier (RFC). We show that silencing SHMT1 in cells with low RFC expression impairs pyrimidine biosynthesis and tumor growth in vivo. Overall, our findings reveal major diversity in cancer cell utilization of the cytosolic versus mitochondrial folate cycle across tumors and SLC19A1 expression as a marker for increased reliance on SHMT1.
MeSH term(s)	Animals ; CRISPR-Cas Systems/genetics ; Carbon Cycle/genetics ; Cell Line ; Cytosol/metabolism ; Folic Acid/genetics ; Folic Acid/metabolism ; Glycine Hydroxymethyltransferase/deficiency ; Glycine Hydroxymethyltransferase/genetics ; Glycine Hydroxymethyltransferase/metabolism ; Humans ; Male ; Mice ; Mice, Inbred NOD ; Mice, Knockout ; Mice, SCID ; Mitochondria/metabolism ; Neoplasms/metabolism ; Neoplasms/pathology ; Reduced Folate Carrier Protein/genetics ; Reduced Folate Carrier Protein/metabolism
Chemical Substances	Reduced Folate Carrier Protein ; SLC19A1 protein, human ; Folic Acid (935E97BOY8) ; Glycine Hydroxymethyltransferase (EC 2.1.2.1) ; SHMT protein, human (EC 2.1.2.1)
Language	English
Publishing date	2020-12-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2020.12.002
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Zs.A 6169: Show issues

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Article ; Online: Cross-talk between mutant p53 and p62/SQSTM1 augments cancer cell migration by promoting the degradation of cell adhesion proteins.

Proceedings of the National Academy of Sciences of the United States of America

2022 Volume 119, Issue 17, Page(s) e2119644119

Abstract: Missense mutations in the p53 tumor suppressor abound in human cancer. Common (“hotspot”) mutations endow mutant p53 (mutp53) proteins with oncogenic gain of function (GOF), including enhanced cell migration and invasiveness, favoring cancer progression. ...

Abstract	Missense mutations in the p53 tumor suppressor abound in human cancer. Common (“hotspot”) mutations endow mutant p53 (mutp53) proteins with oncogenic gain of function (GOF), including enhanced cell migration and invasiveness, favoring cancer progression. GOF is usually attributed to transcriptional effects of mutp53. To elucidate transcription-independent effects of mutp53, we characterized the protein interactome of the p53R273H mutant in cells derived from pancreatic ductal adenocarcinoma (PDAC), where p53R273H is the most frequent p53 mutant. We now report that p53R273H, but not the p53R175H hotspot mutant, interacts with SQSTM1/p62 and promotes cancer cell migration and invasion in a p62-dependent manner. Mechanistically, the p53R273H-p62 axis drives the proteasomal degradation of several cell junction–associated proteins, including the gap junction protein Connexin 43, facilitating scattered cell migration. Concordantly, down-regulation of Connexin 43 augments PDAC cell migration, while its forced overexpression blunts the promigratory effect of the p53R273H-p62 axis. These findings define a mechanism of mutp53 GOF.
MeSH term(s)	Cell Adhesion/genetics ; Cell Line, Tumor ; Cell Movement/genetics ; Genes, p53 ; Humans ; Mutation ; Pancreatic Neoplasms/genetics ; Sequestosome-1 Protein/genetics ; Sequestosome-1 Protein/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	SQSTM1 protein, human ; Sequestosome-1 Protein ; Tumor Suppressor Protein p53
Language	English
Publishing date	2022-04-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2119644119
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Article ; Online: Refinement of breast cancer molecular classification by miRNA expression profiles.

Søkilde, Rolf / Persson, Helena / Ehinger, Anna / Pirona, Anna Chiara / Fernö, Mårten / Hegardt, Cecilia / Larsson, Christer / Loman, Niklas / Malmberg, Martin / Rydén, Lisa / Saal, Lao / Borg, Åke / Vallon-Christerson, Johan / Rovira, Carlos

BMC genomics

2019 Volume 20, Issue 1, Page(s) 503

Abstract: Background: Accurate classification of breast cancer using gene expression profiles has contributed to a better understanding of the biological mechanisms behind the disease and has paved the way for better prognostication and treatment prediction.: ... ...

Abstract	Background: Accurate classification of breast cancer using gene expression profiles has contributed to a better understanding of the biological mechanisms behind the disease and has paved the way for better prognostication and treatment prediction. Results: We found that miRNA profiles largely recapitulate intrinsic subtypes. In the case of HER2-enriched tumors a small set of miRNAs including the HER2-encoded mir-4728 identifies the group with very high specificity. We also identified differential expression of the miR-99a/let-7c/miR-125b miRNA cluster as a marker for separation of the Luminal A and B subtypes. High expression of this miRNA cluster is linked to better overall survival among patients with Luminal A tumors. Correlation between the miRNA cluster and their precursor LINC00478 is highly significant suggesting that its expression could help improve the accuracy of present day's signatures. Conclusions: We show here that miRNA expression can be translated into mRNA profiles and that the inclusion of miRNA information facilitates the molecular diagnosis of specific subtypes, in particular the clinically relevant sub-classification of luminal tumors.
MeSH term(s)	Breast Neoplasms/classification ; Breast Neoplasms/genetics ; Cluster Analysis ; Cohort Studies ; Computational Biology/methods ; Gene Expression Profiling ; Humans ; MicroRNAs/genetics ; Unsupervised Machine Learning
Chemical Substances	MIRN125 microRNA, human ; MIRN99 microRNA, human ; MicroRNAs ; mirnlet7 microRNA, human
Language	English
Publishing date	2019-06-17
Publishing country	England
Document type	Journal Article
ISSN	1471-2164
ISSN (online)	1471-2164
DOI	10.1186/s12864-019-5887-7
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Article ; Online: Frequent miRNA-convergent fusion gene events in breast cancer.

Persson, Helena / Søkilde, Rolf / Häkkinen, Jari / Pirona, Anna Chiara / Vallon-Christersson, Johan / Kvist, Anders / Mertens, Fredrik / Borg, Åke / Mitelman, Felix / Höglund, Mattias / Rovira, Carlos

Nature communications

2017 Volume 8, Issue 1, Page(s) 788

Abstract: Studies of fusion genes have mainly focused on the formation of fusions that result in the production of hybrid proteins or, alternatively, on promoter-switching events that put a gene under the control of aberrant signals. However, gene fusions may also ...

Abstract	Studies of fusion genes have mainly focused on the formation of fusions that result in the production of hybrid proteins or, alternatively, on promoter-switching events that put a gene under the control of aberrant signals. However, gene fusions may also disrupt the transcriptional control of genes that are encoded in introns downstream of the breakpoint. By ignoring structural constraints of the transcribed fusions, we highlight the importance of a largely unexplored function of fusion genes. Here, we show, using breast cancer as an example, that miRNA host genes are specifically enriched in fusion genes and that many different, low-frequency, 5' partners may deregulate the same miRNA irrespective of the coding potential of the fusion transcript. These results indicate that the concept of recurrence, defined by the rate of functionally important aberrations, needs to be revised to encompass convergent fusions that affect a miRNA independently of transcript structure and protein-coding potential.Fusion gene research traditionally focuses on fusions that result in hybrid proteins or promoter switching events. Here, the authors demonstrate enrichment of fusions in miRNA host genes in breast cancer, highlighting that disparate fusions could have convergent impact on miRNA.
MeSH term(s)	Breast Neoplasms/genetics ; Female ; Gene Expression Regulation, Neoplastic/genetics ; Gene Fusion/genetics ; Humans ; Introns ; MicroRNAs/genetics ; Promoter Regions, Genetic ; RNA, Messenger/genetics
Chemical Substances	MicroRNAs ; RNA, Messenger
Language	English
Publishing date	2017-10-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2041-1723
ISSN (online)	2041-1723
DOI	10.1038/s41467-017-01176-1
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