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Article: p16: cycling off the beaten path.

Buj, Raquel / Aird, Katherine M

Molecular & cellular oncology

2019 Volume 6, Issue 6, Page(s) e1677140

Abstract: ... ...

Abstract	p16
Language	English
Publishing date	2019-10-15
Publishing country	United States
Document type	Journal Article
ISSN	2372-3556
ISSN	2372-3556
DOI	10.1080/23723556.2019.1677140
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Loss of p16: A Bouncer of the Immunological Surveillance?

Leon, Kelly E / Tangudu, Naveen Kumar / Aird, Katherine M / Buj, Raquel

Life (Basel, Switzerland)

2021 Volume 11, Issue 4

Abstract: ... ...

Abstract	p16
Language	English
Publishing date	2021-04-02
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2662250-6
ISSN	2075-1729
ISSN	2075-1729
DOI	10.3390/life11040309
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Suppression of p16 alleviates the senescence-associated secretory phenotype.

Buj, Raquel / Leon, Kelly E / Anguelov, Marlyn A / Aird, Katherine M

Aging

2021 Volume 13, Issue 3, Page(s) 3290–3312

Abstract: Oncogene-induced senescence (OIS) is characterized by increased expression of the cell cycle inhibitor p16, leading to a hallmark cell cycle arrest. Suppression of p16 in this context drives proliferation, senescence bypass, and contributes to ... ...

Abstract	Oncogene-induced senescence (OIS) is characterized by increased expression of the cell cycle inhibitor p16, leading to a hallmark cell cycle arrest. Suppression of p16 in this context drives proliferation, senescence bypass, and contributes to tumorigenesis. OIS cells are also characterized by the expression and secretion of a widely variable group of factors collectively termed the senescence-associated secretory phenotype (SASP). The SASP can be both beneficial and detrimental and affects the microenvironment in a highly context-dependent manner. The relationship between p16 suppression and the SASP remains unclear. Here, we show that knockdown of p16 decreases expression of the SASP factors and pro-inflammatory cytokines
MeSH term(s)	Cell Cycle Checkpoints/genetics ; Cell Line, Tumor ; Cellular Senescence/genetics ; Cyclin-Dependent Kinase Inhibitor p16/genetics ; Cyclin-Dependent Kinase Inhibitor p16/metabolism ; Gene Knockdown Techniques ; Humans ; Interleukin-6/genetics ; Interleukin-6/metabolism ; Interleukin-8/genetics ; Interleukin-8/metabolism ; Lamin Type B/metabolism
Chemical Substances	CDKN2A protein, human ; CXCL8 protein, human ; Cyclin-Dependent Kinase Inhibitor p16 ; IL6 protein, human ; Interleukin-6 ; Interleukin-8 ; Lamin Type B
Language	English
Publishing date	2021-02-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.202640
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Article: Deoxyribonucleotide Triphosphate Metabolism in Cancer and Metabolic Disease.

Buj, Raquel / Aird, Katherine M

Frontiers in endocrinology

2018 Volume 9, Page(s) 177

Abstract: The maintenance of a healthy deoxyribonucleotide triphosphate (dNTP) pool is critical for the proper replication and repair of both nuclear and mitochondrial DNA. Temporal, spatial, and ratio imbalances of the four dNTPs have been shown to have a ... ...

Abstract	The maintenance of a healthy deoxyribonucleotide triphosphate (dNTP) pool is critical for the proper replication and repair of both nuclear and mitochondrial DNA. Temporal, spatial, and ratio imbalances of the four dNTPs have been shown to have a mutagenic and cytotoxic effect. It is, therefore, essential for cell homeostasis to maintain the balance between the processes of dNTP biosynthesis and degradation. Multiple oncogenic signaling pathways, such as c-Myc, p53, and mTORC1 feed into dNTP metabolism, and there is a clear role for dNTP imbalances in cancer initiation and progression. Additionally, multiple chemotherapeutics target these pathways to inhibit nucleotide synthesis. Less is understood about the role for dNTP levels in metabolic disorders and syndromes and whether alterations in dNTP levels change cancer incidence in these patients. For instance, while deficiencies in some metabolic pathways known to play a role in nucleotide synthesis are pro-tumorigenic (e.g., p53 mutations), others confer an advantage against the onset of cancer (G6PD). More recent evidence indicates that there are changes in nucleotide metabolism in diabetes, obesity, and insulin resistance; however, whether these changes play a mechanistic role is unclear. In this review, we will address the complex network of metabolic pathways, whereby cells can fuel dNTP biosynthesis and catabolism in cancer, and we will discuss the potential role for this pathway in metabolic disease.
Language	English
Publishing date	2018-04-18
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2018.00177
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Article: Tumor-Associated Macrophages Expand Chemoresistant, Ovarian Cancer Stem-Like Cells.

Sharrow, Allison C / Ho, Madeline / Dua, Aakriti / Buj, Raquel / Blenman, Kim R M / Orsulic, Sandra / Buckanovich, Ronald / Aird, Katherine M / Wu, Lily

bioRxiv : the preprint server for biology

2023

Abstract: The persistence of ovarian cancer stem-like cells (OvCSCs) after chemotherapy resistance has been implicated in relapse. However, the ability of these relatively quiescent cells to produce the robust tumor regrowth necessary for relapse remains an enigma. ...

Abstract	The persistence of ovarian cancer stem-like cells (OvCSCs) after chemotherapy resistance has been implicated in relapse. However, the ability of these relatively quiescent cells to produce the robust tumor regrowth necessary for relapse remains an enigma. Since normal stem cells exist in a niche, and tumor-associated macrophages (TAMs) are the highest abundance immune cell within ovarian tumors, we hypothesized that TAMs may influence OvCSC proliferation. To test this, we optimized OvCSC enrichment by sphere culture and in vitro polarization of monocytes to a TAM-like M2 phenotype. Using cocultures that permitted the exchange of only soluble factors, we found that M2 macrophages increased the proliferation of sphere cells. Longer-term exposure (5-7 days) to soluble TAM factors led to retention of some stem cell features by OvCSCs but loss of others, suggesting that TAMs may support an intermediate stemness phenotype in OvCSCs. Although TAM coculture decreased the percentage of OvCSCs surviving chemotherapy, it increased the overall number. We therefore sought to determine the influence of this interaction on chemotherapy efficacy in vivo and found that inhibiting macrophages improved chemotherapy response. Comparing the gene expression changes in OvCSCs cocultured with TAMs to publicly available patient data identified 34 genes upregulated in OvCSCs by exposure to soluble TAM factors whose expression correlates with outcome. Overall, these data suggest that TAMs may influence OvCSC proliferation and impact therapeutic response.
Language	English
Publishing date	2023-10-16
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.07.17.549067
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Article ; Online: Overexpression of oncogenic H-Ras in hTERT-immortalized and SV40-transformed human cells targets replicative and specialized DNA polymerases for depletion.

Tsao, Wei-Chung / Buj, Raquel / Aird, Katherine M / Sidorova, Julia M / Eckert, Kristin A

PloS one

2021 Volume 16, Issue 5, Page(s) e0251188

Abstract: DNA polymerases play essential functions in replication fork progression and genome maintenance. DNA lesions and drug-induced replication stress result in up-regulation and re-localization of specialized DNA polymerases η and κ. Although oncogene ... ...

Abstract	DNA polymerases play essential functions in replication fork progression and genome maintenance. DNA lesions and drug-induced replication stress result in up-regulation and re-localization of specialized DNA polymerases η and κ. Although oncogene activation significantly alters DNA replication dynamics, causing replication stress and genome instability, little is known about DNA polymerase expression and regulation in response to oncogene activation. Here, we investigated the consequences of mutant H-RAS G12V overexpression on the regulation of DNA polymerases in h-TERT immortalized and SV40-transformed human cells. Focusing on DNA polymerases associated with the replication fork, we demonstrate that DNA polymerases are depleted in a temporal manner in response to H-RAS G12V overexpression. The polymerases targeted for depletion, as cells display markers of senescence, include the Pol α catalytic subunit (POLA1), Pol δ catalytic and p68 subunits (POLD1 and POLD3), Pol η, and Pol κ. Both transcriptional and post-transcriptional mechanisms mediate this response. Pol η (POLH) depletion is sufficient to induce a senescence-like growth arrest in human foreskin fibroblast BJ5a cells, and is associated with decreased Pol α expression. Using an SV-40 transformed cell model, we observed cell cycle checkpoint signaling differences in cells with H-RasG12V-induced polymerase depletion, as compared to Pol η-deficient cells. Our findings contribute to our understanding of cellular events following oncogene activation and cellular transformation.
MeSH term(s)	Cell Line ; DNA Damage/genetics ; DNA Repair/genetics ; DNA Replication/genetics ; DNA-Directed DNA Polymerase/genetics ; Fibroblasts/metabolism ; Genes, ras/genetics ; Humans
Chemical Substances	DNA-Directed DNA Polymerase (EC 2.7.7.7)
Language	English
Publishing date	2021-05-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0251188
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: ATR promotes mTORC1 activation via de novo cholesterol synthesis in p16-low cancer cells.

Tangudu, Naveen Kumar / Huang, Zhentai / Fang, Richard / Buj, Raquel / Uboveja, Apoorva / Cole, Aidan R / Happe, Cassandra / Sun, Mai / Gelhaus, Stacy L / MacDonald, Matthew L / Hempel, Nadine / Snyder, Nathaniel W / Aird, Katherine M

bioRxiv : the preprint server for biology

2023

Abstract: DNA damage and cellular metabolism are intricately linked with bidirectional feedback. Two of the main effectors of the DNA damage response and control of cellular metabolism are ATR and mTORC1, respectively. Prior work has placed ATR upstream of mTORC1 ... ...

Abstract	DNA damage and cellular metabolism are intricately linked with bidirectional feedback. Two of the main effectors of the DNA damage response and control of cellular metabolism are ATR and mTORC1, respectively. Prior work has placed ATR upstream of mTORC1 during replication stress, yet the direct mechanism for how mTORC1 is activated in this context remain unclear. We previously published that p16-low cells have mTORC1 hyperactivation, which in part promotes their proliferation. Using this model, we found that ATR, but not ATM, is upstream of mTORC1 activation via
Language	English
Publishing date	2023-10-27
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.10.27.564195
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Article: De novo purine metabolism is a metabolic vulnerability of cancers with low p16 expression.

Tangudu, Naveen Kumar / Buj, Raquel / Wang, Hui / Wang, Jiefei / Cole, Aidan R / Uboveja, Apoorva / Fang, Richard / Amalric, Amandine / Sajjakulnukit, Peter / Lyons, Maureen A / Cooper, Kristine / Hempel, Nadine / Snyder, Nathaniel W / Lyssiotis, Costas A / Chandran, Uma R / Aird, Katherine M

bioRxiv : the preprint server for biology

2023

Abstract: p16 is a tumor suppressor encoded by ... ...

Abstract	p16 is a tumor suppressor encoded by the
Language	English
Publishing date	2023-09-23
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.07.15.549149
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Article: ATM inhibition synergizes with fenofibrate in high grade serous ovarian cancer cells.

Chen, Chi-Wei / Buj, Raquel / Dahl, Erika S / Leon, Kelly E / Aird, Katherine M

Heliyon

2020 Volume 6, Issue 9, Page(s) e05097

Abstract: While therapies targeting deficiencies in the homologous recombination (HR) pathway are emerging as the standard treatment for high grade serous ovarian cancer (HGSOC) patients, this strategy is limited to the ~50% of patients with a deficiency in this ... ...

Abstract	While therapies targeting deficiencies in the homologous recombination (HR) pathway are emerging as the standard treatment for high grade serous ovarian cancer (HGSOC) patients, this strategy is limited to the ~50% of patients with a deficiency in this pathway. Therefore, patients with HR-proficient tumors are likely to be resistant to these therapies and require alternative strategies. We found that the HR gene Ataxia Telangiectasia Mutated (ATM) is wildtype and its activity is upregulated in HGSOC compared to normal fallopian tube tissue. Interestingly, multiple pathways related to metabolism are inversely correlated with
Language	English
Publishing date	2020-09-29
Publishing country	England
Document type	Journal Article
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2020.e05097
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Article ; Online: Loss of p16

Kelly E. Leon / Naveen Kumar Tangudu / Katherine M. Aird / Raquel Buj

Life, Vol 11, Iss 309, p

A Bouncer of the Immunological Surveillance?

2021 Volume 309

Abstract: p16 INK4A (hereafter called p16) is an important tumor suppressor protein frequently suppressed in human cancer and highly upregulated in many types of senescence. Although its role as a cell cycle regulator is very well delineated, little is known about ...

Abstract	p16 INK4A (hereafter called p16) is an important tumor suppressor protein frequently suppressed in human cancer and highly upregulated in many types of senescence. Although its role as a cell cycle regulator is very well delineated, little is known about its other non-cell cycle-related roles. Importantly, recent correlative studies suggest that p16 may be a regulator of tissue immunological surveillance through the transcriptional regulation of different chemokines, interleukins and other factors secreted as part of the senescence-associated secretory phenotype (SASP). Here, we summarize the current evidence supporting the hypothesis that p16 is a regulator of tumor immunity.
Keywords	senescence-associated secretory phenotype (SASP) ; senescence ; cell-cycle ; melanoma ; pancreatic adenocarcinoma ; tumor infiltration ; Science ; Q
Language	English
Publishing date	2021-04-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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