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Article: E2F1 mediates competition, proliferation and response to cisplatin in cohabitating resistant and sensitive ovarian cancer cells.

Valdivia, Andres / Cowan, Matthew / Cardenas, Horacio / Isac, Ana Maria / Zhao, Guangyuan / Huang, Hao / Matei, Daniela

2024 Volume 14, Page(s) 1304691

Abstract: Background: Tumor heterogeneity is one of the key factors leading to chemo-resistance relapse. It remains unknown how resistant cancer cells influence sensitive cells during cohabitation and growth within a heterogenous tumors. The goal of our study was ...

Abstract	Background: Tumor heterogeneity is one of the key factors leading to chemo-resistance relapse. It remains unknown how resistant cancer cells influence sensitive cells during cohabitation and growth within a heterogenous tumors. The goal of our study was to identify driving factors that mediate the interactions between resistant and sensitive cancer cells and to determine the effects of cohabitation on both phenotypes. Methods: We used isogenic ovarian cancer (OC) cell lines pairs, sensitive and resistant to platinum: OVCAR5 vs. OVCAR5 CisR and PE01 vs. PE04, respectively, to perform long term direct culture and to study the phenotypical changes of the interaction of these cells. Results: Long term direct co-culture of sensitive and resistant OC cells promoted proliferation (p < 0.001) of sensitive cells and increased the proportion of cells in the G1 and S cell cycle phase in both PE01 and OVCAR5 cells. Direct co-culture led to a decrease in the IC50 to platinum in the cisplatin-sensitive cells (5.92 µM to 2.79 µM for PE01, and from 2.05 µM to 1.51 µM for OVCAR5). RNAseq analysis of co-cultured cells showed enrichment of Cell Cycle Control, Cyclins and Cell Cycle Regulation pathways. The transcription factor E2F1 was predicted as the main effector responsible for the transcriptomic changes in sensitive cells. Western blot and qRT-PCR confirmed upregulation of E2F1 in co-cultured vs monoculture. Furthermore, an E2F1 inhibitor reverted the increase in proliferation rate induced by co-culture to baseline levels. Conclusion: Our data suggest that long term cohabitation of chemo-sensitive and -resistant cancer cells drive sensitive cells to a higher proliferative state, more responsive to platinum. Our results reveal an unexpected effect caused by direct interactions between cancer cells with different proliferative rates and levels of platinum resistance, modelling competition between cells in heterogeneous tumors.
Language	English
Publishing date	2024-01-26
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2024.1304691
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: N6-Methyladenosine RNA Modifications Regulate the Response to Platinum Through Nicotinamide N-methyltransferase.

Huang, Hao / Zhao, Guangyuan / Cardenas, Horacio / Valdivia, Andres Felipe / Wang, Yinu / Matei, Daniela

Molecular cancer therapeutics

2023 Volume 22, Issue 3, Page(s) 393–405

Abstract: Development of resistance to platinum (Pt) in ovarian cancer remains a major clinical challenge. Here we focused on identifying epitranscriptomic modifications linked to Pt resistance. Fat mass and obesity-associated protein (FTO) is a N6-methyladenosine ...

Abstract	Development of resistance to platinum (Pt) in ovarian cancer remains a major clinical challenge. Here we focused on identifying epitranscriptomic modifications linked to Pt resistance. Fat mass and obesity-associated protein (FTO) is a N6-methyladenosine (m6A) RNA demethylase that we recently described as a tumor suppressor in ovarian cancer. We hypothesized that FTO-induced removal of m6A marks regulates the cellular response of ovarian cancer cells to Pt and is linked to the development of resistance. To study the involvement of FTO in the cellular response to Pt, we used ovarian cancer cells in which FTO was knocked down via short hairpin RNA or overexpressed and Pt-resistant (Pt-R) models derived through repeated cycles of exposure to Pt. We found that FTO was significantly downregulated in Pt-R versus sensitive ovarian cancer cells. Forced expression of FTO, but not of mutant FTO, increased sensitivity to Pt in vitro and in vivo (P < 0.05). Increased numbers of γ-H2AX foci, measuring DNA double-strand breaks, and increased apoptosis were observed after exposure to Pt in FTO-overexpressing versus control cells. Through integrated RNA sequencing and MeRIP sequencing, we identified and validated the enzyme nicotinamide N-methyltransferase (NNMT), as a new FTO target linked to Pt response. NNMT was upregulated and demethylated in FTO-overexpressing cells. Treatment with an NNMT inhibitor or NNMT knockdown restored sensitivity to Pt in FTO-overexpressing cells. Our results support a new function for FTO-dependent m6A RNA modifications in regulating the response to Pt through NNMT, a newly identified RNA methylated gene target.
MeSH term(s)	Female ; Humans ; Adenosine/chemistry ; Alpha-Ketoglutarate-Dependent Dioxygenase FTO/genetics ; Alpha-Ketoglutarate-Dependent Dioxygenase FTO/metabolism ; Nicotinamide N-Methyltransferase ; Ovarian Neoplasms/drug therapy ; Ovarian Neoplasms/metabolism ; Platinum/pharmacology ; Platinum/therapeutic use ; RNA/chemistry ; RNA/metabolism
Chemical Substances	Adenosine (K72T3FS567) ; Alpha-Ketoglutarate-Dependent Dioxygenase FTO (EC 1.14.11.33) ; FTO protein, human (EC 1.14.11.33) ; Nicotinamide N-Methyltransferase (EC 2.1.1.1) ; Platinum (49DFR088MY) ; RNA (63231-63-0) ; N-methyladenosine (CLE6G00625)
Language	English
Publishing date	2023-01-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-22-0278
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Zs.A 5750: Show issues

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Article: Distribution of the acoustic occurrence of dolphins during the summers 2011 to 2015 in the Upper Gulf of California, Mexico.

Cárdenas Hinojosa, Gustavo / de la Cueva, Horacio / Gerrodette, Tim / Jaramillo-Legorreta, Armando M

PeerJ

2020 Volume 8, Page(s) e9121

Abstract: Baseline knowledge of spatial and temporal distribution patterns is essential for cetacean management and conservation. Such knowledge is particularly important in areas where gillnet fishing occurs, as the Upper Gulf of California, which increases the ... ...

Abstract	Baseline knowledge of spatial and temporal distribution patterns is essential for cetacean management and conservation. Such knowledge is particularly important in areas where gillnet fishing occurs, as the Upper Gulf of California, which increases the probability of bycatch of cetaceans. In this area, the vaquita porpoise (
Language	English
Publishing date	2020-05-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2703241-3
ISSN	2167-8359
ISSN	2167-8359
DOI	10.7717/peerj.9121
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Article ; Online: Nanoparticle Targeting in Chemo-Resistant Ovarian Cancer Reveals Dual Axis of Therapeutic Vulnerability Involving Cholesterol Uptake and Cell Redox Balance.

Wang, Yinu / Calvert, Andrea E / Cardenas, Horacio / Rink, Jonathon S / Nahotko, Dominik / Qiang, Wenan / Ndukwe, C Estelle / Chen, Fukai / Keathley, Russell / Zhang, Yaqi / Cheng, Ji-Xin / Thaxton, C Shad / Matei, Daniela

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

2024 Volume 11, Issue 13, Page(s) e2305212

Abstract: Platinum (Pt)-based chemotherapy is the main treatment for ovarian cancer (OC); however, most patients develop Pt resistance (Pt-R). This work shows that Pt-R OC cells increase intracellular cholesterol through uptake via the HDL receptor, scavenger ... ...

Abstract	Platinum (Pt)-based chemotherapy is the main treatment for ovarian cancer (OC); however, most patients develop Pt resistance (Pt-R). This work shows that Pt-R OC cells increase intracellular cholesterol through uptake via the HDL receptor, scavenger receptor type B-1 (SR-B1). SR-B1 blockade using synthetic cholesterol-poor HDL-like nanoparticles (HDL NPs) diminished cholesterol uptake leading to cell death and inhibition of tumor growth. Reduced cholesterol accumulation in cancer cells induces lipid oxidative stress through the reduction of glutathione peroxidase 4 (GPx4) leading to ferroptosis. In turn, GPx4 depletion induces decreased cholesterol uptake through SR-B1 and re-sensitizes OC cells to Pt. Mechanistically, GPx4 knockdown causes lower expression of the histone acetyltransferase EP300, leading to reduced deposition of histone H3 lysine 27 acetylation (H3K27Ac) on the sterol regulatory element binding transcription factor 2 (SREBF2) promoter and suppressing expression of this key transcription factor involved in the regulation of cholesterol metabolism. SREBF2 downregulation leads to decreased SR-B1 expression and diminished cholesterol uptake. Thus, chemoresistance and cancer cell survival under high ROS burden obligates high GPx4 and SR-B1 expression through SREBF2. Targeting SR-B1 to modulate cholesterol uptake inhibits this axis and causes ferroptosis in vitro and in vivo in Pt-R OC.
MeSH term(s)	Humans ; Female ; Scavenger Receptors, Class B/metabolism ; Cholesterol/metabolism ; Transcription Factors/metabolism ; Nanoparticles ; Ovarian Neoplasms/drug therapy ; Oxidation-Reduction
Chemical Substances	Scavenger Receptors, Class B ; Cholesterol (97C5T2UQ7J) ; Transcription Factors
Language	English
Publishing date	2024-01-23
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2808093-2
ISSN	2198-3844 ; 2198-3844
ISSN (online)	2198-3844
ISSN	2198-3844
DOI	10.1002/advs.202305212
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Article ; Online: Preclinical Evaluation of NTX-301, a Novel DNA Hypomethylating Agent in Ovarian Cancer.

Wang, Yinu / Situ, Xiaolei / Cardenas, Horacio / Siu, Ellie / Alhunayan, Sayedabdulrazzaq A / Keathley, Russell / Tanner, Edward / Wei, Jian-Jun / Tan, Yuying / Prabhu Dessai, Chinmayee Vallabh / Cheng, Ji-Xin / Matei, Daniela

Clinical cancer research : an official journal of the American Association for Cancer Research

2024 Volume 30, Issue 6, Page(s) 1175–1188

Abstract: Purpose: DNA methylation causes silencing of tumor-suppressor and differentiation-associated genes, being linked to chemoresistance. Previous studies demonstrated that hypomethylating agents (HMA) resensitize ovarian cancer to chemotherapy. NTX-301 is a ...

Abstract	Purpose: DNA methylation causes silencing of tumor-suppressor and differentiation-associated genes, being linked to chemoresistance. Previous studies demonstrated that hypomethylating agents (HMA) resensitize ovarian cancer to chemotherapy. NTX-301 is a highly potent and orally bioavailable HMA, in early clinical development. Experimental design: The antitumor effects of NTX-301 were studied in ovarian cancer models by using cell viability, stemness and ferroptosis assays, RNA sequencing, lipidomic analyses, and stimulated Raman spectroscopy. Results: Ovarian cancer cells (SKOV3, IC50 = 5.08 nmol/L; OVCAR5 IC50 = 3.66 nmol/L) were highly sensitive to NTX-301 compared with fallopian tube epithelial cells. NTX-301 downregulated expression of DNA methyltransferases 1-3 and induced transcriptomic reprogramming with 15,000 differentially expressed genes (DEG, P < 0.05). Among them, Gene Ontology enrichment analysis identified regulation of fatty acid biosynthesis and molecular functions related to aldehyde dehydrogenase (ALDH) and oxidoreductase, known features of cancer stem cells. Low-dose NTX-301 reduced the ALDH(+) cell population and expression of stemness-associated transcription factors. Stearoyl-coenzyme A desaturase 1 (SCD), which regulates production of unsaturated fatty acids (UFA), was among the top DEG downregulated by NTX-301. NTX-301 treatment decreased levels of UFA and increased oxidized lipids, and this was blunted by deferoxamine, indicating cell death via ferroptosis. NTX-301-induced ferroptosis was rescued by oleic acid. In vivo, monotherapy with NTX-301 significantly inhibited ovarian cancer and patient-derived xenograft growth (P < 0.05). Decreased SCD levels and increased oxidized lipids were detected in NTX-301-treated xenografts. Conclusions: NTX-301 is active in ovarian cancer models. Our findings point to a new mechanism by which epigenetic blockade disrupts lipid homeostasis and promotes cancer cell death.
MeSH term(s)	Humans ; Female ; Cell Line, Tumor ; Ovarian Neoplasms/drug therapy ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/pathology ; Enzyme Inhibitors/therapeutic use ; Aldehyde Dehydrogenase/genetics ; DNA ; Lipids/therapeutic use
Chemical Substances	Enzyme Inhibitors ; Aldehyde Dehydrogenase (EC 1.2.1.3) ; DNA (9007-49-2) ; Lipids
Language	English
Publishing date	2024-01-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-23-2368
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Zs.A 4223: Show issues

Location:
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bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Metabolic reprogramming from glycolysis to fatty acid uptake and beta-oxidation in platinum-resistant cancer cells

Yuying Tan / Junjie Li / Guangyuan Zhao / Kai-Chih Huang / Horacio Cardenas / Yinu Wang / Daniela Matei / Ji-Xin Cheng

Nature Communications, Vol 13, Iss 1, Pp 1-

2022 Volume 16

Abstract: Metabolic reprogramming is associated with cancer initiation, progression and resistance to therapy. Here, the authors show that metabolic reprogramming from glycolysis to fatty acid uptake and beta-oxidation is associated with cancer-cell platinum-based ...

Abstract	Metabolic reprogramming is associated with cancer initiation, progression and resistance to therapy. Here, the authors show that metabolic reprogramming from glycolysis to fatty acid uptake and beta-oxidation is associated with cancer-cell platinum-based chemotherapy resistance.
Keywords	Science ; Q
Language	English
Publishing date	2022-08-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Information policies and libraries, beginning at the beginning

Horacio Cardenas Zardoni

Biblios, Vol 0, Iss 54, Pp 88-

2015 Volume 94

Abstract: Information policies do not occur in the abstract, as part of a theory or science of information, they do not exist in isolation, isolated from the organized action of society as a whole. While the productive sector may have a clear perspective of where ... ...

Abstract	Information policies do not occur in the abstract, as part of a theory or science of information, they do not exist in isolation, isolated from the organized action of society as a whole. While the productive sector may have a clear perspective of where they want to go, the field of information policy corresponds to national governments. In order to achieve the goals that Information policy has raised in the information society, they necessarily have to enroll as part of public policies, especially those related to social development strategies, and with each country's educational effort. The library as a social entity has always served as a repository, making available materials that meet the information needs of the population, as such it should be seen as an integral part of public and information policy.
Keywords	Políticas de información ; Políticas públicas ; Desarrollo social ; Políticas educativas ; Bibliotecas ; Bibliography. Library science. Information resources ; Z
Subject code	306
Language	Spanish
Publishing date	2015-02-01T00:00:00Z
Publisher	University Library System, University of Pittsburgh
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Ovarian Cancer-Why Lipids Matter.

Zhao, Guangyuan / Cardenas, Horacio / Matei, Daniela

Cancers

2019 Volume 11, Issue 12

Abstract: This review highlights recent advances in the understanding of the relevance of altered lipid metabolic pathways contributing to the poor prognosis of high grade serous ovarian cancer, as they relate to cancer metastasis and cancer stemness. Increased ... ...

Abstract	This review highlights recent advances in the understanding of the relevance of altered lipid metabolic pathways contributing to the poor prognosis of high grade serous ovarian cancer, as they relate to cancer metastasis and cancer stemness. Increased lipid uptake regulated by the receptor CD36 and the transport protein FABP4 has been implicated in ovarian cancer metastasis. The symbiotic relationship between ovarian cancer cells and adipocytes was shown to be important for sustaining widespread peritoneal and omental metastasis. Increased lipogenesis dependent on the fatty acid desaturase SCD1 was detected in ovarian cancer stem cells. Furthermore, response to therapy, specifically to platinum, was linked to increased fatty acid biogenesis, while the survival of drug tolerant cells was shown to depend on lipid peroxidation. These recent findings suggest that lipids are necessary elements supporting oncogenic signaling and the energetic needs of rapidly proliferating cancer cells. New strategies targeting key enzymes involved in lipid uptake or utilization in cancer cells have been shown to exert anti-tumor effects and are being developed as cancer interventions in combination with chemotherapy or immunotherapy.
Language	English
Publishing date	2019-11-26
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers11121870
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Article ; Online: Are public policies to school libraries necessary? Latin America situation

Horacio Cárdenas Zardoni

Biblios, Vol 0, Iss 48, Pp 21-

2012 Volume 30

Abstract: School libraries are one of te main resources to enhance learning in students in the educational system in any nation. Every country invests important amounts of money in library resources in schools, which have the quality of stay and increase, as time ... ...

Abstract	School libraries are one of te main resources to enhance learning in students in the educational system in any nation. Every country invests important amounts of money in library resources in schools, which have the quality of stay and increase, as time passes, the school library may have an important collection to offer to students. Despite its undeniable value as contributor to the education of millions of citizens studying in the latin american schools, its potencial and ability are far from being used to its maximum. The reason for this is the lack of public policies that incorporate it to the education process.
Keywords	Bibliotecas escolares ; Políticas públicas ; Política educativa ; Políticas de información ; Bibliography. Library science. Information resources ; Z
Language	Spanish
Publishing date	2012-08-01T00:00:00Z
Publisher	University Library System, University of Pittsburgh
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Metabolic reprogramming from glycolysis to fatty acid uptake and beta-oxidation in platinum-resistant cancer cells.

Tan, Yuying / Li, Junjie / Zhao, Guangyuan / Huang, Kai-Chih / Cardenas, Horacio / Wang, Yinu / Matei, Daniela / Cheng, Ji-Xin

Nature communications

2022 Volume 13, Issue 1, Page(s) 4554

Abstract: Increased glycolysis is considered as a hallmark of cancer. Yet, cancer cell metabolic reprograming during therapeutic resistance development is under-studied. Here, through high-throughput stimulated Raman scattering imaging and single cell analysis, we ...

Abstract	Increased glycolysis is considered as a hallmark of cancer. Yet, cancer cell metabolic reprograming during therapeutic resistance development is under-studied. Here, through high-throughput stimulated Raman scattering imaging and single cell analysis, we find that cisplatin-resistant cells exhibit increased fatty acids (FA) uptake, accompanied by decreased glucose uptake and lipogenesis, indicating reprogramming from glucose to FA dependent anabolic and energy metabolism. A metabolic index incorporating glucose derived anabolism and FA uptake correlates linearly to the level of cisplatin resistance in ovarian cancer (OC) cell lines and primary cells. The increased FA uptake facilitates cancer cell survival under cisplatin-induced oxidative stress by enhancing beta-oxidation. Consequently, blocking beta-oxidation by a small molecule inhibitor combined with cisplatin or carboplatin synergistically suppresses OC proliferation in vitro and growth of patient-derived xenografts in vivo. Collectively, these findings support a rapid detection method of cisplatin-resistance at single cell level and a strategy for treating cisplatin-resistant tumors.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Cell Line, Tumor ; Cisplatin/pharmacology ; Cisplatin/therapeutic use ; Drug Resistance, Neoplasm ; Fatty Acids/pharmacology ; Female ; Glucose/metabolism ; Glycolysis ; Humans ; Ovarian Neoplasms/pathology ; Platinum/pharmacology
Chemical Substances	Antineoplastic Agents ; Fatty Acids ; Platinum (49DFR088MY) ; Glucose (IY9XDZ35W2) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2022-08-05
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-32101-w
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