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Article ; Online: RNA helicase DDX5 modulates sorafenib sensitivity in hepatocellular carcinoma via the Wnt/β-catenin-ferroptosis axis.

Li, Zhili / Caron de Fromentel, Claude / Kim, Woojun / Wang, Wen-Hung / Sun, Jiazeng / Yan, Bingyu / Utturkar, Sagar / Lanman, Nadia Atallah / Elzey, Bennett D / Yeo, Yoon / Zhang, Hao / Kazemian, Majid / Levrero, Massimo / Andrisani, Ourania

Cell death & disease

2023 Volume 14, Issue 11, Page(s) 786

Abstract: Reduced expression of the RNA helicase DDX5 associated with increased hepatocellular carcinoma (HCC) tumor grade and poor patient survival following treatment with sorafenib. While immunotherapy is the first-line treatment for HCC, sorafenib and other ... ...

Abstract	Reduced expression of the RNA helicase DDX5 associated with increased hepatocellular carcinoma (HCC) tumor grade and poor patient survival following treatment with sorafenib. While immunotherapy is the first-line treatment for HCC, sorafenib and other multi-tyrosine kinase inhibitors (mTKIs) are widely used when immunotherapy is contra-indicated or fails. Herein, we elucidate the role of DDX5 in sensitizing HCC to sorafenib, offering new therapeutic strategies. Treatment of various human HCC cell lines with sorafenib/mTKIs downregulated DDX5 in vitro and in preclinical HCC models. Conversely, DDX5 overexpression reduced the viability of sorafenib-treated cells via ferroptosis, suggesting a role for DDX5 in sorafenib sensitivity. RNAseq of wild-type vs. DDX5-knockdown cells treated with or without sorafenib identified a set of common genes repressed by DDX5 and upregulated by sorafenib. This set significantly overlaps with Wnt signaling genes, including Disheveled-1 (DVL1), an indispensable Wnt activator and prognostic indicator of poor survival for sorafenib-treated patients. DDX5-knockout (DDX5
MeSH term(s)	Humans ; Carcinoma, Hepatocellular/drug therapy ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Sorafenib/pharmacology ; Sorafenib/therapeutic use ; Liver Neoplasms/drug therapy ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Ferroptosis ; RNA Helicases/metabolism ; beta Catenin/metabolism ; Cell Line, Tumor ; Wnt Signaling Pathway
Chemical Substances	Sorafenib (9ZOQ3TZI87) ; RNA Helicases (EC 3.6.4.13) ; beta Catenin
Language	English
Publishing date	2023-11-30
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-023-06302-0
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Article: GNS561, a New Autophagy Inhibitor Active against Cancer Stem Cells in Hepatocellular Carcinoma and Hepatic Metastasis from Colorectal Cancer.

Brun, Sonia / Pascussi, Jean-Marc / Gifu, Elena Patricia / Bestion, Eloïne / Macek-Jilkova, Zuzana / Wang, Guanxiong / Bassissi, Firas / Mezouar, Soraya / Courcambeck, Jérôme / Merle, Philippe / Decaens, Thomas / Pannequin, Julie / Halfon, Philippe / Caron de Fromentel, Claude

Journal of Cancer

2021 Volume 12, Issue 18, Page(s) 5432–5438

Abstract: Patients with advanced hepatocellular carcinoma (HCC) or metastatic colorectal cancer (mCRC) have a very poor prognosis due to the lack of efficient treatments. As observed in several other tumors, the effectiveness of treatments is mainly hampered by ... ...

Abstract	Patients with advanced hepatocellular carcinoma (HCC) or metastatic colorectal cancer (mCRC) have a very poor prognosis due to the lack of efficient treatments. As observed in several other tumors, the effectiveness of treatments is mainly hampered by the presence of a highly tumorigenic sub-population of cancer cells called cancer stem cells (CSCs). Indeed, CSCs are resistant to chemotherapy and radiotherapy and can regenerate the tumor bulk. Hence, innovative drugs that are efficient against both bulk tumor cells and CSCs would likely improve cancer treatment. In this study, we demonstrated that GNS561, a new autophagy inhibitor that induces lysosomal cell death, showed significant activity against not only the whole tumor population but also a sub-population displaying CSC features (high ALDH activity and tumorsphere formation ability) in HCC and in liver mCRC cell lines. These results were confirmed
Language	English
Publishing date	2021-07-13
Publishing country	Australia
Document type	Journal Article
ZDB-ID	2573318-7
ISSN	1837-9664
ISSN	1837-9664
DOI	10.7150/jca.58533
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Article ; Online: The 5th International p63/p73 Workshop: much more than just tumour suppression.

Kadakia, M P / Caron de Fromentel, C / de-Fromentel, C C / Sabapathy, K

Cell death and differentiation

2012 Volume 19, Issue 3, Page(s) 549–550

MeSH term(s)	Animals ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Disease Models, Animal ; Education ; France ; Genome-Wide Association Study ; Humans ; Mice ; Mice, Mutant Strains ; Mutation ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Tumor Protein p73 ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism
Chemical Substances	DNA-Binding Proteins ; Nuclear Proteins ; Phosphoproteins ; TP63 protein, human ; TP73 protein, human ; Trans-Activators ; Transcription Factors ; Trp63 protein, mouse ; Trp73 protein, mouse ; Tumor Protein p73 ; Tumor Suppressor Proteins
Language	English
Publishing date	2012-01-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/cdd.2011.204
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Zs.A 4230: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) 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: Les deux visages de p63, Janus de la famille p53.

Caron de Fromentel, Claude / Aberdam, Edith / Aberdam, Daniel

Medecine sciences : M/S

2012 Volume 28, Issue 4, Page(s) 381–387

Abstract: The TP53 family member TP63 encodes two main isoforms TAp63 and ΔNp63 with distinct, often opposite functions during development and in the adult. ΔNp63 is crucial for the formation of the ectodermal derivatives and epidermis, while TAp63 is essential ... ...

Title translation	The two faces of p63, Janus of the p53 gene family.
Abstract	The TP53 family member TP63 encodes two main isoforms TAp63 and ΔNp63 with distinct, often opposite functions during development and in the adult. ΔNp63 is crucial for the formation of the ectodermal derivatives and epidermis, while TAp63 is essential for heart development. In the adult, ΔNp63 behaves as a cell survival factor, controlling cell proliferation, adhesion and cell differentiation. In contrast, TAp63 is a proapoptotic factor that protects oocytes from genotoxic insults and prevents premature aging of dermal stem cells. In agreement with these activities, TAp63 is often lost and ΔNp63 overexpressed in cancer cells. Because of their opposite and competitive effects, p63 isoforms could be viewed as Janus two faces. The review focuses on the accumulating data on the p63 functions and regulation in the last decade.
MeSH term(s)	Adult ; Animals ; Epidermis/embryology ; Epidermis/metabolism ; Epidermis/physiology ; Gene Expression Regulation, Developmental ; Genes, p53/physiology ; Humans ; Models, Biological ; Multigene Family/physiology ; Protein Isoforms ; Transcription Factors/genetics ; Transcription Factors/physiology ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/physiology
Chemical Substances	Protein Isoforms ; TP63 protein, human ; Transcription Factors ; Tumor Suppressor Proteins
Language	French
Publishing date	2012-04
Publishing country	France
Document type	English Abstract ; Journal Article ; Review
ZDB-ID	632733-3
ISSN	1958-5381 ; 0767-0974
ISSN (online)	1958-5381
ISSN	0767-0974
DOI	10.1051/medsci/2012284015
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Zs.B 2872: Show issues

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Article ; Online: Rôle de la transition épithéliomésenchymateuse dans la progression tumorale.

Ansieau, S / Caron de Fromentel, C / Bastid, J / Morel, A-P / Puisieux, A

Bulletin du cancer

2010 Volume 97, Issue 1, Page(s) 7–15

Abstract: The epithelial-mesenchymal transition (EMT) is a morphogenetic program that converts epithelial into mesenchymal cells during the embryonic development. This mechanism is frequently reactivated during tumor progression and provides cells with motility ... ...

Title translation	Role of the epithelial-mesenchymal transition during tumor progression.
Abstract	The epithelial-mesenchymal transition (EMT) is a morphogenetic program that converts epithelial into mesenchymal cells during the embryonic development. This mechanism is frequently reactivated during tumor progression and provides cells with motility and invasive capabilities favoring the metastatic dissemination from epithelial tumors. Various EMT-inducing transcription factors, such as the TWIST proteins, were also shown to inhibit oncogene-induced fail-safe programs (senescence and apoptosis), thereby promoting the progression from benign to malignant stages. Altogether, these observations suggest that EMT could play an important role in favoring both tumor development and metastatic dissemination.
MeSH term(s)	Animals ; Cell Movement/physiology ; Cell Transdifferentiation/genetics ; Cell Transdifferentiation/physiology ; Cellular Senescence/physiology ; Disease Progression ; Epithelial Cells/pathology ; Humans ; Mesoderm/pathology ; Mice ; Neoplasm Invasiveness ; Neoplasm Metastasis/genetics ; Neoplasm Metastasis/pathology ; Neoplastic Stem Cells/physiology ; Signal Transduction/physiology ; Transcription Factors/physiology ; Transcriptional Activation
Chemical Substances	Transcription Factors
Language	French
Publishing date	2010-01
Publishing country	France
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	213270-9
ISSN	1769-6917 ; 0007-4551
ISSN (online)	1769-6917
ISSN	0007-4551
DOI	10.1684/bdc.2009.1025
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Article: Quand les mutants de p53 se livrent à des trafics !

Caron de Fromentel, Claude / Maguer-Satta, Véronique

Medecine sciences : M/S

2010 Volume 26, Issue 10, Page(s) 814–816

Title translation	When p53 mutants engage in trafficking!.
MeSH term(s)	Cell Division ; Genes, p53 ; Humans ; Mutation ; Neoplasms/genetics ; Neoplasms/pathology ; Neuroblastoma/genetics ; Polymorphism, Genetic
Language	French
Publishing date	2010-10
Publishing country	France
Document type	News
ZDB-ID	632733-3
ISSN	1958-5381 ; 0767-0974
ISSN (online)	1958-5381
ISSN	0767-0974
DOI	10.1051/medsci/20102610814
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Article ; Online: In vitro transformation of primary human hepatocytes: Epigenetic changes and stemness properties.

Pez, Floriane / Gifu, Patricia / Degli-Esposti, Davide / Fares, Nadim / Lopez, Anaïs / Lefrançois, Lydie / Michelet, Maud / Rivoire, Michel / Bancel, Brigitte / Sylla, Bakary S / Herceg, Zdenko / Merle, Philippe / Caron de Fromentel, Claude

Experimental cell research

2019 Volume 384, Issue 2, Page(s) 111643

Abstract: Human hepatocarcinogenesis is a complex process with many unresolved issues, including the cell of origin (differentiated and/or progenitor/stem cells) and the initial steps leading to tumor development. With the aim of providing new tools for studying ... ...

Abstract	Human hepatocarcinogenesis is a complex process with many unresolved issues, including the cell of origin (differentiated and/or progenitor/stem cells) and the initial steps leading to tumor development. With the aim of providing new tools for studying hepatocellular carcinoma initiation and progression, we developed an innovative model based on primary human hepatocytes (PHHs) lentivirus-transduced with SV40
MeSH term(s)	Animals ; Biomarkers, Tumor/genetics ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/pathology ; Cell Differentiation/genetics ; Cell Line ; Cell Line, Tumor ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/pathology ; Epigenesis, Genetic/genetics ; Epithelial-Mesenchymal Transition/genetics ; Female ; HEK293 Cells ; Hepatocytes/pathology ; Humans ; Liver Neoplasms/genetics ; Liver Neoplasms/pathology ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplastic Stem Cells/pathology
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2019-09-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1493-x
ISSN	1090-2422 ; 0014-4827
ISSN (online)	1090-2422
ISSN	0014-4827
DOI	10.1016/j.yexcr.2019.111643
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Zs.A 563: Show issues

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Article ; Online: TP63 gene in stress response and carcinogenesis: a broader role than expected.

Petitjean, Audrey / Hainaut, Pierre / Caron de Fromentel, Claude

Bulletin du cancer

2006 Volume 93, Issue 12, Page(s) E126–35

Abstract: The TP63 gene is a member of the TP53 gene family. In contrast with TP53, this gene is not frequently inactivated by mutation in cancer. Initial experiments with disrupted TP63 have allowed specifying p63 protein a role in the regulation of ... ...

Abstract	The TP63 gene is a member of the TP53 gene family. In contrast with TP53, this gene is not frequently inactivated by mutation in cancer. Initial experiments with disrupted TP63 have allowed specifying p63 protein a role in the regulation of differentiation and morphogenesis in epithelial and mesenchymal tissues. Nevertheless, there is growing evidence that p63 is also involved in oncogenesis through several mechanisms. Indeed, amplification of TP63 is detected in about 25% of squamous cell carcinomas of lung, head and neck and oesophagus. This results in overexpression of a truncated form of p63 (DeltaNp63) that may counteract growth suppression induced by full length p63 (TAp63), as well as by the other family members, p53 and TAp73. Moreover, mice heterozygous for TP63 develop spontaneous tumours. Whereas p53 plays a major role in response to numerous DNA-damaging agents, the involvement of p63 in this process is not well documented. Nevertheless, several groups recently reported that TAp63 can induce cell cycle arrest and apoptosis in DNA-damaged cells, alone or in synergy with chemotherapeutic agents, and thus appears as a chemosensitivity factor. Overall, in addition to non-redundant, specific functions in differentiation and morphogenesis, p63 appears to exert biological functions similar to those of p53 and to take a growing place in oncogenesis and modulation of responses to anti-cancer therapy.
MeSH term(s)	Animals ; Apoptosis ; Cell Differentiation/drug effects ; Cells/drug effects ; Cells/radiation effects ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/physiology ; Genes, p53/physiology ; Humans ; Mice ; Neoplasms/diagnosis ; Neoplasms/genetics ; Protein Isoforms/genetics ; Protein Isoforms/physiology ; Trans-Activators/genetics ; Trans-Activators/physiology ; Transcription Factors ; Tumor Suppressor Protein p53/physiology ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/physiology
Chemical Substances	DNA-Binding Proteins ; Protein Isoforms ; TP63 protein, human ; Trans-Activators ; Transcription Factors ; Tumor Suppressor Protein p53 ; Tumor Suppressor Proteins
Language	English
Publishing date	2006-12
Publishing country	France
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	213270-9
ISSN	1769-6917 ; 0007-4551
ISSN (online)	1769-6917
ISSN	0007-4551
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Article ; Online: Properties of the six isoforms of p63: p53-like regulation in response to genotoxic stress and cross talk with DeltaNp73.

Petitjean, A / Ruptier, C / Tribollet, V / Hautefeuille, A / Chardon, F / Cavard, C / Puisieux, A / Hainaut, P / Caron de Fromentel, C

Carcinogenesis

2008 Volume 29, Issue 2, Page(s) 273–281

Abstract: TP63, a member of the TP53 gene family, encodes two groups of three isoforms (alpha, beta and gamma). The TAp63 isoforms act as transcription factors. The DeltaNp63 isoforms lack the main transcription activation domain and act as dominant-negative ... ...

Abstract	TP63, a member of the TP53 gene family, encodes two groups of three isoforms (alpha, beta and gamma). The TAp63 isoforms act as transcription factors. The DeltaNp63 isoforms lack the main transcription activation domain and act as dominant-negative inhibitors of transactivation (TA) isoforms. To clarify the role of these isoforms and to better understand their functional overlap with p53, we ectopically expressed each p63 isoform in the p53-null hepatocellular carcinoma cell line Hep3B. All TA isoforms, as well as DeltaNp63alpha, had a half-life of <1 h when transiently expressed and were degraded by the proteasome pathway. The most stable form was DeltaNp63gamma, with a half-life of >8 h. As expected, TA isoforms differed in their transcriptional activities toward genes regulated by p53, TAp63gamma being the most active form. In contrast, DeltaNp63 isoforms were transcriptionally inactive on genes studied and inhibited TA isoforms in a dose-dependent manner. When stably expressed in polyclonal cell populations, TAp63beta and gamma isoforms were undetectable. However, when treated with doxorubicin (DOX), p63 proteins rapidly accumulated in the cells. This stabilization was associated with an increase in phosphorylation. Strikingly, in DOX-treated polyclonal populations, increase in TAp63 levels was accompanied by overexpression of DeltaNp73. This observation suggests complex regulatory cross talks between the different isoforms of the p53 family. In conclusion, p63 exhibits several transcriptional and stress-response properties similar to those of p53, suggesting that p63 activities should be taken into consideration in approaches to improve cancer therapies based on genotoxic agents.
MeSH term(s)	Apoptosis ; Cell Adhesion ; Cell Line, Tumor ; DNA Damage ; DNA-Binding Proteins/metabolism ; Gene Expression Regulation, Neoplastic ; Genes, Dominant ; Humans ; Membrane Proteins/chemistry ; Models, Biological ; Nuclear Proteins/metabolism ; Plasmids/metabolism ; Protein Isoforms ; Reverse Transcriptase Polymerase Chain Reaction ; Transcriptional Activation ; Tumor Suppressor Protein p53/physiology ; Tumor Suppressor Proteins/metabolism
Chemical Substances	CKAP4 protein, human ; DNA-Binding Proteins ; Membrane Proteins ; Nuclear Proteins ; Protein Isoforms ; TP53 protein, human ; Tumor Suppressor Protein p53 ; Tumor Suppressor Proteins
Language	English
Publishing date	2008-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603134-1
ISSN	1460-2180 ; 0143-3334
ISSN (online)	1460-2180
ISSN	0143-3334
DOI	10.1093/carcin/bgm258
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Zs.A 1558: Show issues

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Article ; Online: Functional interplay between p63 and p53 controls RUNX1 function in the transition from proliferation to differentiation in human keratinocytes.

Masse, I / Barbollat-Boutrand, L / Molina, M / Berthier-Vergnes, O / Joly-Tonetti, N / Martin, M T / Caron de Fromentel, C / Kanitakis, J / Lamartine, J

Cell death & disease

2012 Volume 3, Page(s) e318

Abstract: The interfollicular epidermis is continuously renewed, thanks to a regulated balance between proliferation and differentiation. The ΔNp63 transcription factor has a key role in the control of this process. It has been shown that ΔNp63 directly regulates ... ...

Abstract	The interfollicular epidermis is continuously renewed, thanks to a regulated balance between proliferation and differentiation. The ΔNp63 transcription factor has a key role in the control of this process. It has been shown that ΔNp63 directly regulates Runt-related transcription factor 1 (RUNX1) transcription factor expression in mouse keratinocytes. The present study showed for the first time that RUNX1 is expressed in normal human interfollicular epidermis and that its expression is tightly regulated during the transition from proliferation to differentiation. It demonstrated that ΔNp63 directly binds two different RUNX1 regulatory DNA sequences and modulates RUNX1 expression differentially in proliferative or differentiated human keratinocytes. It also showed that the regulation of RUNX1 expression by ΔNp63 is dependent on p53 and that this coregulation relies on differential binding and activation of RUNX1 regulatory sequences by ΔNp63 and p53. We also found that RUNX1 inhibits keratinocyte proliferation and activates directly the expression of KRT1, a critical actor in early keratinocyte differentiation. Finally, we described that RUNX1 expression, similar to ΔNp63 and p53, was strongly expressed and downregulated in basal cell carcinomas and squamous cell carcinomas respectively. Taken together, these data shed light on the importance of tight control of the functional interplay between ΔNp63 and p53 in regulating RUNX1 transcription factor expression for proper regulation of interfollicular epidermal homeostasis.
MeSH term(s)	Cell Differentiation ; Cell Proliferation ; Cells, Cultured ; Core Binding Factor Alpha 2 Subunit/genetics ; Core Binding Factor Alpha 2 Subunit/metabolism ; Down-Regulation ; Epidermal Cells ; Epidermis/metabolism ; Humans ; Keratinocytes/cytology ; Keratinocytes/metabolism ; Membrane Proteins/metabolism ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	CKAP4 protein, human ; Core Binding Factor Alpha 2 Subunit ; Membrane Proteins ; RUNX1 protein, human ; Tumor Suppressor Protein p53
Language	English
Publishing date	2012-06-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/cddis.2012.62
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