Laetitia Barbollat‐Boutrand

Université Claude Bernard Lyon 1

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Ingrid Masse

Université Claude Bernard Lyon 1

Odile Berthier‐Vergnes

Laboratoire de Génétique Cellulaire

Jérôme Lamartine

Biologie Tissulaire et Ingénierie Thérapeutique

Manale El Kharbili

Université Claude Bernard Lyon 1

Julie Caramel

Centre de Recherche en Cancérologie de Lyon

Stéphane Dalle

Hospices Civils de Lyon

Roxane M. Pommier

Centre Léon Bérard

Maxime Grimont

Centre de Recherche en Cancérologie de Lyon

Arnaud de la Fouchardière

Université Claude Bernard Lyon 1

Gweltaz Agaësse

Université Claude Bernard Lyon 1

Cooperative Institutions

Inserm

Centre National de la Recherche Scientifique

Université Claude Bernard Lyon 1

Centre Léon Bérard

Centre de Recherche en Cancérologie de Lyon

Cancer Research Center

Commissariat à l'Énergie Atomique et aux Énergies Alternatives

Hospices Civils de Lyon

Hôpital Edouard Herriot

Université Grenoble Alpes

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GATA3 inhibits proliferation and induces expression of both early and late differentiation markers in keratinocytes of the human epidermis

Archives of Dermatological Research (2013)

Ingrid Masse Laetitia Barbollat‐Boutrand Manale El Kharbili Odile Berthier‐Vergnes Damien Aubert

Loricrin

GATA3

Epidermis (zoology)

10.1007/s00403-013-1435-5

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Citations (24)

Profil génomique et épigénétique de fibroblastes cutanés de patients atteints par la naevomatose basocellulaire ou syndrome de Gorlin

Annales de Dermatologie et de Vénéréologie (2014)

Aurora Pignata M. Monchanin Laetitia Barbollat‐Boutrand Mheni Ben Abdallah Marielle Martin

10.1016/j.annder.2014.04.143

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Functional interplay between p63 and p53 controls RUNX1 function in the transition from proliferation to differentiation in human keratinocytes

Cell Death and Disease (2012)

Ingrid Masse Laetitia Barbollat‐Boutrand María José Molina Odile Berthier‐Vergnes Nicolas Joly‐Tonetti

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.

RUNX1

Epidermis (zoology)

10.1038/cddis.2012.62

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Citations (44)

Tspan8-β-catenin positive feedback loop promotes melanoma invasion

Oncogene (2019)

Manale El Kharbili Gweltaz Agaësse Laetitia Barbollat‐Boutrand Roxane M. Pommier Arnaud de la Fouchardière

Tumor progression

Beta-catenin

10.1038/s41388-019-0691-z

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Cancer Cell Biomechanical Properties Accompany Tspan8-Dependent Cutaneous Melanoma Invasion

Cancers (2024)

Gaël Runel Noémie Lopez-Ramirez Laetitia Barbollat‐Boutrand Muriel Cario Simon Durand

The intrinsic biomechanical properties of cancer cells remain poorly understood. To decipher whether cell stiffness modulation could increase melanoma cells’ invasive capacity, we performed both in vitro and in vivo experiments exploring cell stiffness by atomic force microscopy (AFM). We correlated stiffness properties with cell morphology adaptation and the molecular mechanisms underlying epithelial-to-mesenchymal (EMT)-like phenotype switching. We found that melanoma cell stiffness reduction was systematically associated with the acquisition of invasive properties in cutaneous melanoma cell lines, human skin reconstructs, and Medaka fish developing spontaneous MAP-kinase-induced melanomas. We observed a systematic correlation of stiffness modulation with cell morphological changes towards mesenchymal characteristic gains. We accordingly found that inducing melanoma EMT switching by overexpressing the ZEB1 transcription factor, a major regulator of melanoma cell plasticity, was sufficient to decrease cell stiffness and transcriptionally induce tetraspanin-8-mediated dermal invasion. Moreover, ZEB1 expression correlated with Tspan8 expression in patient melanoma lesions. Our data suggest that intrinsic cell stiffness could be a highly relevant marker for human cutaneous melanoma development.

10.3390/cancers16040694

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p53 targets TSPAN8 to prevent invasion in melanoma cells

Oncogenesis (2017)

Gweltaz Agaësse Laetitia Barbollat‐Boutrand Manale El Kharbili Odile Berthier‐Vergnes Ingrid Masse

Cutaneous melanoma is a very deadly cancer because of its proclivity to metastasize. Despite the recent development of targeted and immune therapies, patient survival remains low. It is therefore crucial to enhance understanding of the molecular mechanisms underlying invasion. We previously identified tetraspanin 8 (TSPAN8) as an important modulator of melanoma invasiveness, and several of its transcriptional regulators, which affect TSPAN8 expression during melanoma progression toward an invasive stage. This study found that TSPAN8 promoter contains consensus-binding sites for p53 transcription factor. We demonstrated that p53 silencing was sufficient to turn on Tspan8 expression in non-invasive melanoma cells and that p53 acts as a direct transcriptional repressor of TSPAN8. We also showed that p53 modulated matrigel invasion in melanoma cells in a TSPAN8-dependent manner. In conclusion, this study reveals p53 as a negative regulator of Tspan8 expression. As TP53 gene is rarely mutated in melanoma, it was hitherto poorly studied but its role in apoptosis and growth suppression in melanoma is increasingly becoming clear. The study highlights the importance of p53 as a regulator of melanoma invasion and the concept that reactivating p53 could provide a strategy for modulating not only proliferative but also invasive capacity in melanoma treatment.

Matrigel

10.1038/oncsis.2017.11

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Citations (21)

MicroRNA‐23b‐3p regulates human keratinocyte differentiation through repression of TGIF1 and activation of the TGF‐ß–SMAD2 signalling pathway

Experimental Dermatology (2016)

Laetitia Barbollat‐Boutrand Nicolas Joly‐Tonetti Morgan Dos Santos Élodie Metral Aurélie Boher

MicroRNAs (miRNAs) are a class of short non-coding RNAs capable of repressing gene expression at the post-transcriptional level. miRNAs participate in the control of numerous cellular mechanisms, including skin homeostasis and epidermal differentiation. However, few miRNAs involved in these processes have been identified so far in human skin, and the gene networks they control remain largely unknown. Here, we focused on miR-23b-3p, a miRNA that is expressed during the late step of human keratinocyte differentiation. We report that miR-23b-3p silencing modulates epidermal differentiation in human skin reconstructs. The SMAD transcriptional corepressor TGIF1 was identified on bioinformatic analysis as a potential target of miR-23b-3p. Expression analysis and reporter gene assays confirmed direct regulation of TGIF1 expression by miR-23b-3p. Finally, we showed that miR-23-3p was able to activate TGF-ß signalling in human keratinocytes by increasing SMAD2 phosphorylation through TGIF1 repression. Taken together, these data identify miR-23b-3p as a new regulator of human epidermal differentiation in line with TGF-ß signalling.

Corepressor

10.1111/exd.13119

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Citations (28)

Identification des régulateurs transcriptionnels de la tétraspanine-8 dans l’invasion précoce du mélanome cutané

Annales de Dermatologie et de Vénéréologie (2013)

Gweltaz Agaësse Laetitia Barbollat‐Boutrand Eric Sulpice Stéphanie Combe Patricia Obeïd

10.1016/j.annder.2013.09.596

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CDYL2 Epigenetically Regulates MIR124 to Control NF-κB/STAT3-Dependent Breast Cancer Cell Plasticity

iScience (2020)

Maha Siouda Audrey D. Dujardin Laetitia Barbollat‐Boutrand Marco Antonio Mendoza-Parra Benjamin Gibert

Epigenetic deregulation of gene transcription is central to cancer cell plasticity and malignant progression but remains poorly understood. We found that the uncharacterized epigenetic factor chromodomain on Y-like 2 (CDYL2) is commonly over-expressed in breast cancer, and that high CDYL2 levels correlate with poor prognosis. Supporting a functional role for CDYL2 in malignancy, it positively regulated breast cancer cell migration, invasion, stem-like phenotypes, and epithelial-to-mesenchymal transition. CDYL2 regulation of these plasticity-associated processes depended on signaling via p65/NF-κB and STAT3. This, in turn, was downstream of CDYL2 regulation of MIR124 gene transcription. CDYL2 co-immunoprecipitated with G9a/EHMT2 and GLP/EHMT1 and regulated the chromatin enrichment of G9a and EZH2 at MIR124 genes. We propose that CDYL2 contributes to poor prognosis in breast cancer by recruiting G9a and EZH2 to epigenetically repress MIR124 genes, thereby promoting NF-κB and STAT3 signaling, as well as downstream cancer cell plasticity and malignant progression.

10.1016/j.isci.2020.101141

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Citations (30)

Tetraspanin8 expression predicts an increased metastatic risk and is associated with cancer-related death in human cutaneous melanoma

Molecular Cancer (2021)

Odile Berthier‐Vergnes Laetitia Barbollat‐Boutrand Roxane M. Pommier Arnaud de la Fouchardière P. Combemale

10.1186/s12943-021-01429-0

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Citations (3)