MAML1 drives Notch and Hedgehog oncogenic pathways by inhibiting Itch activity in triple-negative breast cancer Article Swipe
Sabrina Zema
,
Francesca Di Fazio
,
Maria Pelullo
,
Sara Di Savino
,
Bruna Cerbelli
,
Martina Leopizzi
,
Laura Di Magno
,
Carmine Nicoletti
,
Giovanna Peruzzi
,
Daniel D’Andrea
,
Maria V. Giuli
,
Samantha Cialfi
,
Biagio Palmisano
,
Alice Turdo
,
Rocco Palermo
,
Giulia D'Amati
,
Gianluca Canettieri
,
Antongiulio Faggiano
,
Lucia Di Marcotullio
,
Matilde Todaro
,
Isabella Screpanti
,
Claudio Talora
,
Saula Checquolo
,
Diana Bellavia
·
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1038/s41418-025-01613-5
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1038/s41418-025-01613-5
Triple-negative breast cancer (TNBC) is an aggressive and heterogeneous breast cancer subtype with poor patient outcomes. TNBC heterogeneity arises from multiple dysregulated pathways, including Notch and Hedgehog, which contribute to tumor initiation, progression, and drug resistance. Identifying common molecular regulators of TNBC aggressiveness is crucial for developing effective therapeutic strategies. Here, we demonstrate that the transcriptional coactivator MAML1 drives TNBC aggressiveness by regulating Notch1 and Gli1 stability through the E3 ubiquitin ligase Itch, functioning as an Itch-negative regulator. Mechanistically, MAML1 interacts with Itch via its PPQY motif and promotes K63-linked self-ubiquitylation of Itch, deregulating its expression/activity. Using a Maml1-deficient mouse model, we reveal an inverse correlation between MAML1 and Itch levels, where the loss of MAML1 stabilizes Itch and suppresses Notch1 and Gli1 activity. Conversely, MAML1 upregulation enhances Notch1 and Gli1 expression, driving accelerated TNBC tumor growth and faster multiorgan metastasis in vivo. Accordingly, we show that MAML1 is overexpressed in a cohort of TNBC patients, and the combined overexpression of MAML1/Notch1 and MAML1/Gli1 correlates with poor clinical outcomes by in silico analysis. Our findings establish a dual role for MAML1 as a transcriptional coactivator and a post-translational regulator of Itch, thereby amplifying Notch and Hedgehog oncogenic signaling. This study uncovers MAML1 as a key driver of TNBC progression and a potential therapeutic target for fighting TNBC aggressiveness and heterogeneity.
Related Topics
Concepts
GLI1
Cancer research
Breast cancer
Hedgehog
Downregulation and upregulation
Notch signaling pathway
Coactivator
Medicine
Hedgehog signaling pathway
Suppressor
Ubiquitin ligase
Regulator
Carcinogenesis
Biology
Triple-negative breast cancer
Metastasis
Cancer
Sonic hedgehog
Smoothened
Ubiquitin
Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1038/s41418-025-01613-5
- OA Status
- hybrid
- References
- 67
- OpenAlex ID
- https://openalex.org/W7106439923
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W7106439923Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1038/s41418-025-01613-5Digital Object Identifier
- Title
-
MAML1 drives Notch and Hedgehog oncogenic pathways by inhibiting Itch activity in triple-negative breast cancerWork title
- Type
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articleOpenAlex work type
- Language
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enPrimary language
- Publication year
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2025Year of publication
- Publication date
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2025-11-21Full publication date if available
- Authors
-
Sabrina Zema, Francesca Di Fazio, Maria Pelullo, Sara Di Savino, Bruna Cerbelli, Martina Leopizzi, Laura Di Magno, Carmine Nicoletti, Giovanna Peruzzi, Daniel D’Andrea, Maria V. Giuli, Samantha Cialfi, Biagio Palmisano, Alice Turdo, Rocco Palermo, Giulia D'Amati, Gianluca Canettieri, Antongiulio Faggiano, Lucia Di Marcotullio, Matilde Todaro, Isabella Screpanti, Claudio Talora, Saula Checquolo, Diana BellaviaList of authors in order
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https://doi.org/10.1038/s41418-025-01613-5Publisher landing page
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YesWhether a free full text is available
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hybridOpen access status per OpenAlex
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https://doi.org/10.1038/s41418-025-01613-5Direct OA link when available
- Concepts
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GLI1, Cancer research, Breast cancer, Hedgehog, Downregulation and upregulation, Notch signaling pathway, Coactivator, Medicine, Hedgehog signaling pathway, Suppressor, Ubiquitin ligase, Regulator, Carcinogenesis, Biology, Triple-negative breast cancer, Metastasis, Cancer, Sonic hedgehog, Smoothened, UbiquitinTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
0Total citation count in OpenAlex
- References (count)
-
67Number of works referenced by this work
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| primary_location.raw_type | journal-article |
| primary_location.license_id | https://openalex.org/licenses/cc-by |
| primary_location.is_accepted | True |
| primary_location.is_published | True |
| primary_location.raw_source_name | Cell Death & Differentiation |
| primary_location.landing_page_url | https://doi.org/10.1038/s41418-025-01613-5 |
| publication_date | 2025-11-21 |
| publication_year | 2025 |
| referenced_works | https://openalex.org/W3128646645, https://openalex.org/W4311588716, https://openalex.org/W1058934875, https://openalex.org/W2069624136, https://openalex.org/W1508234976, https://openalex.org/W2158421326, https://openalex.org/W2955046614, https://openalex.org/W2128160901, https://openalex.org/W1964032340, https://openalex.org/W2044626217, https://openalex.org/W2113724558, https://openalex.org/W2163798555, https://openalex.org/W2736866570, https://openalex.org/W3029224395, https://openalex.org/W2982337925, https://openalex.org/W2087898777, https://openalex.org/W2013248580, https://openalex.org/W1974096298, https://openalex.org/W2082983359, https://openalex.org/W1993775542, https://openalex.org/W2547826289, https://openalex.org/W2070268999, https://openalex.org/W2117754842, https://openalex.org/W3012099338, https://openalex.org/W2913266125, https://openalex.org/W2285812380, https://openalex.org/W2093230990, https://openalex.org/W2738729362, https://openalex.org/W2029093937, https://openalex.org/W2036385874, https://openalex.org/W2783850750, https://openalex.org/W2898679675, https://openalex.org/W2936511529, https://openalex.org/W3012253666, https://openalex.org/W3037127899, https://openalex.org/W2940947272, https://openalex.org/W2038164707, https://openalex.org/W2943589671, https://openalex.org/W2105481533, https://openalex.org/W2059194853, https://openalex.org/W2028622010, https://openalex.org/W2134805829, https://openalex.org/W2062487788, https://openalex.org/W2794222046, https://openalex.org/W1975206161, https://openalex.org/W2331898954, https://openalex.org/W1971166655, https://openalex.org/W3212723841, https://openalex.org/W2509400142, https://openalex.org/W2140843725, https://openalex.org/W2020553511, https://openalex.org/W2902679159, https://openalex.org/W2170725518, https://openalex.org/W2925631060, https://openalex.org/W2007514087, https://openalex.org/W2465716717, https://openalex.org/W2924616875, https://openalex.org/W4386895445, https://openalex.org/W2094328127, https://openalex.org/W4283764180, https://openalex.org/W2972637542, https://openalex.org/W4286854843, https://openalex.org/W2068430088, https://openalex.org/W2920863604, https://openalex.org/W2005895632, https://openalex.org/W2795989238, https://openalex.org/W2607211817 |
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| abstract_inverted_index.cancer | 3, 11 |
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| abstract_inverted_index.growth | 137 |
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