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Marselina Arshakyan on Muck Rack

Marselina Arshakyan

As seen in: Nature
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Articles

Antagonistic SMAD2/3 control of TIMP-1, VEGF-A, and hypoxia signaling in myofibroblasts shapes histotype-specific angiogenesis in lung cancer

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By Natalia Díaz-Valdivia, Paula Duch, Rafael Ikemori, Amelia Parker, Marselina Arshakyan, Alejandro Llorente, Alejandro García Bernardo, José Rodríguez-Rojas, Josep Lluís Carrasco, Danielle Park, Erik Sahai, Cristina Fillat, Manel Juan, Ernest Nadal, Noemí Reguart, Derek C. Radisky, Oriol Casanovas, Jordi Alcaraz
| Nature Verified
Abstract Non-small cell lung cancer (NSCLC) exhibits disparate responses to anti-angiogenic therapies between its two major histologic subtypes, lung adenocarcinoma (LUAD) and squamous cell carcinoma (LUSC), suggesting a histotype-dependent angiogenesis regulation. Tumor-associated fibroblasts (TAFs) exhibit an activated/myofibroblast-like phenotype in NSCLC, and are emerging as major regulators of tumor progression; yet, their role in controlling angiogenesis in NSCLC remains undefined.
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3D collagen migration patterns reveal a SMAD3-dependent and TGF-β1-independent mechanism of recruitment for tumour-associated fibroblasts in lung adenocarcinoma | British Journal of Cancer

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By Natalia Díaz-Valdivia, Alejandro Llorente, Alejandro García Bernardo, Marselina Arshakyan, Carlos Borau, José Carlos Ruffinelli, Ernest Nadal, José M. García-Aznar
| Nature Verified
Abstract Background The TGF-β1 transcription factor SMAD3 is epigenetically repressed in tumour-associated fibroblasts (TAFs) from lung squamous cell carcinoma (SCC) but not adenocarcinoma (ADC) patients, which elicits a compensatory increase in SMAD2 that renders SCC-TAFs less fibrotic. Here we examined the effects of altered SMAD2/3 in fibroblast migration and its impact on the desmoplastic stroma formation in lung cancer.
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