Ana Luísa Silva

Assistant Professor

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Ciência Vitae

Ana Luísa Silva

Assistant Professor

Bio

Participation in Católica Medical School

Tutor for the curricular unit Growth and Development I (IMM)
Tutor for the curricular unit Regulation and Integration (IMM)
Coordinator of the curricular unit Molecular Biology - (BSc in Systems and Cognitive Neuroscience)
Principal Investigator of the Molecular Endocrinology and Signaling Laboratory

Field of Work

Endocrinology| Molecular Signaling| Oncobiology | Gene expression | Targeted Therapies

Professional Activity

Católica Medical School
CatólicaMed Platform - Centre for Interdisciplinary Research in Health

Education

Degree in Biochemistry — Faculdade de Ciências da Universidade de Lisboa, Portugal
PhD in Biochemistry- Molecular Genetics — Faculdade de Ciências da Universidade de Lisboa, Portugal

Professional Career Summary

Ana Luísa Silva is a Portuguese researcher and academic specializing in molecular endocrinology and oncology. She holds a PhD in Biochemistry, with a specialization in molecular genetics, from the Faculty of Sciences of the University of Lisbon.

She is currently an Assistant Professor at Católica Medical School, Universidade Católica Portuguesa, and leads the Molecular Endocrinology and Signaling Laboratory within the CatólicaMed Platform of the Centre for Interdisciplinary Research in Health.

Beyond her research, Ana Luísa is committed to education and mentoring. She teaches and supervises medical, master’s, and doctoral students in molecular biology, genetics, oncology, and endocrinology. Her career bridges basic science and clinical application, reflecting her dedication to advancing the diagnosis and treatment of endocrine tumors.

The Molecular Endocrinology and Signaling Laboratory

Ana Luísa Silva’s Lab focuses on understanding the molecular pathways that drive endocrine tumors—particularly of the thyroid and pituitary glands—with the goal of developing novel therapeutic approaches to improve patient outcomes.

Our group investigates the molecular mechanisms that regulate endocrine cell function and drive endocrine tumor progression, with a particular focus on radioiodine-refractory thyroid carcinomas and aggressive pituitary adenomas.

A key area of our work is the Sodium Iodide Symporter (NIS), a protein essential for iodine uptake in thyroid cells and critical to the success of radioiodine therapy. We investigate how extracellular matrix components and tumor microenvironment signals affect NIS function and localization, offering insights that may guide future strategies to restore or enhance treatment efficacy in iodine-refractory thyroid cancers.

Pituitary research lines are led by Prof. Pedro Marques, focusing on the molecular determinants of tumor invasiveness, resistance to conventional therapies, and biomarker discovery for clinically aggressive pituitary adenomas.

We study how disruptions in cell signaling, epithelial adhesion, and the inflammatory microenvironment influence tumor aggressiveness and therapy resistance. Our research integrates transcriptomic and proteomic profiling, molecular and cell biology, biochemistry, and live-cell imaging to identify actionable therapeutic targets.

Using thyroid and pituitary tumor-derived cell models, functional in vitro assays, and drug screening platforms, we explore strategies to restore sodium-iodide symporter (NIS) function or block inflammation-related pathways. Our ultimate goal is to contribute to the development of personalized therapies for endocrine neoplasia.

Languages

Portuguese | English

Programs:

Integrated Master's in Medicine
BSc in Systems and Cognitive Neuroscience

Publications

Paper

The Role of Programmed Cell Death Ligand 1 Expression in Pituitary Tumours: Lessons from the Current Literature

Ana Luísa Silva (with Lopes-Pinto, Mariana). 2024. Neuroendocrinology

Universidade Católica launches webinars to facilitate integration and boost academic success

Isaura Martins wins Pain Research Grant with project on spinal cord injuries

NERQ Training on Responsible Conduct of Research (RCR)

Ana Luísa Silva

Ana Luísa Silva

Bio

The Role of Programmed Cell Death Ligand 1 Expression in Pituitary Tumours: Lessons from the Current Literature

Therapeutical Usefulness of PD-1/PD-L1 Inhibitors in Aggressive or Metastatic Pituitary Tumours

A integridade das adesões célula-célula é um determinante chave para a expressão funcional de NIS.

Usefulness of a clinicopathological classification in predicting treatment-related outcomes and multimodal therapeutic approaches in pituitary adenoma patients: retrospective analysis on a Portuguese cohort of 129 patients from a tertiary pituitary center

A role for RAC1 in the rescue of functional NIS expression at the plasma membrane induced by MEK inhibition.

Análise de polimorfismos no gene NLRP1 na Diabetes mellitus tipo1.

MAPK e RAC1 exercem efeitos opostos na expressão de NIS em células de carcinoma da tiróide.

Modulação da expressão funcional de NIS: Uma comparação entre tecido tiroideu e mamário.

The microenvironment of pituitary adenomas: biological, clinical and therapeutical implications

Um papel para a tirosina cinase SRC na expressão funcional de NIS na membrana plasmática.

Analysis of NIS Plasma Membrane Interactors Discloses Key Regulation by a SRC/RAC1/PAK1/PIP5K/EZRIN Pathway with Potential Implications for Radioiodine Re-Sensitization Therapy in Thyroid Cancer

Gß¿-mediated signaling regulates NIS abundance at the plasma membrane

MAPK Inhibition Requires Active RAC1 Signaling to Effectively Improve Iodide Uptake by Thyroid Follicular Cells

Modulação combinada das vias de sinalização RAC1 e MAPK para potenciar a captação de iodo radioactivo.

Inflammatory Microenvironment Modulation of Alternative Splicing in Cancer: A Way to Adapt

Targeting RAC1 signaling to potentiate the positive effect of MAPK pathway inhibition on radioiodine uptake

TNFα-mediated activation of NF-κB downregulates sodium-iodide symporter expression in thyroid cells

A role for the small GTPases RAC1 and RAC1b in the modulation of NIS expression: potentiation of therapy with radioactive iodine in differentiated thyroid carcinoma

Antagonistic effects of RAC1 and tumor-related RAC1b on NIS expression in thyroid

Identificação de novos moduladores da abundância de NIS na membrana plasmática

Impacto do TNF-alpha na ativação de vias pró-proliferativas e de sobrevivência em linhas celulares de tiróide.

Modulation of Sodium Iodide Symporter expression by tumor-associated signaling pathways.

Unravelling the Signaling Pathways Influencing the NIS regulation

Impact of RAC1/1b signalling on Sodium Iodide symporter regulation

RAC1b overexpression stimulates proliferation and NF-kB-mediated anti-apoptotic signaling in thyroid cancer cells

Extending the Impact of RAC1b Overexpression to Follicular Thyroid Carcinomas.

RAC1b overexpression in papillary thyroid carcinomas: an activator of NF-kB pathway that contributes to thyroid tumorigenesis?

RAC1b: A New Player in the Scenario of Thyroid Tumorigenesis?

Coexistence of paraganglioma/pheochromocytoma and papillary thyroid carcinoma: a four-case series analysis

Expression of Human Hemojuvelin (HJV) Is Tightly Regulated by Two Upstream Open Reading Frames in HJV mRNA That Respond to Iron Overload in Hepatic Cells

Identification and characterization of two novel germline RET variants associated with medullary thyroid carcinoma

Resistance of mRNAs with AUG-proximal nonsense mutations to nonsense-mediated decay reflects variables of mRNA structure and translational activity

Functional characterization of two novel RET variants associated with medullary thyroid carcinoma

RAC1b overexpression in papillary thyroid carcinoma: A role to unravel

Rac1B: a prognostic marker for papillary thyroid carcinoma?

Alternative polyadenylation and nonsense-mediated decay coordinately regulate the human HFE mRNA levels

Interaction of PABPC1 with the translation initiation complex is critical to the NMD resistance of AUG-proximal nonsense mutations

Molecular analysis of TTF-1 and TTF-2 genes in patients with early onset papillary thyroid carcinoma

Unspliced precursors of NMD-sensitive β-globin transcripts exhibit decreased steady-state levels in erythroid cells

Control of human β-globin mRNA stability and its impact on beta-thalassemia phenotype

Nonsense-mediated decay resistance of AUG-proximal nonsense-mutated transcripts relies on the link between translation initiation and premature stop codon definition.

Abnormal nuclear distribution of human beta-globin transcripts committed to nonsense-mediated mRNA decay, in erythoid cells.

How the secondary structure of the open reading frame affects the efficiency of nonsense-mediated decay in transcripts with AUG-proximal nonsense codons. .

Human beta-globin transcripts commited to nonsense-mediated mRNA decay have na abnormal nuclear distribution in erythoid cells.

Interactions between 5’ and 3’ end-associated proteins during mRNA translation protects AUG-proximal nonsense-mutated mRNAs from nonsense-mediated decay.

The mammalian nonsense-mediated mRNA decay pathway: To decay or not to decay! Which players make the decision?

Mammalian nonsense mediated mRNA decay: new determinants that make transcripts bearing a small open reading frame resistant to rapid decay

Proximity of the poly(A)-binding protein to a premature termination codon inhibits mammalian nonsense-mediated mRNA decay

Comment on 'Nonsense-mediated mRNA decay modulates clinical outcome of genetic disease' [1]

Controlo de Qualidade do RNA Mensageiro em Mamíferos: Mecanismos de Degradação

The canonical UPF1-dependent nonsense-mediated mRNA decay is inhibited in transcripts carrying a short open reading frame independent of sequence context

Nonsense mutations in close proximity to the initiation codon fail to trigger full nonsense-mediated mRNA decay

Human mammaglobin RT-PCR assay for detection of occult breast cancer cells in hemotapoietic products

Cytokeratin 20 is not a reliable molecular marker for occult breast cancer cell detection in hematological tissues

The PML-RARα transcript in long-term follow-up of acute promyelocytic leukemia patients