Valentina Celestini

ORCID: 0000-0002-0908-6037
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About
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Research Areas
  • FOXO transcription factor regulation
  • Retinoids in leukemia and cellular processes
  • ATP Synthase and ATPases Research
  • Sirtuins and Resveratrol in Medicine
  • Mitochondrial Function and Pathology
  • Peroxisome Proliferator-Activated Receptors
  • Cancer, Lipids, and Metabolism
  • Genomics, phytochemicals, and oxidative stress
  • Genetics, Aging, and Longevity in Model Organisms
  • Colorectal Cancer Treatments and Studies
  • RNA Research and Splicing
  • Genetic factors in colorectal cancer
  • Epigenetics and DNA Methylation
  • Cancer Treatment and Pharmacology
  • PI3K/AKT/mTOR signaling in cancer
  • Histone Deacetylase Inhibitors Research

University of Bari Aldo Moro
2014-2019

Mario Negri Institute for Pharmacological Research
2018-2019

University of Perugia
2019

Istituti di Ricovero e Cura a Carattere Scientifico
2018

University of Washington
2018

Seattle University
2018

Gastroenterology Hospital "Saverio de Bellis"
2018

Abstract While aberrant cancer cell growth is frequently associated with altered biochemical metabolism, normal mitochondrial functions are usually preserved and necessary for full malignant transformation. The transcription factor FoxO3A a key determinant of homeostasis, playing dual role in survival/death response to metabolic stress therapeutics. We recently described novel arm the AMPK-FoxO3A axis cells upon nutrient shortage. Here, we show that metabolically stressed cells, recruited...

10.1038/s41419-018-0336-0 article EN cc-by Cell Death and Disease 2018-02-14

All-trans-retinoic-acid (ATRA) is a promising agent in the prevention/treatment of breast-cancer. There growing evidence that reprogramming cellular lipid metabolism contributes to malignant transformation and progression. Lipid implicated cell differentiation metastatic colonization it involved mechanisms sensitivity/resistance different anti-tumor agents. The role played by lipids activity ATRA has never been studied.We used 16 breast cancer cell-lines whose degree sensitivity...

10.1186/s13046-019-1438-y article EN cc-by Journal of Experimental & Clinical Cancer Research 2019-10-29

Hamartomatous polyposis syndromes (HPS) are inherited conditions associated with high cancer risk. They include the Peutz-Jeghers and PTEN hamartoma tumor syndromes, which caused by mutations in LKB1 genes, respectively. Estimation of risk is crucial order to optimize surveillance, but no prognostic markers currently available for these conditions. Our study relies on a 'signal transduction' hypothesis based crosstalk between LKB1/AMPK PI3K/PTEN/Akt signaling at level suppressor protein...

10.1186/1471-2407-14-661 article EN cc-by BMC Cancer 2014-09-11

Abstract Background: All-trans retinoic acid (ATRA) is the active metabolite of vitamin A and a promising agent in prevention treatment breast cancer. We recently demonstrated that approximately 70% estrogen-receptor-positive (ER+) cancer cell lines primary tumors are sensitive to anti-proliferative effects ATRA (1,2). In contrast only 10-20% HER2-positive triple-negative counterparts respond retinoid. The significance lipids growth, progression drug sensitivity specific types solid tumors,...

10.1158/1538-7445.sabcs18-p2-02-15 article EN Cancer Research 2019-02-15

Introduction c-Myc plays a central role in cellular proliferation, differentiation, and apoptosis. Therefore its deregulation represents powerful trigger of tumorigenesis, particularly colorectal cancer (CRC). It has been shown that the MEK/ERK pathway phosphorylates on serine 62, which stabilises by preventing ubiquitin/proteasomal degradation. We recently reported inhibition is counteracted over-activation p38α MAPK. Here, we identified mechanisms lead to deregulation, crucial issue for...

10.1136/esmoopen-2018-eacr25.51 article EN cc-by-nc ESMO Open 2018-06-01

Introduction While aberrant cancer cell growth is frequently associated with altered biochemical metabolism, normal mitochondrial functions are usually preserved and necessary for full malignant transformation. The transcription factor FoxO3A a key determinant of homeostasis, playing dual role in survival/death response. We recently described novel arm the AMPK-FoxO3A axis cells upon nutrient shortage. Material methods After extensive characterisation function vitro several lines tumours, we...

10.1136/esmoopen-2018-eacr25.276 article EN cc-by-nc ESMO Open 2018-06-01

Introduction Human cancers arise from a combination of genetic and epigenetic changes. Epigenetic factors regulate chromatin structure, affecting biological processes promoting cancer. Drugs that target modifiers are new therapeutic challenge, due to the reversibility epi-modifications. Indeed, drugs might sensitise cancer resistant cells chemotherapy. The SMYD3 histone methyltransferase has an oncogenic role in several types. It is overexpressed various promotes cell proliferation, making...

10.1136/esmoopen-2018-eacr25.510 article EN cc-by-nc ESMO Open 2018-06-01

Introduction TP53 is the most frequently mutated gene in human cancer.However, metastatic melanoma mutations of occur infrequently and p53 fails to function as a tumour suppressor.The altered expression family members, including p53/p73 isoforms, well interactions among them could affect normal p53.Furthermore, somatic BRAF have been found 37%-50% all melanomas, which almost 90% harbour activating V600E mutation.Although initial response inhibitors highly effective, resistant clones develop,...

10.1136/esmoopen-2018-eacr25.683 article EN cc-by-nc ESMO Open 2018-06-01

Abstract Background: All-trans retinoic acid (ATRA) is a promising agent in the treatment of breast cancer. In view ATRA-based therapeutic strategies aimed at personalized mammary tumors, we recently demonstrated that approximately 70% estrogen-receptor-positive (ER+) cancer sensitive to anti-proliferative effects ATRA (1). contrast only 10-20% HER2-positive and triple-negative counterparts respond retinoid. On basis these data available basal gene-expression profiles cell lines primary...

10.1158/1538-7445.sabcs18-p5-05-09 article EN Cancer Research 2019-02-15
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