Giulia Anichini

ORCID: 0000-0002-7146-3489
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About
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Research Areas
  • Hedgehog Signaling Pathway Studies
  • Cancer-related gene regulation
  • Cholangiocarcinoma and Gallbladder Cancer Studies
  • Epigenetics and DNA Methylation
  • Islamic Finance and Communication
  • Oral and gingival health research
  • DNA Repair Mechanisms
  • Genomic variations and chromosomal abnormalities
  • Phagocytosis and Immune Regulation
  • Cancer-related Molecular Pathways
  • Cancer Cells and Metastasis
  • Immunotherapy and Immune Responses
  • Cancer Mechanisms and Therapy
  • Glycosylation and Glycoproteins Research

Piedmont Reference Center for Epidemiology and Cancer Prevention
2020-2024

Understanding the molecular events controlling melanoma progression is of paramount importance for development alternative treatment options this devastating disease. Here we report a mechanism regulated by oncogenic SOX2-GLI1 transcriptional complex driving invasion through induction sialyltransferase ST3GAL1. Using in vitro and vivo studies, demonstrate that ST3GAL1 drives metastasis. Silencing enzyme suppresses significantly reduces ability aggressive cells to enter blood stream, colonize...

10.1038/s41467-020-19575-2 article EN cc-by Nature Communications 2020-11-17

Aberrant activation of Hedgehog (HH) signaling in cancer is the result genetic alterations upstream pathway components (canonical) or other oncogenic mechanisms (noncanonical), that ultimately concur to activate zinc-finger transcription factors GLI1 and GLI2. Therefore, inhibition GLI activity a good therapeutic option suppress both canonical noncanonical HH pathway. However, only few inhibitors are available, none them have profile required for clinical development due poor metabolic...

10.1016/j.phrs.2023.106858 article EN cc-by-nc-nd Pharmacological Research 2023-07-19

Abstract Background Melanoma progression is based on a close interaction between cancer cells and immune in the tumor microenvironment (TME). Thus, better understanding of mechanisms controlling TME dynamics composition will help improve management this dismal disease. Work from our other groups has reported requirement an active Hedgehog-GLI (HH-GLI) signaling for melanoma growth stemness. However, role downstream GLI1 transcription factor remains largely unexplored. Methods The...

10.1186/s13046-024-03138-0 article EN cc-by Journal of Experimental & Clinical Cancer Research 2024-08-02

Abstract Cholangiocarcinoma (CCA) is characterized by resistance to chemotherapy and a poor prognosis. Therefore, treatments that can effectively suppress tumor growth are urgently needed. Aberrant activation of hedgehog (HH) signaling has been implicated in several cancers, including those the hepatobiliary tract. However, role HH intrahepatic CCA (iCCA) not completely elucidated. In this study, we addressed function main transducer Smoothened (SMO) transcription factors (TFs) GLI1 GLI2...

10.1158/1535-7163.mct-22-0379 article EN cc-by-nc-nd Molecular Cancer Therapeutics 2022-12-02

<div>Abstract<p>Cholangiocarcinoma (CCA) is characterized by resistance to chemotherapy and a poor prognosis. Therefore, treatments that can effectively suppress tumor growth are urgently needed. Aberrant activation of hedgehog (HH) signaling has been implicated in several cancers, including those the hepatobiliary tract. However, role HH intrahepatic CCA (iCCA) not completely elucidated. In this study, we addressed function main transducer Smoothened (SMO) transcription factors...

10.1158/1535-7163.c.6543811 preprint EN 2023-04-03

<div>Abstract<p>Cholangiocarcinoma (CCA) is characterized by resistance to chemotherapy and a poor prognosis. Therefore, treatments that can effectively suppress tumor growth are urgently needed. Aberrant activation of hedgehog (HH) signaling has been implicated in several cancers, including those the hepatobiliary tract. However, role HH intrahepatic CCA (iCCA) not completely elucidated. In this study, we addressed function main transducer Smoothened (SMO) transcription factors...

10.1158/1535-7163.c.6543811.v1 preprint EN 2023-04-03
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