Marina De Rosa

University of Naples Federico II

Title: Role of Lithium Chloride in Colorectal cancer therapy

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Biography

Marina De Rosa (MDR) is Associated Professor of "Biochemistry" at the University of Naples Federico II. She received the title of PhD in Biotechnology in 1998. In 2000 she obtained the title of specialist in Biochemistry and Clinical Chemistry. 

She is Editorial Board Member of the Experimental and Therapeutic Medicine journal-Spandidos publications. Reviewer Board member of the "Cancers" journal-MDPI journal. and "Membranes" journal-MDPI journal. 

She is author of more than 95 papers. Of these, 45 are articles on indexed scientific journals with a total of 862 citations, achieving an h-index of 18, according to Scopus and PubMed database

Abstract

Colorectal cancer is the third most prevalent of all cancers worldwide, representing the 10.2 % of all cancer cases, and the second most common cause of cancer mortality, accounting for about 9.2% of all cancer death in 2018, mainly due to resistance to therapy, in accordance with GLOBOCAN 2018. Treatments for CRC include surgery, chemotherapy, radiation therapy, and combination therapy. However, chemoradiotherapy often kills only differentiated cancer cells, while the more undifferentiated cells, the mesenchymal and stem cells, are resistant and can survive after therapy, giving rise to therapy-resistant tumours.

We isolated two primary colon adenocarcinoma cell cultures that had undergone epithelial-to-mesenchymal transition, one with a high microsatellite instability phenotype (T88) and one with a chromosomal instability phenotype (T93). Since GSK3? is an important regulator of cell survival which promotes tumourigenesis in colon cells, we explored the effects of the specific GSK-3? inhibitor LiCl on cell motility and plasticity, demonstrating that LiCl reduced cell migration, stemness features and cell plasticity. We also investigated the effect of X-ray alone or in combination with LiCl treatment on viability of T88 primary colon cancer cells. As expected, we observed that LiCl sensitises primary colon cancer cells to photon radiation treatment. We explored the molecular bases of this response by analysing the effect of all treatments on the expression of proteins involved in the apoptotic mechanism and in death escape, such as Bax, Bcl-2, p53 and Survivin proteins. We found that LiCl treatment downregulates survivin and Bcl-2, while up-regulate p53, BAX and beta-catenin proteins. These effects were additive in irradiated cells pre-treated with LiCl. In our opinion, these data suggest that LiCl could represent an interesting drug useful to sensitise resistant colon cancer cells to photon radiation.