http://www.cnr.it/ontology/cnr/individuo/prodotto/ID59204

Thymosin beta4 targeting impairs tumorigenic activity of colon cancer stem cells. (Articolo in rivista)

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Thymosin beta4 targeting impairs tumorigenic activity of colon cancer stem cells. (Articolo in rivista) (literal)

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Ricci-Vitiani, L1; Mollinari, C2,3; di Martino, S1; Biffoni, M1; Pilozzi, E4; Pagliuca, A1; de Stefano, MC2; Circo, R5; Merlo, D2,6; De Maria, R1,5; Garaci, E7 First two authors equally contributed to this work (2010)
Thymosin beta4 targeting impairs tumorigenic activity of colon cancer stem cells.
in The FASEB journal
(literal)

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Ricci-Vitiani, L1; Mollinari, C2,3; di Martino, S1; Biffoni, M1; Pilozzi, E4; Pagliuca, A1; de Stefano, MC2; Circo, R5; Merlo, D2,6; De Maria, R1,5; Garaci, E7 First two authors equally contributed to this work (literal)

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1. Ist Super Sanita, Dept Hematol Oncol & Mol Med, I-00161 Rome, Italy 2. Ist Super Sanita, Dept Cell Biol & Neurosci, I-00161 Rome, Italy 3. CNR, Dept Neurobiol & Mol Med, Rome, Italy 4. Univ Roma La Sapienza, Dept Lab Med & Pathol, St Andrea Hosp, Rome, Italy 5. Mediterranean Inst Oncol, Catania, Italy 6. IRCCS San Raffaele Pisana, Rome, Italy 7. Univ Roma Tor Vergata, Dept Expt Med & Biochem Sci, I-00133 Rome, Italy (literal)

Titolo

Thymosin beta4 targeting impairs tumorigenic activity of colon cancer stem cells. (literal)

Abstract

Thymosin beta4 (Tb4) is an actin-binding peptide overexpressed in several tumors, including colon carcinomas. The aim of this study was to investigate the role of Tb4 in promoting the tumorigenic properties of colorectal cancer stem cells (CR-CSCs), which are responsible for tumor initiation and growth. We first found that CR-CSCs from different patients have higher Tb4 levels than normal epithelial cells. Then, we used a lentiviral strategy to down-regulate Tb4 expression in CR-CSCs and analyzed the effects of such modulation on proliferation, survival, and tumorigenic activity of CR-CSCs. Empty vector-transduced CR-CSCs were used as a control. Targeting of the Tb4 produced CR-CSCs with a lower capacity to grow and migrate in culture and, interestingly, reduced tumor size and aggressiveness of CR-CSC-based xenografts in mice. Moreover, such loss in tumorigenic activity was accompanied by a significant increase of phosphatase and tensin homologue (PTEN) and a concomitant reduction of the integrin-linked kinase (ILK) expression, which resulted in a decreased activation of protein kinase B (Akt). Accordingly, exogenous expression of an active form of Akt rescued all the protumoral features lost after Tb4 targeting in CR-CSCs. In conclusion, T?4 may have important implications for therapeutic intervention for treatment of human colon carcinoma. (literal)

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