Obesity and low-grade inflammation are associated with an increased risk of hepatocellular carcinoma (HCC), a leading cause of cancer-related death worldwide. The tissue inhibitor of metalloproteinase (TIMP) 3, an endogenous inhibitor of protease activity that represents a key mediator of inflammation, is reduced in inflammatory metabolic disorders and cancer. In contrast, Timp3-deficient mice (Timp3-/-) are highly resistant to developing HCC in response to a diethylnitrosamine (DEN); therefore, we aimed to elucidate the biological role of genetic loss of Timp3 in obesity-related hepatocarcinogenesis.
Casagrande, V., Mauriello, A., Anemona, L., Mavilio, M., Iuliani, G., De Angelis, L., et al. (2019). Timp3 deficiency affects the progression of DEN-related hepatocellular carcinoma during diet-induced obesity in mice. ACTA DIABETOLOGICA, 56(12), 1265-1274 [10.1007/s00592-019-01382-x].
Timp3 deficiency affects the progression of DEN-related hepatocellular carcinoma during diet-induced obesity in mice
Casagrande V.;Mauriello A.;Anemona L.;Mavilio M.;Iuliani G.;De Angelis L.;Federici M.;Menghini R.
2019-01-01
Abstract
Obesity and low-grade inflammation are associated with an increased risk of hepatocellular carcinoma (HCC), a leading cause of cancer-related death worldwide. The tissue inhibitor of metalloproteinase (TIMP) 3, an endogenous inhibitor of protease activity that represents a key mediator of inflammation, is reduced in inflammatory metabolic disorders and cancer. In contrast, Timp3-deficient mice (Timp3-/-) are highly resistant to developing HCC in response to a diethylnitrosamine (DEN); therefore, we aimed to elucidate the biological role of genetic loss of Timp3 in obesity-related hepatocarcinogenesis.| File | Dimensione | Formato | |
|---|---|---|---|
|
Casagrande2019_ACTA DIABETOL Article_Timp3DeficiencyAffectsTheProgr.pdf
solo utenti autorizzati
Tipologia:
Versione Editoriale (PDF)
Licenza:
Non specificato
Dimensione
4.29 MB
Formato
Adobe PDF
|
4.29 MB | Adobe PDF | Visualizza/Apri Richiedi una copia |
I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
