To the Editor,Portal hypertension(PH)is defined by a pathological increase in the pressure of the portal venous system,1 with liver cirrhosis as the most common cause.However,some other noncirrhotic diseases might cau...To the Editor,Portal hypertension(PH)is defined by a pathological increase in the pressure of the portal venous system,1 with liver cirrhosis as the most common cause.However,some other noncirrhotic diseases might cause PH;a condition referred to as noncirrhotic PH(NCPH).2 NCPH is a rare disease characterized by clinical signs of PH in the absence of cirrhosis,presenting with complications of PH including ascites,splenomegaly,esophagogastric varices,and variceal bleeding.3 Because of the similarities in clinical manifestations and imaging signs,NCPH is easily misdiagnosed as liver cirrhosis and thus raises difficulties in differential diagnosis.Although liver biopsy is still the gold standard for diagnosis,4 extensive workup including laboratory testing,hepatic imaging and liver biopsy is recommended for comprehensive NCPH diagnosis.展开更多
Hepatocellular carcinoma(HCC) is the major form of primary liver cancer and one of the most prevalent and life-threatening malignancies globally. One of the hallmarks in HCC is the sustained cell survival and prolifer...Hepatocellular carcinoma(HCC) is the major form of primary liver cancer and one of the most prevalent and life-threatening malignancies globally. One of the hallmarks in HCC is the sustained cell survival and proliferative signals, which are determined by the balance between oncogenes and tumor suppressors.Transforming growth factor beta(TGF-β) is an effective growth inhibitor of epithelial cells including hepatocytes, through induction of cell cycle arrest, apoptosis, cellular senescence, or autophagy. The antitumorigenic effects of TGF-β are bypassed during liver tumorigenesis via multiple mechanisms.Furthermore, along with malignant progression, TGF-β switches to promote cancer cell survival and proliferation. This dichotomous nature of TGF-β is one of the barriers to therapeutic targeting in liver cancer. Thereafter, understanding the underlying molecular mechanisms is a prerequisite for discovering novel antitumor drugs that may specifically disable the growth-promoting branch of TGF-β signaling or restore its tumor-suppressive arm. This review summarizes how TGF-β inhibits or promotes liver cancer cell survival and proliferation, highlighting the functional switch mechanisms during the process.展开更多
基金supported by the National Natural Science Foundation of China(grant number 82103655).
文摘To the Editor,Portal hypertension(PH)is defined by a pathological increase in the pressure of the portal venous system,1 with liver cirrhosis as the most common cause.However,some other noncirrhotic diseases might cause PH;a condition referred to as noncirrhotic PH(NCPH).2 NCPH is a rare disease characterized by clinical signs of PH in the absence of cirrhosis,presenting with complications of PH including ascites,splenomegaly,esophagogastric varices,and variceal bleeding.3 Because of the similarities in clinical manifestations and imaging signs,NCPH is easily misdiagnosed as liver cirrhosis and thus raises difficulties in differential diagnosis.Although liver biopsy is still the gold standard for diagnosis,4 extensive workup including laboratory testing,hepatic imaging and liver biopsy is recommended for comprehensive NCPH diagnosis.
基金supported by grants from the National Natural Science Foundation of China(31671460,31871378 and 32060148)the Natural Science Foundation of Jiangxi Province of China(20171ACB21004)to X.Y。
文摘Hepatocellular carcinoma(HCC) is the major form of primary liver cancer and one of the most prevalent and life-threatening malignancies globally. One of the hallmarks in HCC is the sustained cell survival and proliferative signals, which are determined by the balance between oncogenes and tumor suppressors.Transforming growth factor beta(TGF-β) is an effective growth inhibitor of epithelial cells including hepatocytes, through induction of cell cycle arrest, apoptosis, cellular senescence, or autophagy. The antitumorigenic effects of TGF-β are bypassed during liver tumorigenesis via multiple mechanisms.Furthermore, along with malignant progression, TGF-β switches to promote cancer cell survival and proliferation. This dichotomous nature of TGF-β is one of the barriers to therapeutic targeting in liver cancer. Thereafter, understanding the underlying molecular mechanisms is a prerequisite for discovering novel antitumor drugs that may specifically disable the growth-promoting branch of TGF-β signaling or restore its tumor-suppressive arm. This review summarizes how TGF-β inhibits or promotes liver cancer cell survival and proliferation, highlighting the functional switch mechanisms during the process.
