21 research outputs found
Hepatectomy for Hepatocellular Carcinoma in Patients with End-Stage Renal Disease on Hemodialysis
Hepatectomy for Hepatocellular Carcinoma in Patients with End-Stage Renal Disease on Hemodialysis
Expression of N-acetylglucosaminyltransferase V in Intrahepatic Cholangiocarcinoma and Its Association with Clinicopathological Findings
Efficient induction of apoptosis by wee1 kinase inhibition in hepatocellular carcinoma cells.
Transforming growth factor-β1 (TGF-β1) potently inhibits human hepatocellular carcinoma (HCC) cell growth. Here we demonstrated that TGF-β1-induced apoptosis is mediated by decreased phosphorylation of cdc2 at Tyr15 accompanied by down-regulation of Wee1 kinase expression. As expected from these results, a Wee1 kinase inhibitor efficiently induced apoptosis in HCC cells in the absence of TGF-β1 treatment. In surgically resected samples, Wee1 kinase was expressed in moderately to poorly differentiated HCC, whereas no Wee1 kinase expression was observed in non-cancerous tissue, including cirrhotic tissue. Our results suggest that Wee1 kinase inhibitors may be a practical novel therapeutic option against advanced HCC
Safe anatomical hepatectomy with Glissonean pedicle approach for patients with hepatocellular carcinoma
Intrahepatic metastasis and lymph node metastasis are useful for determination of indications for surgery, borderline, or non-surgery in intrahepatic cholangiocarcinoma
Targeting Wee1 kinase induces apoptosis in HCC cells.
<p>A, The number of sub-G1 HuH7 cells significantly increased after PD166285 treatment (200 nM). PD166285-mediated apoptosis of HuH7 cells was completely inhibited by pretreatment with 20 µM roscovitine (Ros). * indicates significant differences between each group (P<0.05). The results are presented as means ± S.D. of three experiments. <b>B,</b> PD166285 decreased the number of HuH7 cells in a concentration-dependent manner after 72 h. * indicates significant differences between each group (P<0.05). The representative results of three independent experiments are shown. <b>C</b> and D, Wee1 kinase-specific siRNAs (18-2 or 18-3) significantly reduced the total number of cells and increased the sub-G1 cell population 48 h after transfection in a concentration-dependent manner compared with control-vector transfectants. * indicates significant differences between each group (P<0.05).</p
TGF-B1 induces apoptosis through cdc2 activation.
<p><b>A,</b> FACS analyses showed that the sub-G1 phase HuH7 cell population increased from approximately 0.7% to 7.7%, and cells in the G1 phase increased from approximately 69% to 87% 48 h after TGF-β1 treatment. Data represent the means ± S.D. of three experiments. * indicates significant differences between each group (P<0.05). B, Cdc2 kinase activity was determined based on the level of phosphorylated histone H1 using histone H1 as a substrate. Cdc2 was activated 48 h after TGF-β1 treatment in HuH7 cells. However, cdc2 was not activated in HuH7R cells, which were isolated as an apoptosis-resistant clone from TGF-β1-treated HuH7 cells. Roscovitine (Ros)-pretreated HuH7 cells did not show cdc2 activation. A representative image from three independent experiments is shown. <b>C,</b> After TGF-β1 treatment (48 h), we observed cdc2 Tyr15 dephosphorylation in association with Wee1 kinase down-regulation in apoptotic cells. Pretreatment with 20 µM roscovitine completely abolished apoptosis and restored Wee1 kinase expression. TGF-β1 treatment induced G1 cell cycle arrest in HuH7R cells; however, Wee1 kinase expression and non-phosphorylated cdc2 Tyr 15 were similar to those of roscovitine-pretreated HuH7 cells. A representative image of three experiments is shown. <b>D,</b> Wee1 down-regulation and cdc2 Tyr15 dephosphorylation commenced approximately 24 h after TGF-β1 treatment, which was similar to thea initiation of apoptosis. A representative Western blot image is shown in the upper panels. The results in the lower graphs represent the means ± S.D. of three experiments. * indicates significant differences between each group (P<0.05).</p