Integrated ubiquitomics characterization of hepatocellular carcinomas.

Background And Aims: Patients with aggressive HCC have limited therapeutic options. Therefore, a better understanding of HCC pathogenesis is needed to improve treatment. Genomic studies of HCC have improved our understanding of cancer biology.

FBXW10-S6K1 promotes ANXA2 polyubiquitination and KRAS activation to drive hepatocellular carcinoma development in males.

The incidence rate of human hepatocellular carcinoma (HCC) is approximately three times higher in males than in females. A better understanding of the mechanisms underlying HCC development in males could lead to more effective therapies for HCC. Our previous study found that FBXW10 played a critical role in promoting HCC development in male mice and patients, but the mechanism remains unknown.

Degradation of helicase-like transcription factor (HLTF) by β-TrCP promotes hepatocarcinogenesis via activation of the p62/mTOR axis.

Helicase-like transcription factor (HLTF) has been found to be involved in the maintenance of genome stability and tumour suppression, but whether its downregulation in cancers is associated with posttranslational regulation remains unclear. Here, we observed that HLTF was significantly downregulated in hepatocellular carcinoma (HCC) tissues and positively associated with the survival of HCC patients. Mechanistically, the decreased expression of HLTF in HCC was attributed to elevated β-TrCP-mediated ubiquitination and degradation.

Hepatic sinusoidal obstruction syndrome induced by tacrolimus following liver transplantation: Three case reports.

Background: Hepatic sinusoidal obstruction syndrome (HSOS) is a rare complication in solid organ transplant recipients, especially in liver transplantation recipients. However, the consequences of HSOS occurrence are pernicious, which could result in severe liver or renal failure, and even death. In addition to previously reported azathioprine and acute rejection, tacrolimus is also considered as one predisposing factor to induce HSOS after liver transplantation, although the underlying mechanism remains unclear.

Mutant Kras and mTOR crosstalk drives hepatocellular carcinoma development via PEG3/STAT3/BEX2 signaling.

Abnormal activation of mTOR through loss of tuberous sclerosis complex (Tsc) frequently occurs in hepatocellular carcinoma (HCC). Mutant Kras could induce aggressive HCCs. Here, we aim to identify the predictive or prognostic biomarkers for HCC patients with Kras mutant and mTOR hyperactivation, and to provide potential therapeutic approaches for this subtype of HCCs.

Gastroduodenal artery disconnection during liver transplantation decreases non-anastomotic stricture incidence.

Background: The hepatic artery is the only blood source nourishing the biliary duct and associated with biliary complication after liver transplantation (LT). Gastroduodenal artery (GDA) disconnection increased proper hepatic artery flow. Whether this procedure attenuates biliary non-anastomotic stricture (NAS) is not clear.

Elevated preoperative CA125 levels predicts poor prognosis of hilar cholangiocarcinoma receiving radical surgery.

Background: Preoperative serum carbohydrate antigen 125 (CA125) is used to judge the diagnosis and prognosis of various tumors. However, the relationship between preoperative serum CA125 and prognosis of hilar cholangiocarcinoma (HCCA) has not been proven. This study aims to evaluate preoperative serum CA125 in predicting the prognosis of HCCA after resection.

liver resection followed by autotransplantation in radical resection of gastric cancer liver metastases: A case report.

Background: Radical resection of gastric cancer liver metastases (GCLM) can increase the 5-year survival rate of GCLM patients. However, patients may lose the theoretical feasibility of surgery due to the critical location of liver metastasis in some cases.

Case Summary: A 29-year-old woman had a chief complaint of chronic abdominal pain for 1 year.

Reduced IκBα promotes hepatocellular carcinoma cell proliferation and migration via regulation of NF-κB/Erbin axis.

Aberrantly low expression of NF-κB inhibitor α (IκBα) is observed in hepatocellular carcinoma (HCC), yet the underlying mechanism via which IκBα regulates HCC remains largely unknown. Therefore, to determine the potential function of IκBα in hepatocarcinogenesis, the present study used immunohistochemistry (IHC) staining to analyze the associations between IκBα protein expression and clinicopathologic characteristics of 107 patients with HCC. It was found that expression of IκBα was significantly associated with tumor recurrence.

Impact of body mass index on postoperative outcomes in patients undergoing radical resection for hilar cholangiocarcinoma.

Background: Body mass index (BMI) has been widely used as a prognostic indicator. The association between preoperative BMI and postoperative morbidity in patients with hilar cholangiocarcinoma (HCCA) has not been proved. This study aimed to identify the association between preoperative BMI and postoperative morbidity following radical resection of HCCA.

p53 haploinsufficiency and increased mTOR signalling define a subset of aggressive hepatocellular carcinoma.

Background & Aims: p53 mutations occur frequently in human HCC. Activation of the mammalian target of rapamycin (mTOR) pathway is also associated with HCC. However, it is still unknown whether these changes together initiate HCC and can be targeted as a potential therapeutic strategy.

Prognostic and predicted significance of Ubqln2 in patients with hepatocellular carcinoma.

Purpose: Hepatocellular carcinoma (HCC) is a common malignant cancer and the third leading cause of death worldwide. The molecular mechanism of HCC remains unclear. Recent studies have demonstrated that the ubiquitin-proteasome system (UPS) is associated with HCC.

Impact of iatrogenic biliary injury during laparoscopic cholecystectomy on surgeon's mental distress: a nationwide survey from China.

Background: Iatrogenic biliary injury (IBI) following laparoscopic cholecystectomy (LC) is the most serious iatrogenic complications. Little is known whether LC-IBI would lead to surgeon's severe mental distress (SMD).

Methods: A cross-sectional survey in the form of electronic questionnaire was conducted among Chinese general surgeons who have caused LC-IBI.

LNC00673 suppresses proliferation and metastasis of pancreatic cancer via target miR-504/ HNF1A.

Pancreatic cancer is a highly invasive malignant tumor of the digestive system. To explore the mechanism of pancreatic cancer development, development, invasion and metastasis, in this study we focused on long non-coding RNA (LncRNA), which has been reported to be involved in tumorigenesis. We identified a LINC00673, which is highly correlated with the pancreatic cancer risk.

FBXW10 promotes hepatocarcinogenesis in male patients and mice.

Hepatocellular carcinoma (HCC) is reported to associate with abnormal expression of SCF E3 ubiquitin ligases. FBXW10, an F-box protein of the E3 ubiquitin ligases, was abnormally regulated in HCC patients. However, whether FBXW10 is associated with HCC has not yet been evaluated.

Neuron-glial antigen 2 overexpression in hepatocellular carcinoma predicts poor prognosis.

Aim: To investigate whether neuron-glial antigen 2 (NG2) could be an effective prognostic marker in hepatocellular carcinoma (HCC).

Methods: NG2 expression was semi-quantitatively scored from the immunohistochemistry (IHC) data based on the number of positive cells and the staining intensity. A total of 132 HCC specimens and 96 adjacent noncancerous tissue samples were analyzed by IHC for NG2 protein expression.

siRNA-mediated knockdown against NUF2 suppresses pancreatic cancer proliferation in vitro and in vivo.

NUF2 (NUF2, Ndc80 kinetochore complex component) plays an important role in kinetochore-microtubule attachment. It has been reported that NUF2 is associated with multiple human cancers. However, the functional role of NUF2 in pancreatic cancer remains unclear.

Apigenin potentiates the growth inhibitory effects by IKK-β-mediated NF-κB activation in pancreatic cancer cells.

Apigenin is a potential chemopreventive agent for cancer prevention. Because of the central role of transcription factor nuclear factor-κB (NF-κB) in pancreatic cancer, we investigated the roles of NF-κB in apigenin-induced growth inhibition in pancreatic cancer cells. It showed that apigenin reduced cell growth and induced apoptosis in the cells.

Increased liver-infiltrating CD8+FoxP3+ regulatory T cells are associated with tumor stage in hepatocellular carcinoma patients.

Hepatocellular carcinoma (HCC) is the most common primary malignant tumor of the liver, and patients who are diagnosed with this tumor typically have a poor prognosis. The suppressive effects of CD4(+)FoxP3(+) regulatory T cells on antitumor immune response in HCC have been studied in great detail. CD8(+)FoxP3(+) regulatory T cells have recently been detected in tumors; however, the role of CD8(+)FoxP3(+) regulatory T cells in HCC is still unknown.

[Experimental study of epithelial-mesenchymal transition induced by HBx protein in liver cancer cell].

Objective: To explore whether or not HBx protein can induce epithelial-mesenchymal transition (EMT) in liver cancer cell SMMC-7721.

Methods: A recombinant adenovirus vector containing HBx gene was constructed and introduced into SMMC-7721 cell. The morphological changes were observed.

HBx protein induces EMT through c-Src activation in SMMC-7721 hepatoma cell line.

The relationships between epithelial-to-mesenchymal transition (EMT), hepatitis B virus X protein (HBx), and the non-receptor tyrosine kinase c-Src were investigated. The HBx gene transfected SMMC-7721 cells underwent morphological changes from a classic epithelial morphology to a spindle-like shape. The HBx transfection increased the invasive potential of these cells.

[Vascular endothelial growth factor receptor-1 activation induces epithelial to mesenchmal transition in hepatocellular carcinoma cell line MHCC97-H.].

Objective: To evaluate the mechanism of increased invasion and migration of hepatocellular carcinoma (HCC) cells induced by vascular endothelial growth factor receptor-1 (VEGFR-1) activation.

Methods: Vascular endothelial growth factor-B (VEGF-B) was used to induce and stimulate hepatocellular carcinoma cell line MHCC97-H. Morphologic changes of MHCC97-H were investigated.