The application of a single-hand-operated hepatic pedicle clamping clamp in laparoscopic hepatectomy.

OBJECTIVE: In this paper, a single-hand-operated hepatic pedicle clamp was introduced, and its application value in laparoscopic liver tumor resection was preliminarily discussed. METHODS: The clinical data of 67 patients who underwent laparoscopic liver tumor resection at the First Affiliated Hospital of Wannan Medical College from March 2019 to October 2023 were retrospectively analyzed. The Pringle maneuver was performed with a hepatic pedicle clamp during the operation. The preoperative, intraoperative and postoperative clinical data were observed and recorded. RESULTS: Sixty-seven patients had a median block number, block time, intraoperative blood loss, and postoperative length of hospital stay of 4, 55 min, 400 ml, and 7 days, respectively. The average operation time was 304.9±118.4 min, the time required for each block was 3.2±2.4 s, and the time required for each removed block was 2.6±0.7 s. None of the patients developed portal vein thrombosis or hepatic artery aneurysm formation. CONCLUSION: The hepatic pedicle clamping clamp is simple to use in laparoscopic hepatectomy, optimizes the operation process, and has a reliable blocking effect. It is recommended for clinical application.

GCNT3 Promotes Hepatocellular Carcinoma Progression and EMT by Activating the PI3K/AKT Pathway.

Primary liver cancer, specifically hepatocellular carcinoma (HCC), is a major global health concern. GCNT3 has been identified as an oncogene in various human malignancies. This investigation aimed to discover the GCNT3 function in HCC. The present study employed integrated bioinformatics analyses to assess the expression pattern, prognostic implications, and putative function of GCNT3 in HCC. Transwell flow cytometry, CCK-8, and wound healing assays were performed to examine HCC cell growth, cell cycle, apoptosis, invasion, and migration. In addition, the epithelial-mesenchymal transition (EMT) markers and PI3K/AKT mechanism markers were examined via western blot analysis to elucidate the underlying mechanisms. In HCC, GCNT3 was significantly overexpressed, which was connected with enhanced tumor aggressiveness and an unfavorable prognosis of individuals. In vitro experiments demonstrated that elevated levels of GCNT3 promoted cell growth, migration, cell cycle development, and invasion, in addition to EMT, while suppressing apoptosis. Conversely, knockdown of GCNT3 exerted the opposite effects. GCNT3 overexpression increased PI3K/AKT phosphorylation in HCC cells, and LY294002 counteracted the impacts of upregulated GCNT3 on cell cycle, migration, invasion, proliferation, and EMT in HCC. The investigation showed that GCNT3 may enhance HCC progression and EMT by stimulating PI3K/AKT mechanism.

Exploring the Mechanism of KLF15 on the Biological Activity and Autophagy of Gastric Cancer Cells based on PI3K/Akt/Mtor Signaling Pathway.

OBJECTIVE: To explore the mechanism of KLF15 on the biological activity and autophagy of gastric cancer cells based on the PI3K/Akt/mTOR signaling pathway. MATERIAL AND METHODS: The gastric cancer AGS cells were divided into the Con group, pcDNANC group, pcDNA-KLF15 group, LY294002 group and IGF-1 group. RT-PCR was used to detect the expression of KLF15 in human gastric mucosal cells and gastric cancer cells; MTT method to detect cell proliferation; Transwell method to detect cell invasion; flow cytometry to detect cell apoptosis; Western blotting to detect PI3K, Akt, mTOR in cells, LC3, Beclin1, p62 protein expression.P<0.05 was used to indicate statistical significance. RESULTS: Compared with the human gastric mucosal cell line GES-1 cells, the expression of KLF15 in human gastric cancer cell lines MKN-28, MFC, SCG-7901 and AGS cells was significantly decreased, And the expression of KLF15 in AGS cells, was the lowest (P=0.006). Compared with the Con group, The expression of KLF15 in the cells of the PCDNA-KLF15 group was significantly increased (P=0.018); There was no significant difference in the expression of KLF15 between the Con group and the PCDNA-NC group (P=0.225). Compared with the Con group, the proliferation and invasion abilities of the cells in the pcDNA-KLF15 group were significantly reduced, And the apoptosis ability was significantly increased (P=0.019). The ratio of LC3II/LC31 and the expression of Beclin1 Protein in the control group were significantly higher than those in the Con group (P=0.017). CONCLUSION: Overexpression of KLF15 can inhibit the proliferation and invasion of Gastric cancer cells and promote cell apoptosis and autophagy, and its mechanism may be related to the regulation of the PI3K/Akt/mTOR signaling pathway.

Enucleation versus hepatectomy for hepatic hemangiomas: A meta-analysis.

Objective: To compare the safety and efficacy of enucleation and hepatectomy for the treatment of hepatic hemangioma (HH). Methods: A systematic literature search was conducted to identify studies evaluating enucleation versus hepatectomy for HH starting from the time of database creation to February 2022. Extraction of the data used in this study was done from the literature. The differences between the two surgical approaches were evaluated by comparing and analyzing the relevant data by means of meta-analysis. Results: A total of 1,384 patients (726 underwent enucleation, and 658 with hepatectomy) were included in our meta-analysis from 12 studies. Enucleations were associated with favorable outcomes in terms of operation time [mean difference (MD): -39.76, 95% confidence interval (CI): -46.23, -33.30], blood loss (MD: -300.42, 95% CI: -385.64, -215.19), length of hospital stay (MD: -2.33, 95% CI: -3.22, -1.44), and postoperative complications (OR: 0.57, 95% CI: 0.44-0.74). There were no differences between the groups in terms of patients needing transfusion (OR: 0.85, 95% CI: 0.50, 1.42), inflow occlusion time (MD: 1.72, 95% CI: -0.27, 3.71), and 30-day postoperative mortality (OR: 0.23, 95% CI: 0.02-2.17). Conclusion: Compared with hepatectomy, enucleation is found to be effective at reducing postoperative complications, blood loss, and operation time and shortening the length of hospital stay. Enucleation is similar to hepatectomy in terms of inflow occlusion time, 30-day postoperative mortality, and patients needing transfusing to hepatectomy.

LATS1 exerts tumor suppressor functions via targeting Gli1 in colorectal cancer.

Background: The Hippo pathway's primary kinase component, large tumor suppressor 1 (LATS1), has been hypothesized as a tumor suppressor in a variety of cancers. LATS1's biological effects on colorectal cancer (CRC) are yet to be determined. Methods: The analysis of LATS1 mRNA expression in CRC was conducted using public databases from the Gene Expressing Profiling Interactive Analysis database (GEPIA). Investigation for the expression of LATS1 protein in 102 CRC tumor tissues and 57 normal tissues was performed using immunohistochemistry (IHC) analysis. In vitro genetic manipulation was used to explore the potential role and mechanism of LATS1 in the regulation of proliferation and migration of CRC cells. Results: LATS1 was found to be considerably downregulated in CRC tissues, with much lower levels in individuals with bigger tumors of size (≥5 cm), deeper invasion (T3-4), positive lymph node metastasis (LNM), and advanced tumor-node-metastasis (TNM) stage (III-IV). As exhibited by clinical data analysis, LATS1 loss was significantly associated with TNM and LNM staging in CRC patients. Furthermore, our in vitro investigations revealed that LATS1 depletion increased CRC cell proliferation and migration in HCT116 cells, whereas overexpressing LATS1 had the opposite effect in SW620 cells. LATS1 suppressed the expression of glioma-associated oncogene-1 (Gli1), and LATS1's tumor-suppressive actions in CRC are dependent on Gli1. Moreover, LATS1 could modulate Yes-associated protein 1 (YAP1) expression and mTOR activation in CRC cells. Conclusion: Our findings identify the LATS1 as a unique Gli1 regulator in CRC cell migration and proliferation, and suggest that LATS1 may serve as a potential therapeutic target for CRC.

Yes-Associated Protein Contributes to Cell Proliferation and Migration of Gastric Cancer via Activation of Gli1.

OBJECTIVE: In the present study, we aimed to explore the potential oncogenic property and the internal mechanism of yes-associated protein (YAP) in gastric cancer (GC). MATERIALS AND METHODS: YAP protein levels were evaluated in human GC tissues and paired normal tissues using immunohistochemistry (IHC). The role of YAP in regulating GC cell proliferation and migration was verified by genetic manipulation in vitro. Western blot analysis was used to determine the molecular signaling to explain the mechanism of the observed YAP effects in GC. RESULTS: Nuclear YAP protein expression was upregulated in GC tissues, and high nuclear YAP level was significantly correlated with lymph node metastasis (LNM) and tumor node metastasis (TNM) stage in patients suffered from GC. YAP knockdown inhibited GC cell proliferation, migration and epithelial-mesenchymal transition (EMT) progress in vitro, whereas YAP elevation did the opposite. YAP regulated glioma-associated oncogene-1 (Gli1) expression independent of smoothened homolog (SMO). YAP modulated protein kinase B (AKT)/mechanistic target of rapamycin (mTOR) signaling pathway in GC cells. CONCLUSION: YAP enhanced GC cell proliferation and migration potentially via its regulation of Gli1 expression through the non-classical Hedgehog pathway, indicating suppression of YAP/Gli1 signaling axis may highlight a new entry point for combination therapy of GC.

Silencing of keratin 17 by lentivirus-mediated short hairpin RNA inhibits the proliferation of PANC-1 human pancreatic cancer cells.

Keratin 17 (KRT17) has been demonstrated to be a potential biological marker for the prediction of prognosis in particular types of cancer. The aim of the present study was to investigate the molecular mechanisms underlying the function of KRT17 in the pancreatic cancer (PAC) cell line PANC-1 and the potential of KRT17 as a therapeutic target for PAC. KRT17 expression levels were analyzed using quantitative PCR and compared with histological data using bioinformatics tools in PAC samples and three human PAC cell lines. Cell proliferation was determined using an MTT assay, in addition to cell cycle distribution and apoptosis analysis using flow cytometry, colony formation assay using Giemsa staining and cell motility analysis using a Transwell migration assay. Tumor growth was evaluated in vivo in nude mice. The expression levels of a number of signaling molecules were measured to establish the potential mechanism by which silencing KRT17 expression affected PAC PANC-1 cells. Increased levels of KRT17 expression were observed in human PAC compared with normal tissues, as well as in three human PAC cell lines (MIA PaCa-2, PANC-1 and KP-3 cells) compared with the H6c7 human immortal pancreatic duct epithelial cell line. High expression levels of KRT17 in PAC samples were associated with poor overall survival (P=0.036) and disease-free survival (P=0.017). Lentivirus-mediated KRT17 silencing inhibited cell proliferation, colony formation and migration, but promoted apoptosis and resulted in cell cycle arrest in the G0/G1 phase in PANC-1 cells. In addition, KRT17 knockdown inhibited in vivo tumor growth. KRT17 knockdown induced dysregulation of ERK1/2 and upregulation of the pro-apoptotic Bcl-2 protein Bad. In conclusion, the present study demonstrated that elevated KRT17 levels are positively associated with pancreatic cancer progression; KRT17 knockdown suppressed cell growth, colony formation, migration and tumor growth, and induced apoptosis and cell cycle arrest, affecting ERK1/2/Bad signaling. Therefore, the results of the present study suggested that KRT17 may be a potential target for the treatment of pancreatic cancer.

Prognostic significance of peritumoral fibrosis after resection of pancreatic head cancer.

Prognostic value of peritumoral fibrosis (PF) in pancreatic head cancer after resection was evaluated. A total of 143 pancreatic cancer patients who underwent tumor resection were enrolled. All patients underwent routine preoperative examination, including contrast-enhanced computed tomography (CT) or magnetic resonance imaging (MRI). Patients receiving preoperative chemoradiation were excluded because it affects the proportion of fibrosis and cancer cells. Histopathological confirmation and classification of pancreatic head cancer (PHC) was made according to the standards of World Health Organization and the American Joint Committee on Cancer (AJCC). The presence of fibrosis was assessed histologically, and correlated with the clinicopathological characteristics and overall survival using univariate Kaplan-Meier analysis and a stepwise multivariable Cox regression model. Vein resection, resection margin, grading, nodal status, preoperative CA19-9 levels and PF were significantly associated with overall survival. Multivariate analysis showed that all the aforementioned were independent predictive factors of survival. In addition, the survival of patients with PF was significantly worse compared to those without (HR 1.392; P=0.027). Tumor necrosis is a valuable prognostic tool that can be included in the routine post-resection histopathological evaluation of pancreatic head cancer patients.

MicroRNA-493-5p promotes apoptosis and suppresses proliferation and invasion in liver cancer cells by targeting VAMP2.

The aim of the present study was to explore the role of miR­493-5p in liver cancer tissues and cell lines, and its effect on cell behavioral characteristics. The expression of miR-493-5p was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) in liver cancer tissues and cell lines (hepatic cell line HL-7702 and the liver cancer cell lines HCCC-9810, HuH-7 and HepG2). In addition, the mechanism by which miR-493-5p mediates its effects was analyzed via the transfection of miR-493-5p mimic and negative control miRNA into HepG2 cells. The viability, proliferation, apoptosis and invasion of the cells were analyzed using MTT assay, flow cytometry and Transwell chamber experiments. Furthermore, the effect of miR-493-5p on the expression of vesicle associated membrane protein 2 (VAMP2) was assayed using a dual-luciferase reporter system, and VAMP2 protein levels were determined by western blot analysis. In addition, following the cotransfection of HepG2 cells with pcDNA3.1­VAMP2 plasmid and miR­493-5p mimic, the role of miR-493-5p as a regulator of VAMP2 was evaluated using MTT assay, flow cytometry and Transwell chamber experiments. RT-qPCR analysis indicated that the expression of miR-493-5p in liver cancer tissues and cell lines was decreased significantly compared with that in adjacent normal liver tissues and normal liver cell lines, respectively. Compared with the control group, the cells transfected with miR-493-5p mimic (the miR-493-5p overexpression group) exhibited reduced cell viability, a reduced percentage of cells in the S phase and an increased percentage of apoptotic cells. In addition, fewer cells passed through the Transwell membrane in the miR-493-5p overexpression group compared with the control group. In the dual-luciferase reporter assay, luciferase activity in the miR­493-5p overexpression group was attenuated compared with that in the control group. In addition, western blot analysis indicated that the VAMP2 protein levels in the miR­493-5p overexpression group were lower than those in the control group. Furthermore, in cells overexpressing miR-493-5p and VAMP2 simultaneously, the biological behavior of the cells, including cell viability, cell cycle and cell invasiveness, was significantly rescued compared with that of the control group transfected with miR­493-5p alone. In conclusion, miR-493-5p is indicated to be a tumor suppressor gene, and is downregulated in human liver cancer. miR-493-5p overexpression promotes cell apoptosis and inhibits the proliferation and migration of liver cancer cells by negatively regulating the expression of VAMP. These observations suggest the potential of treating liver cancer by the overexpression of microRNA-493-5p.

Inferoposterior duodenal approach for laparoscopic pancreaticoduodenectomy.

AIM: To investigate the advantages of inferoposterior duodenal approach (IPDA) for laparoscopic pancreaticoduodenectomy (LPD). METHODS: A total of 36 patients subjected to LPD were admitted to the Affiliated Yijishan Hospital of Wannan Medical College from December 2009 to February 2015. These patients were diagnosed with an ampullary tumour or a pancreatic head tumour through computed tomography, magnetic resonance imaging or endoscopic retrograde cholangiopancreatography preoperatively. The cases were selected on the basis of the following criteria: tumour diameter < 4 cm; no signs of peripheral vascular invasion; evident lymph node swelling; and distant metastasis. Of the 36 cases, 20 were subjected to anterior approach (AA; AA group) and 16 were subjected to IPDA (IPDA group). Specimen removal time, intraoperative blood loss and postoperative complications in the two groups were observed, and their differences were compared. RESULTS: During the operation, 2 cases in the AA group and 2 cases in the IPDA group were converted to laparotomy; these cases were excluded from statistical analysis. The remaining 32 cases successfully completed the surgery. The AA group and IPDA group exhibited the specimen removal time of 205 ± 52 and 160 ± 35 min, respectively, and the difference was significant (P < 0.01). The AA group and IPDA group revealed the intraoperative blood loss of 360 ± 210 mL and 310 ± 180 mL, respectively, but these values were not significantly different. Postoperative pathological results revealed 4 cases of inferior common bile duct cancer, 8 cases of duodenal papillary cancer, 6 cases of ampullary cancer, 13 cases of pancreatic cancer, 3 cases of chronic pancreatitis accompanied with cyst formation or duct expansion, and 2 cases of mucinous cystic tumour in the pancreatic head. The postoperative complications were pulmonary Staphylococcus aureus infection, incision faulty union, ascites induced poor drainage accompanied with infection, bile leakage, pancreatic leakage and delayed abdominal bleeding. CONCLUSION: In IPDA, probing for important steps can be performed in early stages, surgical procedures can be optimised and operation time can be shortened.

[Laparoscopic pancreaticoduodenectomy: right-inferior-posterior "artery first" approach].

OBJECTIVE: To discuss the application of right-inferior-posterior "artery first" approach in laparoscopic pancreaticoduodenectomy. METHODS: Clinical data of 17 patients who underwent laparoscopic pancreaticoduodenectomy through right-inferior-posterior "artery first" approach in our department from February 2014 to April 2015 were retrospectively analyzed. The operation began at the inferior flexure of duodenum. After entering the Toldt's space, the left renal vein (LRV) was revealed and the root of superior mesenteric artery (SMA) was exposed just above the LRV. SMA was dissected along its trunk till the horizontal part of duodenum. RESULTS: Of these 17 cases, adenocarcinoma of pancreatic head was observed in 5 cases, adenosquamous carcinoma in 2 cases, mucinous cycstic neoplasm in 1 case, adenocarcinoma of lower common bile duct in 4 cases, and duodenal papilla cancer in 5 cases. Fifteen cases were accomplished successfully with laparoscopy and 2 cases were converted to open approach. The average operating time was (320 ± 85) min and mean intraoperative blood loss was (305 ± 175) ml. The cutting margins were tumor negative in all the patients. The average number of harvested lymph node was 15.4 ± 6.5. Postoperative complication occurred in 5 cases. Two cases of bile leakage and 2 cases of pancreatic fistula were cured with conservative treatment. One case of delayed abdominal hemorrhage was resolved with reoperation. CONCLUSION: Right-inferior-posterior "artery first" approach is safe and feasible in laparoscopic pancreaticoduodenectomy.

Over-expression of regulator of G protein signaling 5 promotes tumor metastasis by inducing epithelial-mesenchymal transition in hepatocellular carcinoma cells.

BACKGROUND AND OBJECTIVES: Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related deaths worldwide. The regulator of G-protein signaling 5 (RGS5) has been reported to be highly expressed in some malignant tumors. However, its expression and role in HCC has not been reported. METHODS: The expression of RGS5 was examined in liver cancer tissues and cell lines by real-time quantitative PCR. The cell migration and invasion was investigated by wound healing and transwell invasion assay. The epithelial-mesenchymal transition markers were detected by Western blotting or immunofluorescence. RESULTS: We observed that RGS5 is over-expressed in most of liver cancer tissue samples and cell lines compared with matched normal samples. Further analysis showed that the over-expression of RGS5 is associated with liver cancer recurrence, venous infiltration, and patients' poor survival. Next, we found that knockdown of RGS5 significantly inhibits liver cancer cell migration and invasion in highly invasive liver cancer cells. Furthermore, we found that over-expression of RGS5 induces epithelial-mesenchymal transition in epithelial liver cancer cells. CONCLUSIONS: These results indicate that over-expression of RGS5 promotes tumor metastasis by inducing epithelial-mesenchymal transition in HCC.