ABSTRACT
Pancreatic cancer is a highly malignant, fast progressive digestive system neoplasm with poor prognosis, and the incidence has increased significantly in the recent years. The treatment mode of pancreatic cancer has been transformed from surgery-first approach to multidisciplinary approach including surgery, chemotherapy, radiotherapy and other comprehensive treatment modalities, accompanying with significant improvement in clinical efficacy. During the last decade, the molecular mechanism of pancreatic cancer has been explored in depth. Indeed, we had a clearer understanding of the disease, which provides clues for translation of basic research into clinical practice. This review summarized recent high quality studies on pancreatic cancer including pathogenic factor, advances in basic research, and clinical treatment.
ABSTRACT
Pancreatic ductal adenocarcinoma (PDAC) is among the most devastating human malignancies. The poor clinical outcome in PDAC is partly attributed to a growth-permissive tumor microenvironment. In the PDAC microenvironment, the stroma is characterized by the development of extensive fibrosis, with stromal components outnumbering pancreatic cancer cells. Each of the components within the stroma has a distinct role in conferring chemoresistance to PDAC, and intrinsic chemoresistance has further worsened this pessimistic prognosis. The nucleoside analog gemcitabine (GEM) is usually the recommended first-line chemotherapeutic agent for PDAC patients and is given alone or in combination with other agents. The mechanisms of intrinsic resistance to GEM are an active area of ongoing research. This review highlights the important role the complex structure of stroma in PDAC plays in the intrinsic resistance to GEM and discusses whether antistroma therapy improves the efficacy of GEM. The addition of antistroma therapy combined with GEM is expected to be a novel therapeutic strategy with significant survival benefits for PDAC patients.
ABSTRACT
With the increase of morbidity and mortality, pancreatic cancer will not only become one of the leading causes of death in China, but also a major public health problem in the world. New onset cases of pancreatic cancer all around the world are expected to increase year by year. The prognosis of patients with pancreatic cancer is poor. The 5-year survival rate is only about 6%. The major reason for the poor prognosis is the lack of typical clinical symptoms in the early stage of disease, which makes it difficult to detect and control its relevant recurrence and metastasis. Moreover, lack of effective chemotherapy drugs and resistance to existing chemotherapy drugs are also important reasons for its dismal status. Radical resection surgery is still the most effective treatment. However, even after radical resection surgery, early recurrence and distant metastasis are still the main problems that bother patients. This article reviews recent high quality studies on pancreatic cancer including epidemiological investigation, advances in basic research, and clinical treatment.
ABSTRACT
Background and purpose:Lower expression of E-cadherin is associated with metastasis of cancer cells, however, the correlation between E-cadherin and glucose metabolism has seldom been reported. This article studied the correlation between E-cadherin and glycolysis effect in PANC-1 cells.Methods:Through treatment of transforming growth factor β (TGF-β) in PANC-1 cells to decrease E-cadherin expression, knock-down the gene of E-cadherin interaction protein β-catenin, and overexpressing of E-cadherin, the effects of E-cadherin on the glucose uptake and lactate production ability and on the expression of key glycolytic genes were assessed.Results:E-cadherin negatively regulated the glycolytic effect of PANC-1 cells by inhibiting glucose uptake and lactate production (P<0.05). Moreover, E-cadherin interacting partner β-catenin signiifcantly promoted glucose metabolism transformation in PANC-1 cells (P<0.05). Moreover, key glycolysis regulator sirtuin 3 (SIRT3) could lower E-cadherin expression.Conclusion:Lower expression of E-cadherin induced the transformation of glucose metabolism transformation in PANC-1 cells and manipulation of E-cadherin expression level could change the glycolysis effect. Moreover, through maneuver glycolysis process could inhibit high metastatic potential of pancreatic cancer cells.