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    Aberrant secreted protein acidic and rich in cysteine (SPARC) expression has been reported to play an important role in the tumor development. However, the pattern and the role of SPARC in pancreatic cancer remain largely unknown. Therefore, we further deciphered the role of SPARC played in pancreatic cancer. We first evaluated the SPARC expression in human pancreatic cancer tissues and pancreatic cancer cells. Then we forced expression and silenced SPARC expression in pancreatic cancer cell lines MIA PaCa2 and PANC-1, respectively, using lentivirus vectors. We characterized the stable cells in vitro. In this study, we found that SPARC expression was weak in cancer cells in specimens which negatively correlated with the expression level of phosphorylated pRB and poorer outcome. Moreover, our results demonstrated that SPARC negatively regulated pancreatic cell growth in vitro. Furthermore, we disclosed that the activation of p53 and p27Kip1 may involve in the effect of SPARC on pancreatic cancer cells. SPARC is downregulated in pancreatic cancer cells and retards the growth of pancreatic cancer cell. Taken together, these results indicate SPARC may be a potential target for pancreatic cancer therapy.
    CA19-9
    Citations (8)
    Pancreatic cancer is one of the most aggressive, drug-resistant and lethal types of cancer with poor prognosis. Various factors including reactive oxygen species, cytokines, growth factors, and extracellular matrix proteins are reported to be involved in the development of pancreatic cancer. However, the pathogenesis of pancreatic cancer has not been completely elucidated. Oxidative stress has been shown to contribute to the development of pancreatic cancer. Evidences supporting the role of reactive oxygen species and cytokines as a risk for pancreatic cancer and the concept of antioxidant supplementation as a preventive approach for pancreatic cancer have been proposed. Here, we review the literature on oxidative stress, cytokine expression, inflammatory signaling, and natural antioxidant supplementation in relation to pancreatic cancer.
    Pathogenesis
    Proinflammatory cytokine
    CA19-9
    Citations (48)
    Early detection of pancreatic cancer is notoriously difficult. A novel cancer diagnostic method using the ability of nematodes to detect odor of urine samples has been developed (N-NOSE). This method has a high sensitivity and specificity for various cancers; however, it has not yet been verified in pancreatic cancer. We examined the usefulness of this method to aid early diagnosis of pancreatic cancer in a cancer center.We collected urine samples and clinical data from patients hospitalized in our division, between July 2017 and February 2019. We excluded patients with a known current or past history of other cancers. We investigated the relationship between the results of N-NOSE and the presence of pancreatic cancer.There were 95 noncancer cases and 104 pancreatic cancer cases. The sensitivity and specificity of N-NOSE for pancreatic cancer were 84.6% (88/104) and 60% (57/95), respectively. N-NOSE was able to detect stages 0 to I pancreatic cancer and had a higher correlation with early-stage pancreatic cancer than advanced stage.N-NOSE has sufficient sensitivity and specificity for use in clinical practice, and it holds great potential as a diagnostic aid for pancreatic cancer, especially for early-stage pancreatic cancer.
    Pancreatic cancer remains one of the deadliest cancers in the world, as a consequence of late diagnosis, early metastasis and limited response to chemotherapy, under which conditions the potential mechanism of pancreatic cancer progression requires further study. Exosomes are membrane vesicles which are important in the progression, metastasis and chemoresistance in pancreatic cancer. Additionally, they have been verified to be potential as biomarkers, targets and drug carriers for pancreatic cancer treatment. Thus, studying the role of exosomes in pancreatic cancer is significant. This paper focuses on the role of exosomes in the proliferation, metastasis and chemoresistance, as well as their potential applications for pancreatic cancer.
    Tumor progression
    Citations (75)
    TP53 gene has been found to have the highest correlation with human tumors, and its mutations occurr in about 50% malignant tumors. Its encoded p53 protein is a well-known tumor-suppressor factor in vivo, which is closely related to tumorigenesis. It is found that tumorigenesis has a close relationship with various abnormal biological processes, including cell cycle regulation, apoptosis, DNA damage repair, cell senescence, autophagy, metabolic regulation. This paper reviews the complex network relationship between p53 protein and tumorigenesis from biological processes affecting the tumorigenesis. Key words: Neoplams; Tumor suppressor protein p53; Biological processes
    Senescence
    Pancreatic cancer carries a dismal prognosis with a 5-year survival rate of about 5%, and researches have shown that the malignant level and tumor associated glucose metabolism abnormality may both influence the pancreatic cancer progression and prognosis. Recently, growing evidence suggest an association of SOX7 with tumor development. However, there are no studies focusing on the prognostic effect of SOX7 in pancreatic cancer, or its relationship with pancreatic cancer associated diabetes. To investigate the association of SOX7 and prognosis in pancreatic cancer, and further to verify whether SOX7 involves in the regulation of pancreatic cancer associated diabetes. 100 pancreatic cancer-related cases with follow-up information were made into tissue microarrays. Subsequently, the relationship between SOX7 and clinicopathological characteristics was analyzed. SOX7 expression level has a positive correlation with the prognosis of pancreatic cancer patients, especially in the subgroup of tumor size < 5 cm with pathological grades I-II (P=0.014). Moreover, the results showed that SOX7 is significantly negative with diabetes history in the same subgroup (r2=-0.405, P=0.014). SOX7 may exert a tumor suppressor effect in pancreatic cancer, and this effect may correlate with the pathogenesis of paraneoplastic islet injury.
    CA19-9
    Tissue microarray
    Citations (1)