FASTKD2 promotes cancer cell progression through upregulating Myc expression in pancreatic ductal adenocarcinoma

2019 ◽  
Vol 121 (3) ◽  
pp. 2458-2466
Author(s):  
Rui Fang ◽  
Bin Zhang ◽  
Xiaoming Lu ◽  
Xin Jin ◽  
Tao Liu
Keyword(s):  
Pancreatic Ductal Adenocarcinoma ◽  
Cancer Cell ◽  
Ductal Adenocarcinoma ◽  
Cell Progression

scholarly journals Fibroblasts as a Biological Marker for Curative Resection in Pancreatic Ductal Adenocarcinoma

2020 ◽  
Vol 21 (11) ◽  
pp. 3890 ◽  
Author(s):  
Eriko Katsuta ◽  
Omar M. Rashid ◽  
Kazuaki Takabe
Keyword(s):  
Pancreatic Ductal Adenocarcinoma ◽  
Cancer Cell ◽  
Cancer Biology ◽  
Curative Resection ◽  
Biological Marker ◽  
Ductal Adenocarcinoma ◽  
R0 Resection ◽  
Small Subset ◽  
Inverse Association ◽  
Anti Cancer

Achievement of microscopic tumor clearance (R0) after pancreatic ductal adenocarcinoma (PDAC) surgery is determined by cancer biology rather than operative technique. Fibroblasts are known to play pro-cancer roles; however, a small subset was recently found to play anti-cancer roles. Therefore, we hypothesized that intratumor fibroblasts contribute to curative resection and a better survival of PDAC. Utilizing a large, publicly available PDAC cohort, we found that fibroblast composition was associated with R0 curative resection. A high amount of fibroblasts in PDACs was significantly associated with a higher amount of mature vessels, but not with blood angiogenesis. A high amount of fibroblasts was also associated with a higher infiltration of anti-cancer immune cells, such as CD8+ T-cells and dendritic cells, together with higher inflammatory signaling, including IL2/STAT5 and IL6/JAK/STAT3 signaling. Further, the fibroblast composition was inversely associated with cancer cell composition in the bulk tumor, along with an inverse association with proliferative characteristics, such as MYC signaling and glycolysis. The patients with high-fibroblast PDACs showed an improved prognosis. In conclusion, we found that PDACs with high fibroblasts were associated with a higher R0 resection rate, resulting in a better prognosis. These findings may be due to less aggressive biology with a higher vascularity and anti-cancer immunity, and a low cancer cell component.

scholarly journals Transcriptional regulation of SLIT2 expression in pancreatic cancer cell lines

2020 ◽  
Author(s):  
Brenna A. Rheinheimer ◽  
Lukas Vrba ◽  
Bernard W Futscher ◽  
Ronald L Heimark
Keyword(s):  
Pancreatic Cancer ◽  
Transcriptional Regulation ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Cell Lines ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Trichostatin A ◽  
Cancer Cell Lines ◽  
Ductal Adenocarcinoma ◽  
Liver Cancers

AbstractBackgroundSLIT2 has been shown to serve as a tumor suppressor in breast, lung, colon, and liver cancers. Additionally, expression of SLIT2 has been shown to be epigenetically regulated in prostate cancer. Therefore, we sought to determine transcriptional regulation of SLIT2 in pancreatic ductal adenocarcinoma.MethodsRNA expression of SLIT2, SLIT3, and ROBO1 was examined in a panel of pancreatic ductal adenocarcinoma cell lines while protein expression of ROBO1 and SLIT2 was examined in tumor tissue. Methylation of the SLIT2 promoter was determined using Sequenom while histone modifications were queried by chromatin immunoprecipitation. Reexpression of SLIT2 was tested by treatment with 5-aza-2’deoxycytidine and Trichostatin A.ResultsPancreatic cancer cell lines fall into three distinct groups based on SLIT2 and ROBO1 expression. The SLIT2 promoter is methylated in pancreatic ductal adenocarcinoma and SLIT2 expression is dependent on the level of methylation at specific CpG sites. Treatment with 5-aza-2’deoxycytidine (but not Trichostatin A) led to SLIT2 reexpression. The SLIT2 promoter is bivalent in pancreatic ductal adenocarcinoma and histone marks around the transcriptional start site are responsible for transcription.ConclusionsLoss of SLIT2 expression modulated by epigenetic silencing may play a role in pancreatic ductal adenocarcinoma progression.

scholarly journals ZFP36L2promotes cancer cell aggressiveness and is regulated by antitumormicroRNA-375in pancreatic ductal adenocarcinoma

2017 ◽  
Vol 108 (1) ◽  
pp. 124-135 ◽  
Author(s):  
Keiichi Yonemori ◽  
Naohiko Seki ◽  
Hiroshi Kurahara ◽  
Yusaku Osako ◽  
Tetsuya Idichi ◽  
...  
Keyword(s):  
Pancreatic Ductal Adenocarcinoma ◽  
Cancer Cell ◽  
Ductal Adenocarcinoma

scholarly journals Suppression of pancreatic ductal adenocarcinoma growth and metastasis by fibrillar collagens produced selectively by tumor cells

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Chenxi Tian ◽  
Ying Huang ◽  
Karl R. Clauser ◽  
Steffen Rickelt ◽  
Allison N. Lau ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Stromal Cells ◽  
Proteinase Activity ◽  
Ductal Adenocarcinoma ◽  
Fibrillar Collagen ◽  
Fibrillar Collagens ◽  
Tumor Growth And Metastasis

AbstractPancreatic ductal adenocarcinoma (PDAC) has a collagen-rich dense extracellular matrix (ECM) that promotes malignancy of cancer cells and presents a barrier for drug delivery. Data analysis of our published mass spectrometry (MS)-based studies on enriched ECM from samples of progressive PDAC stages reveal that the C-terminal prodomains of fibrillar collagens are partially uncleaved in PDAC ECM, suggesting reduced procollagen C-proteinase activity. We further show that the enzyme responsible for procollagen C-proteinase activity, bone morphogenetic protein1 (BMP1), selectively suppresses tumor growth and metastasis in cells expressing high levels of COL1A1. Although BMP1, as a secreted proteinase, promotes fibrillar collagen deposition from both cancer cells and stromal cells, only cancer-cell-derived procollagen cleavage and deposition suppresses tumor malignancy. These studies reveal a role for cancer-cell-derived fibrillar collagen in selectively restraining tumor growth and suggest stratification of patients based on their tumor epithelial collagen I expression when considering treatments related to perturbation of fibrillar collagens.

scholarly journals SCF, Regulated by HIF-1α, Promotes Pancreatic Ductal Adenocarcinoma Cell Progression

PLoS ONE ◽  
2015 ◽  
Vol 10 (3) ◽  
pp. e0121338 ◽  
Author(s):  
Chuntao Gao ◽  
Shasha Li ◽  
Tiansuo Zhao ◽  
Jing Chen ◽  
He Ren ◽  
...  
Keyword(s):  
Pancreatic Ductal Adenocarcinoma ◽  
Ductal Adenocarcinoma ◽  
Adenocarcinoma Cell ◽  
Cell Progression

scholarly journals Effects of neoadjuvant FOLFIRINOX and gemcitabine-based chemotherapy on cancer cell survival and death in patients with pancreatic ductal adenocarcinoma

Oncotarget ◽  
2019 ◽  
Vol 10 (68) ◽  
pp. 7276-7287 ◽  
Author(s):  
Li Xie ◽  
Leizhou Xia ◽  
Ulla Klaiber ◽  
Milena Sachsenmaier ◽  
Ulf Hinz ◽  
...  
Keyword(s):  
Cell Survival ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Cancer Cell ◽  
Ductal Adenocarcinoma ◽  
Cancer Cell Survival
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