Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with few therapeutic options. Recently, insight into cancer biology suggested abnormal lipid metabolism to be a risk factor for human malignancies. As a key enzyme implicated in lipid metabolism, PLD1 was elevated in various human cancer associating with malignant phenotypes. However, little was known about its expression and function in PDAC. We showed that PLD1 was elevated in both the cell lines and clinical samples of PDAC, and it positively correlated with vascular invasion (p = 0.041) and responsible for a poor prognosis (p = 0.009). Meanwhile, we also found Sp1 to be elevated in the disease, correlating with vascular invasion (p = 0.007). Moreover, the correlation assay suggested that PLD1 positively correlated with Sp1 in the clinical sample (r = 0.390; p < 0.001) and the cell lines. Finally, we showed that co-high expression of both the factors confers the poorest prognosis for the patients, and that their simultaneous high expression might be an independent prognostic factor (p = 0.001; HR = 3.427; 95% CI 1.629−7.211).
Highlights
Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with the 5-year survival rate of less than 5% and the median survival of about 6 months, rendering it the fourth most lethal cancer in the United States [1], a frustrating situation had not been changed for decades
As a key enzyme implicated in lipid metabolism, PLD1 was elevated in various human cancer associating with malignant phenotypes
We showed that PLD1 was elevated in both the cell lines and clinical samples of PDAC, and it positively correlated with vascular invasion (p = 0.041) and responsible for a poor prognosis (p = 0.009)
Summary
Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with the 5-year survival rate of less than 5% and the median survival of about 6 months, rendering it the fourth most lethal cancer in the United States [1], a frustrating situation had not been changed for decades. Functionality analysis showed that elevated PLD1 had a positive correlation with angiogenesis, invasion and distant metastasis as well as chemoresistence of human cancer [7, 8]. It had been reported that elevated Sp1 contributes to overexpression of multiple oncogenic genes in human cancers [13], including PDAC [14]. Since PLD1 was reported as an oncogenic gene in various human cancers, we boldly postulated that it positive correlated with Sp1, and they could promote PDAC progression synergistically. We showed that PLD1 was elevated in PDAC, and it positively correlated with vascular invasion and poor survival. We showed that PLD1 positively correlated with Sp1 in PDAC, and their simultaneous high expression was an independent prognostic factor for the patients
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