Abstract
Despite improvements in surgical procedures and comprehensive therapies, pancreatic cancer remains one of the most aggressive and deadly human malignancies. It is therefore necessary to determine which cellular mediators associate with prognosis in pancreatic cancer so as to improve the treatment of this disease. In the present study, mRNA array and immunohistochemical analyses showed that KLF5 is highly expressed in tissue samples from three short-surviving patients with pancreatic cancer. Survival analysis using data from The Cancer Genome Atlas showed that patients highly expressing KLF5 exhibited shorter overall and tumor-free survival times. Mechanistically, KLF5 promoted expression of E2F1, cyclin D1 and Rad51, while inhibiting expression of p16 in pancreatic cancer cells. Finally, flow cytometric analyses verified that KLF5 promotes G1/S progression of the cell cycle in pancreatic cancer cells. Collectively, these findings demonstrate that KLF5 is an important prognostic biomarker in pancreatic cancer patients, and they shed light on the molecular mechanism by which KLF5 stimulates cell cycle progression in pancreatic cancer.
Highlights
Pancreatic cancer is one of the most aggressive and deadly human malignancies, with a 5-year survival rate of only 8% [1]
To further examine the mechanisms by which Krüppel-like factor 5 (KLF5) expression leads to a poorer prognosis in pancreatic cancer patients, we identified the microRNAs activated by KLF5 and their target genes and evaluated their roles in the pancreatic cancer pathway extracted in KEGG
The main reasons for the low survival rate are related to 1) the pancreas being situated deep within the www.aging-us.com anatomical structure of the human body and patients being asymptomatic until the disease has reached an advanced stage [2]; 2) only about 20% of pancreatic cancer patients are candidates for surgical resection [27]; and 3) the malignant behavior of pancreatic cancer often leads to early metastasis, early recurrence, and resistance to chemotherapy and radiotherapy [2]
Summary
Pancreatic cancer is one of the most aggressive and deadly human malignancies, with a 5-year survival rate of only 8% [1]. The American Cancer Society estimates that in 2018, new pancreatic cancer cases will be the fourth leading cause of death among all cancer types in both males and females [1]. This unfavorable prognosis is primarily due the aggressive biological behavior of pancreatic tumors, which show early metastasis, poor responses to chemotherapy and radiotherapy, and late diagnosis [2]. For example, KLF5 promotes cell proliferation, migration and invasion by up-regulating expression of TNFAIP2 [14]. KLF5 has been shown to promote breast cancer cell proliferation and survival by upregulating expression of FGF-BP and mPGES1 [15, 16]. A recent study showed that KLF5 promotes cell proliferation, acinar-to-ductal metaplasia, pancreatic intraepithelial neoplasia, and tumor growth [17]
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