scholarly journals Long non-coding RNA SPRY4-IT1 promotes cell proliferation and invasion by regulation of Cdc20 in pancreatic cancer cells

PLoS ONE ◽  
2018 ◽  
Vol 13 (2) ◽  
pp. e0193483 ◽  
Author(s):  
Wenhao Guo ◽  
Kunhong Zhong ◽  
Heng Wei ◽  
Chunlai Nie ◽  
Zhu Yuan
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Xibao Hu ◽  
Lei Zhang ◽  
Jingjing Tian ◽  
Junhong Ma

Abstract Background and objectives Long non-coding RNA (lncRNA) prostate androgen-regulated transcript 1 (PART1) was previously shown to exert an oncogenic role in several human cancers. However, whether PART1 is associated with the malignant progression of pancreatic cancer remains unclear. In the current study, we aimed to identify the role and potential mechanism of PART1 in pancreatic cancer. Methods qRT-PCR was applied to detect PART1 expression in 45 cases of pancreatic cancer patients. The chi-square test was performed to assess the association between PART1 expression and clinicopathologic features, and Kaplan-Meier method was applied to evaluate overall survival. In vitro CCK-8, transwell invasion, and flow cytometry assays were applied to detect the effects of PART1 on cell proliferation, invasion, and apoptosis, respectively. Luciferase reporter and RNA immunoprecipitation assays were used to identify the regulatory mechanism between PART1 and miR-122. Results PART1 expression was upregulated in pancreatic cancer tissues and cell lines. High PART1 expression was closely correlated with tumor size, T classification, clinical stage, and vascular invasion, and predicted a poor overall survival. PART1 knockdown significantly suppressed cell proliferation and invasion abilities of pancreatic cancer but promoted cell apoptosis. PART1 was found to serve as a molecular sponge of miR-122, and miR-122 inhibition partially reversed the inhibitory phenotypes of PART1 knockdown on pancreatic cancer cells. Conclusions PART1 promotes the malignant progression of pancreatic cancer by sponging miR-122. The PART1/miR-122 axis might be a promising target for anticancer therapy in patients with pancreatic cancer.


2010 ◽  
Vol 138 (5) ◽  
pp. S-448
Author(s):  
Shumei Song ◽  
Baoan Ji ◽  
Vijaya Ramachandran ◽  
Nachman Mazurek ◽  
Huamin Wang ◽  
...  

2018 ◽  
Vol 97 ◽  
pp. 809-817 ◽  
Author(s):  
Zhi-Qiang Gao ◽  
Jun-feng Wang ◽  
De-Hua Chen ◽  
Xue-Song Ma ◽  
Wu Yang ◽  
...  

Oncotarget ◽  
2018 ◽  
Vol 9 (78) ◽  
pp. 34719-34734 ◽  
Author(s):  
Norihiko Sasaki ◽  
Masashi Toyoda ◽  
Hisashi Yoshimura ◽  
Yoko Matsuda ◽  
Tomio Arai ◽  
...  

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Yueqin Feng ◽  
Yuguan Jiang ◽  
Fengjin Hao

Abstract Background Pancreatic cancer is one of the most serious digestive malignancies. At present, there is an extreme lack of effective strategies in clinical treatment. The purpose of this study is to identify key genes and pathways in the development of pancreatic cancer and provide targets for the treatment of pancreatic cancer. Methods GSE15471 and GSE62165 were used to screen differentially expressed genes by GEO2R tool. Hub genes prognostic potential assessed using the GEPIA and Kaplan–Meier plotter databases. The drug susceptibility data of pan-cancer cell lines is provided by The Genomics of Drug Sensitivity in Cancer Project (GDSC). Finally, the effects of PI3K–Akt signaling pathway inhibitors on cell viability of pancreatic cancer cells were detected by cell proliferation and invasion assays. Results A total of 609 differentially expressed genes were screened and enriched in the focal adhesion, phagosome and PI3K–Akt signaling pathway. Of the 15 hub genes we found, four were primarily associated with the PI3K–Akt signaling pathway, including COL3A1, EGF, FN1 and ITGA2. GDSC analysis showed that mTOR inhibitors are very sensitive to pancreatic cancer cells with mutations in EWSR1.FLI1 and RNF43. Cell proliferation and invasion results showed that mTOR inhibitors (GSK2126458) can inhibit the proliferation of pancreatic cancer cells. Conclusions This study suggested that the PI3K–Akt signaling pathway may be a key pathway for pancreatic cancer, our study uncovered the potential therapeutic potential of GSK2126458, a specific mTOR inhibitor, for pancreatic cancer.


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