HNF1A/CASC2 regulates pancreatic cancer cell proliferation through PTEN/Akt signaling

2018 ◽  
Vol 120 (3) ◽  
pp. 2816-2827 ◽  
Author(s):  
Yaqun Yu ◽  
Shuai Liang ◽  
Yingqiong Zhou ◽  
Shuqun Li ◽  
Yixiong Li ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Akt Signaling ◽  
Cancer Cell Proliferation

Devil’s Club Falcarinol-Type Polyacetylenes Inhibit Pancreatic Cancer Cell Proliferation

2019 ◽  
Vol 71 (2) ◽  
pp. 301-311 ◽  
Author(s):  
Susan S. C. Cheung ◽  
David Hasman ◽  
Djamel Khelifi ◽  
Joseph Tai ◽  
Richard W. Smith ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Proliferation

Abstract PO-034: CPSF3 inhibition halts pancreatic cancer cell proliferation by limiting core histone supplies

2021 ◽  
Author(s):  
Abdulrahman A. Alahmari ◽  
Carla Schwarz ◽  
Emily Paterson ◽  
Swati Venkat ◽  
Arwen Tisdale ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Core Histone ◽  
Cancer Cell Proliferation

scholarly journals Keratin 17 Suppresses Cell Proliferation and Epithelial-Mesenchymal Transition in Pancreatic Cancer

2020 ◽  
Vol 7 ◽  
Author(s):  
Yong Zeng ◽  
Min Zou ◽  
Yan Liu ◽  
Keting Que ◽  
Yunbing Wang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Cell Cycle Progression ◽  
Pancreatic Cancer Cell ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Cycle Progression ◽  
Mesenchymal Transition

Keratin 17 (K17), a member of type I acidic epithelial keratin family, has been reported to be upregulated in many malignant tumors and to be involved in promoting the development of tumors. However, the precise role of K17 in progression of pancreatic cancer is still unknown. In this study, we found that K17 expression was highly expressed in pancreatic cancer tissues and cell lines and that upregulated expression was associated with the pathological grade and poor prognosis. K17 expression served as an independent predictor of pancreatic cancer survival. Meanwhile, we showed that knocking down K17 induced pancreatic cancer cell proliferation, colony formation and tumor growth in xenografts in mice. However, K17 upregulation inhibited pancreatic cancer cell proliferation and colony formation. Further mechanistic study revealed that K17 knockdown promoted cell cycle progression by upregulating CyclinD1 expression and repressed cell apoptosis. However, K17 upregulation suppressed cell cycle progression by decreasing CyclinD1 expression, and induced apoptosis by increasing the levels of cleaved Caspase3. In addition, K17 knockdown promoted pancreatic cancer cell migration and invasion, but K17 upregulation suppressed cell migration and invasion. Moreover, knocking down K17 promoted epithelial-mesenchymal transition (EMT) in pancreatic cancer cell by inhibiting E-cadherin expression and inducing Vimentin expression, and the effects of K17 upregulation were opposite to that of K17downregulation. Taken together, our findings suggest that K17 functions as a potential tumor suppressor, even though it is upregulated in pancreatic cancer.

PLS3 predicts poor prognosis in pancreatic cancer and promotes cancer cell proliferation via PI3K/AKT signaling

2020 ◽  
Vol 235 (11) ◽  
pp. 8416-8423 ◽  
Author(s):  
Zechang Xin ◽  
Duguang Li ◽  
Feiyu Mao ◽  
Yan Du ◽  
Xiaodong Wang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Poor Prognosis ◽  
Akt Signaling ◽  
Cancer Cell Proliferation
Sign in / Sign up

Export Citation Format

Share Document