scholarly journals Kinesin family member C1 accelerates bladder cancer cell proliferation and induces epithelial–mesenchymal transition via Akt/ GSK 3β signaling

2019 ◽  
Vol 110 (9) ◽  
pp. 2822-2833 ◽  
Author(s):  
Kang‐hua Xiao ◽  
Kai Teng ◽  
Yun‐lin Ye ◽  
Lei Tan ◽  
Ming‐kun Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Family Member ◽  
Cancer Cell ◽  
Epithelial Mesenchymal Transition ◽  
Bladder Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Mesenchymal Transition ◽  
Gsk 3Β ◽  
Kinesin Family

scholarly journals MiR-205 Dysregulations in Breast Cancer: The Complexity and Opportunities

2019 ◽  
Vol 5 (4) ◽  
pp. 53 ◽  
Author(s):  
Xiao ◽  
Humphries ◽  
Yang ◽  
Wang
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Target Gene ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Metastatic Breast ◽  
Therapy Resistance ◽  
Cancer Cell Proliferation ◽  
Mesenchymal Transition

MicroRNAs (miRNAs) are endogenous non-coding small RNAs that downregulate target gene expression by imperfect base-pairing with the 3′ untranslated regions (3′UTRs) of target gene mRNAs. MiRNAs play important roles in regulating cancer cell proliferation, stemness maintenance, tumorigenesis, cancer metastasis, and cancer therapeutic resistance. While studies have shown that dysregulation of miRNA-205-5p (miR-205) expression is controversial in different types of human cancers, it is generally observed that miR-205-5p expression level is downregulated in breast cancer and that miR-205-5p exhibits a tumor suppressive function in breast cancer. This review focuses on the role of miR-205-5p dysregulation in different subtypes of breast cancer, with discussions on the effects of miR-205-5p on breast cancer cell proliferation, epithelial–mesenchymal transition (EMT), metastasis, stemness and therapy-resistance, as well as genetic and epigenetic mechanisms that regulate miR-205-5p expression in breast cancer. In addition, the potential diagnostic and therapeutic value of miR-205-5p in breast cancer is also discussed. A comprehensive list of validated miR-205-5p direct targets is presented. It is concluded that miR-205-5p is an important tumor suppressive miRNA capable of inhibiting the growth and metastasis of human breast cancer, especially triple negative breast cancer. MiR-205-5p might be both a potential diagnostic biomarker and a therapeutic target for metastatic breast cancer.

miR-144 downregulation increases bladder cancer cell proliferation by targeting EZH2 and regulating Wnt signaling

FEBS Journal ◽  
2013 ◽  
Vol 280 (18) ◽  
pp. 4531-4538 ◽  
Author(s):  
Yuwen Guo ◽  
Liang Ying ◽  
Ye Tian ◽  
Peiqian Yang ◽  
Yichen Zhu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Wnt Signaling ◽  
Cancer Cell ◽  
Bladder Cancer Cell ◽  
Cancer Cell Proliferation

scholarly journals lncRNA CCAT1 promotes bladder cancer cell proliferation, migration and invasion

2019 ◽  
Vol 45 (3) ◽  
pp. 549-559 ◽  
Author(s):  
Caixiang Zhang ◽  
Wenying Wang ◽  
Jun Lin ◽  
Jing Xiao ◽  
Ye Tian
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cell ◽  
Bladder Cancer Cell ◽  
Migration And Invasion ◽  
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.

scholarly journals ADNP Upregulation Promotes Bladder Cancer Cell Proliferation via the AKT Pathway

2020 ◽  
Vol 10 ◽  
Author(s):  
Shuai Zhu ◽  
Zhenzhou Xu ◽  
Yong Zeng ◽  
Ying Long ◽  
Gang Fan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cell ◽  
Bladder Cancer Cell ◽  
Akt Pathway ◽  
Cancer Cell Proliferation
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