GPX2 silencing relieves epithelial–mesenchymal transition, invasion, and metastasis in pancreatic cancer by downregulating Wnt pathway

2019 ◽  
Vol 235 (11) ◽  
pp. 7780-7790 ◽  
Author(s):  
Fuzhou Li ◽  
Lan Dai ◽  
Jixiang Niu
Keyword(s):  
Pancreatic Cancer ◽  
Wnt Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition

CEACAM6 induces epithelial-mesenchymal transition and mediates invasion and metastasis in pancreatic cancer

Pancreatology ◽  
2013 ◽  
Vol 13 (3) ◽  
pp. S27 ◽  
Author(s):  
Jianmin Chen ◽  
Qiang Li ◽  
Yong An ◽  
Nan Lv ◽  
Xiaofeng Xue ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition

Expression Profile of EMT-related Genes and miRNAs Involved in Signal Transduction via the Wnt Pathway and Cadherins in Endometrial Cancer

2020 ◽  
Vol 21 ◽  
Author(s):  
Nikola Zmarzły ◽  
Ewelina Hermyt ◽  
Celina Kruszniewska-Rajs ◽  
Joanna Gola ◽  
Andrzej Witek ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Expression Profile ◽  
Expression Profiling ◽  
Wnt Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Microarray Experiment ◽  
Suppressor Gene ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition ◽  
Low Levels

Background: Epithelial-mesenchymal transition (EMT) is a molecular reprogramming that leads to an increased ability to migrate, which can promote invasion and metastasis. EMT can be initiated in response to the activity of signaling pathways such as Wnt as well as miRNAs. Methods: The study material consisted of 50 endometrial samples: 40 with diagnosed endometrial cancer and 10 without neoplastic changes. Expression profile of EMT-related genes was assessed with microarrays and validated by RT-qPCR. MicroRNA expression profiling was performed using microarrays. It was also determined which miRNAs may participate in the expression regulation of EMT-related genes. Results: CDH1 overexpression was observed in all three endometrial cancer grades using both mRNA microarrays and RTqPCR. Microarray experiment showed a decrease in CDH2 level regardless of the endometrial cancer grade, however it was only partially validated with RT-qPCR. Low levels of WNT2, WNT4, WNT5A have also been observed. Decreased expression of WNT2 and WNT5A may be caused by miR-331-3p and miR-200b-5p, respectively. Conclusions: The Wnt signaling is disrupted in endometrial cancer, which may be due to miR-331-3p and miR-200b-5p activity. In addition, a change in WNT5A level in endometrial cancer compared to control may indicate that it acts as a suppressor gene and that its low expression is associated with tumor progression.

scholarly journals CEACAM6 induces epithelial-mesenchymal transition and mediates invasion and metastasis in pancreatic cancer

2013 ◽  
Vol 43 (3) ◽  
pp. 877-885 ◽  
Author(s):  
JIANMIN CHEN ◽  
QIANG LI ◽  
YONG AN ◽  
NAN LV ◽  
XIAOFENG XUE ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition

scholarly journals Niclosamide and Pyrvinium Are Both Potential Therapeutics for Osteosarcoma, Inhibiting Wnt–Axin2–Snail Cascade

Cancers ◽  
2021 ◽  
Vol 13 (18) ◽  
pp. 4630
Author(s):  
Young Yi ◽  
Young Mi Woo ◽  
Kyu Ho Hwang ◽  
Hyun Sil Kim ◽  
Sang Hyeong Lee
Keyword(s):  
Wnt Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Survival Rates ◽  
Regulatory Mechanisms ◽  
Therapeutic Effects ◽  
Osteosarcoma Cells ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition ◽  
Primary Bone ◽  
Potential Therapeutics

Osteosarcoma, the most common primary bone malignancy, is typically related to growth spurts during adolescence. Prognosis is very poor for patients with metastatic or recurrent osteosarcoma, with survival rates of only 20–30%. Epithelial–mesenchymal transition (EMT) is a cellular mechanism that contributes to the invasion and metastasis of cancer cells, and Wnt signaling activates the EMT program by stabilizing Snail and β-catenin in tandem. Although the Wnt/Snail axis is known to play significant roles in the progression of osteosarcoma, and the anthelmintic agents, niclosamide and pyrvinium, have been studied as inhibitors of the Wnt pathway, their therapeutic effects and regulatory mechanisms in osteosarcoma remain unidentified. In this study, we show that both niclosamide and pyrvinium target Axin2, resulting in the suppression of EMT by the inhibition of the Wnt/Snail axis in osteosarcoma cells. Axin2 and Snail are abundant in patient samples and cell lines of osteosarcoma. The treatment of niclosamide and pyrvinium inhibits the migration of osteosarcoma cells at nanomolar concentrations. These results suggest that Axin2 and Snail are candidate therapeutic targets in osteosarcoma, and that anthelminthic agents, niclosamide and pyrvinium, may be effective for osteosarcoma patients.

scholarly journals Long noncoding RNA LINC00941 promotes pancreatic cancer progression by competitively binding miR-335-5p to regulate ROCK1-mediated LIMK1/Cofilin-1 signaling

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jie Wang ◽  
Zhiwei He ◽  
Jian Xu ◽  
Peng Chen ◽  
Jianxin Jiang
Keyword(s):  
Pancreatic Cancer ◽  
Cell Growth ◽  
Cell Lines ◽  
Cancer Progression ◽  
Noncoding Rna ◽  
Epithelial Mesenchymal Transition ◽  
Loss Of Function ◽  
Mesenchymal Transition

AbstractAn accumulation of evidence indicates that long noncoding RNAs are involved in the tumorigenesis and progression of pancreatic cancer (PC). In this study, we investigated the functions and molecular mechanism of action of LINC00941 in PC. Quantitative PCR was used to examine the expression of LINC00941 and miR-335-5p in PC tissues and cell lines, and to investigate the correlation between LINC00941 expression and clinicopathological features. Plasmid vectors or lentiviruses were used to manipulate the expression of LINC00941, miR-335-5p, and ROCK1 in PC cell lines. Gain or loss-of-function assays and mechanistic assays were employed to verify the roles of LINC00941, miR-335-5p, and ROCK1 in PC cell growth and metastasis, both in vivo and in vitro. LINC00941 and ROCK1 were found to be highly expressed in PC, while miR-335-5p exhibited low expression. High LINC00941 expression was strongly associated with larger tumor size, lymph node metastasis, and poor prognosis. Functional experiments revealed that LINC00941 silencing significantly suppressed PC cell growth, metastasis and epithelial–mesenchymal transition. LINC00941 functioned as a molecular sponge for miR-335-5p, and a competitive endogenous RNA (ceRNA) for ROCK1, promoting ROCK1 upregulation, and LIMK1/Cofilin-1 pathway activation. Our observations lead us to conclude that LINC00941 functions as an oncogene in PC progression, behaving as a ceRNA for miR-335-5p binding. LINC00941 may therefore have potential utility as a diagnostic and treatment target in this disease.

scholarly journals Pancreatic Cancers with High Grade Tumor Budding Exhibit Hallmarks of Diminished Anti-Tumor Immunity

Cancers ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1090
Author(s):  
Hassan Sadozai ◽  
Animesh Acharjee ◽  
Thomas Gruber ◽  
Beat Gloor ◽  
Eva Karamitopoulou
Keyword(s):  
Gene Expression ◽  
Pancreatic Cancer ◽  
Disease Progression ◽  
Immune Escape ◽  
Epithelial Mesenchymal Transition ◽  
Tumor Budding ◽  
Ductal Adenocarcinoma ◽  
Low Grade ◽  
High Grade ◽  
Mesenchymal Transition

Tumor budding is associated with epithelial-mesenchymal transition and diminished survival in a number of cancer types including pancreatic ductal adenocarcinoma (PDAC). In this study, we dissect the immune landscapes of patients with high grade versus low grade tumor budding to determine the features associated with immune escape and disease progression in pancreatic cancer. We performed immunohistochemistry-based quantification of tumor-infiltrating leukocytes and tumor bud assessment in a cohort of n = 111 PDAC patients in a tissue microarray (TMA) format. Patients were divided based on the ITBCC categories of tumor budding as Low Grade (LG: categories 1 and 2) and High Grade (HG: category 3). Tumor budding numbers and tumor budding grade demonstrated a significant association with diminished overall survival (OS). HG cases exhibit notably reduced densities of stromal (S) and intratumoral (IT) T cells. HG cases also display lower M1 macrophages (S) and increased M2 macrophages (IT). These findings were validated using gene expression data from TCGA. A published tumor budding gene signature demonstrated a significant association with diminished survival in PDAC patients in TCGA. Immune-related gene expression revealed an immunosuppressive TME in PDAC cases with high expression of the budding signature. Our findings highlight a number of immune features that permit an improved understanding of disease progression and EMT in pancreatic cancer.

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