scholarly journals CCR9 initiates epithelial–mesenchymal transition by activating Wnt/β-catenin pathways to promote osteosarcoma metastasis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Haoran Kong ◽  
Wenhui Yu ◽  
Zhuning Chen ◽  
Haonan Li ◽  
Guiwen Ye ◽  
...  
Keyword(s):  
Cell Migration ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Lung Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Regulatory Relationship ◽  
Mesenchymal Transition ◽  
Cell Migration And Invasion ◽  
Matrigel Invasion

Abstract Background Osteosarcoma (OS) patients with lung metastasis have poor prognoses, and effective therapeutic strategies for delaying or inhibiting the spread of lung metastasis from the primary OS site are lacking. Hence, it is critical to elucidate the underlying mechanisms of OS metastasis and to identify additional new effective treatment strategies for patients. Methods Differential expression and functional analyses were performed to identify key genes and relevant signaling pathways associated with OS lung metastasis. The expression of CCR9 in OS cell lines and tissues was measured by RT-qPCR, western blotting and immunohistochemistry. Cell migration and invasion were assessed by wound healing and Transwell Matrigel invasion assays, respectively. The regulatory relationship between CCR9 and the Wnt/β-catenin signaling pathway was further evaluated by rescue experiments. Results The expression of CCR9 was elevated in OS cell lines and patients with lung metastasis. CCR9 promoted MG63 and HOS cell migration and invasion by activating the Wnt/β-catenin signaling pathway. Furthermore, knockdown of CCR9 repressed epithelial–mesenchymal transition (EMT) by downregulating mesenchymal markers (N-cadherin and Vimentin) and EMT-associated transcription factors (twist and snail) and upregulating an epithelial marker (E-cadherin). Conclusions Our findings suggest that CCR9 promotes EMT by activating Wnt/β-catenin pathways to promote OS metastasis. CCR9 may be a promising therapeutic target to inhibit lung metastasis and serve as a novel prognostic marker for OS.

scholarly journals The Overexpression of Keratin 23 Promotes Migration of Ovarian Cancer via Epithelial-Mesenchymal Transition

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Meng Ren ◽  
Yan Gao ◽  
Qi Chen ◽  
Hongyu Zhao ◽  
Xiaoting Zhao ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Migration ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Cell Migration And Invasion ◽  
Smad Signaling ◽  
Smad Signaling Pathway

Background. Keratin 23 (KRT23) is a new member of the KRT gene family and known to be involved in the development and migration of various types of tumors. However, the role of KRT23 in ovarian cancer (OC) remains unclear. This study is aimed at investigating the function of KRT23 in OC. Methods. The expression of KRT23 in normal ovarian and OC tissues was determined using the Oncomine database and immunohistochemical staining. Reverse transcription quantitative polymerase chain reaction assay was used to analyze the expression of KRT23 in normal ovarian epithelial cell lines and OC cell lines. Small interfering RNA (siRNA), wound healing assay, and transwell assay were conducted to detect the effects of KRT23 on OC cell migration and invasion. Further mechanistic studies were verified by the Gene Expression Profiling Interactive Analysis platform, Western blotting, and immunofluorescence staining. Results. KRT23 was highly expressed in OC tissues and cell lines. High KRT23 expression could regulate OC cell migration and invasion, and the reduction of KRT23 by siRNA inhibited the migration and invasion of OC cells in vitro. Furthermore, KRT23 mediated epithelial-mesenchymal transition (EMT) by regulating p-Smad2/3 levels in the TGF-β/Smad signaling pathway. Conclusions. These results demonstrate that KRT23 plays an important role in OC migration via EMT by regulating the TGF-β/Smad signaling pathway.

488 SNAIL TRANSFECTION INDUCES EPITHELIAL-MESENCHYMAL TRANSITION WITH PROPERTIES OF CANCER STEM-LIKE CELL IN ESOPHAGEAL SQUAMOUS CELL CANCER

2021 ◽  
Vol 34 (Supplement_1) ◽  
Author(s):  
Ching Tzao ◽  
Meng-Hsun Wu ◽  
Ben-Hen Chen
Keyword(s):  
Cell Migration ◽  
Cell Lines ◽  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Cell Cancer ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Cell Migration And Invasion ◽  
Sphere Formation ◽  
E Cadherin

Abstract   Cancer stem-like cell (CSC) is an important player in tumorigenesis and tumor progression. Snail has been demonstrated as a key driver for epithelial-mesenchymal transition (EMT) that is closely linked with generation of stem-like cell in human cancer. We aim to investigate if Snail transfection induces EMT and properties of stem-like cell in esophageal squamous cell carcinoma (ESCC) cell lines. Methods A lentivirus system was used to transfect human Snail via a plasmid pLV-EF1a-hSnail-Hyg into KYSE-170 and KYSE-510 ESCC cell lines. Immunoblotting was used to determine expression of EMT associated markers including Vimentin, E-cadherin, Fibronectin and N-cadherin. Assays for cell migration and invasion were conducted in Snail-transfected cells and its vector control. Cytotoxicity (MTT) and cell proliferation assay was used to determine cell growth. Sphere formation assay and flow cytometry (FCM) were employed to characterize stem cell properties while examining expression of stemness genes by using real-time polymerase chain reaction (PCR). Results After Snail transfection, mesenchymal markers, Vimentin, N-cadherin increased, whereas epithelial marker E-cadherin decreased. Snail-transfected. ESCC cells presented a significant increase in RNA expression of stemness genes such as Nanog, Oct4, ABCG2 and Sox2 with an induction in sphere formation. Moreover, ability of cell migration and invasion increased after Snail-transfection in ESCC with increased chemoresistance to cisplatin, taxol, and 5-Fluorouracil(5-FU) and an increase in radioresistance as well. Conclusion Our results demonstrated that Snail transfection induced EMT with properties of CSC in ESCC cell lines.

scholarly journals Irisin reverses the IL-6 induced epithelial-mesenchymal transition in osteosarcoma cell migration and invasion through the STAT3/Snail signaling pathway

2017 ◽  
Vol 38 (5) ◽  
pp. 2647-2656 ◽  
Author(s):  
Gang Kong ◽  
Yunpeng Jiang ◽  
Xiujiang Sun ◽  
Zhilin Cao ◽  
Guodong Zhang ◽  
...  
Keyword(s):  
Cell Migration ◽  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Osteosarcoma Cell ◽  
Mesenchymal Transition ◽  
Cell Migration And Invasion

scholarly journals YPEL3 suppresses epithelial–mesenchymal transition and metastasis of nasopharyngeal carcinoma cells through the Wnt/β-catenin signaling pathway

2016 ◽  
Vol 35 (1) ◽  
Author(s):  
Jian Zhang ◽  
Xin Wen ◽  
Xian-Yue Ren ◽  
Ying-Qin Li ◽  
Xin-Ran Tang ◽  
...  
Keyword(s):  
Cell Migration ◽  
Nasopharyngeal Carcinoma ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Western Blotting ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Mesenchymal Transition

Abstract Background Metastasis remains the major cause of death in nasopharyngeal carcinoma (NPC). Yippee-like 3 (YPEL3) plays an important role in tumorigenesis. However, its function and mechanism in NPC has not been systematically explored. Methods We evaluated YPEL3 expression in NPC cell lines and tissues using real-time PCR and western blotting. Then, we established NPC cell lines that stably overexpressed YPEL3 and knocked down YPEL3 expression to explore its function in NPC in vitro and in vivo. Additionally, we investigated the potential mechanism of YPEL3 action by identifying the Wnt/β-catenin signaling pathway downstream genes using western blotting. Results YPEL3 was downregulated in NPC cell lines and tissue samples. Ectopic expression of YPEL3 inhibited NPC cell migration and invasion in vitro; while silencing of YPEL3 promoted NPC cell migration and invasion. Further study indicated that overexpression of YPEL3 inhibited NPC cell epithelial–mesenchymal transition (EMT) and that silencing it enhanced EMT. Overexpression of YPEL3 suppressed NPC cell lung metastasis in vivo. The mechanism study determined that YPEL3 suppressed the expression levels of Wnt/β-catenin signaling pathway downstream genes and the nuclear translocation of β-catenin. Conclusions YPEL3 suppresses NPC EMT and metastasis by suppressing the Wnt/β-catenin signaling pathway, which would help better understanding the molecular mechanisms of NPC metastasis and provide novel therapeutic targets for NPC treatment.

Visfatin facilitates gastric cancer malignancy by targeting snai1 via the NF-κB signaling

2021 ◽  
pp. 096032712110061
Author(s):  
D Cao ◽  
L Chu ◽  
Z Xu ◽  
J Gong ◽  
R Deng ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Migration ◽  
Western Blot ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Cell Migration And Invasion ◽  
Protein Levels

Background: Visfatin acts as an oncogenic factor in numerous tumors through a variety of cellular processes. Visfatin has been revealed to promote cell migration and invasion in gastric cancer (GC). Snai1 is a well-known regulator of EMT process in cancers. However, the relationship between visfatin and snai1 in GC remains unclear. The current study aimed to explore the role of visfatin in GC. Methods: The RT-qPCR and western blot analysis were used to measure RNA and protein levels, respectively. The cell migration and invasion were tested by Trans-well assays and western blot analysis. Results: Visfatin showed upregulation in GC cells. Additionally, Visfatin with increasing concentration facilitated epithelial-mesenchymal transition (EMT) process by increasing E-cadherin and reducing N-cadherin and Vimentin protein levels in GC cells. Moreover, endogenous overexpression and knockdown of visfatin promoted and inhibited migratory and invasive abilities of GC cells, respectively. Then, we found that snai1 protein level was positively regulated by visfatin in GC cells. In addition, visfatin activated the NF-κB signaling to modulate snai1 protein expression. Furthermore, the silencing of snai1 counteracted the promotive impact of visfatin on cell migration, invasion and EMT process in GC. Conclusion: Visfatin facilitates cell migration, invasion and EMT process by targeting snai1 via the NF-κB signaling, which provides a potential insight for the treatment of GC.

scholarly journals Cytoplasmic SIRT1 inhibits cell migration and invasion by impeding epithelial–mesenchymal transition in ovarian carcinoma

2019 ◽  
Vol 459 (1-2) ◽  
pp. 157-169 ◽  
Author(s):  
Tong Yang ◽  
Ru Zhou ◽  
Shentong Yu ◽  
Shuhong Yu ◽  
Zhuqing Cui ◽  
...  
Keyword(s):  
Cell Migration ◽  
Ovarian Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Cell Migration And Invasion
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