scholarly journals Cyclin F Downregulation Affects Epithelial-Mesenchymal Transition Increasing Proliferation and Migration of the A-375 Melanoma Cell Line

2020 ◽  
Vol Volume 12 ◽  
pp. 13085-13097
Author(s):  
Adrian Krajewski ◽  
Maciej Gagat ◽  
Klaudia Mikołajczyk ◽  
Magdalena Izdebska ◽  
Agnieszka Żuryń ◽  
...  
Keyword(s):  
Cell Line ◽  
Melanoma Cell ◽  
Melanoma Cell Line ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
And Migration ◽  
Cyclin F ◽  
Proliferation And Migration

SAHA modulates cell proliferation, colony forming and epithelial-mesenchymal transition in CCA cells

2018 ◽  
Vol 44 (1) ◽  
pp. 70-77
Author(s):  
Gülden Başkol ◽  
Merve Özel ◽  
Çiğdem Uçar ◽  
Büşra Nur Doğru ◽  
Esra Hilal Yüksek ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Line ◽  
Protein Level ◽  
Epithelial Mesenchymal Transition ◽  
Chemotherapeutic Regimen ◽  
Mesenchymal Transition ◽  
Protein Levels ◽  
Cholangiocarcinoma Cell ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Therapeutic options for advanced cholangiocarcinoma (CCA) are limited and ineffective due to the largely incomplete understanding of the molecular pathogenesis of this deadly tumor. So that, we planned to investigate epigenetic regulation of epithelial-mesenchymal transition (EMT) in cholangiocarcinoma cell line by applying Suberoylanilide hydroxamic acid (SAHA). We studied the effect of SAHA on cell proliferation, colony forming, migration and protein level of E-cadherin (E-cad) as an epithelial EMT marker, N-cadherin (N-cad) and Vimentin (Vim), as a mesenchymal markers of EMT, in human CCA cell line. Materials and methods Cell proliferation and migration measurements were performed by flow cytometry and wound healing assay, respectively. E-cad, N-cad and Vim protein levels were determined by Western blot analysis. Results It was found that SAHA significantly inhibits cell viability, proliferation and migration of TFK-1 cells, accompanied by reversing of EMT markers. SAHA, upregulated protein level of E-cad, while downregulated the protein levels of N-cad and Vimentin. Conclusions SAHA treatment may bebeneficial for CCA patients and SAHA might be a potential therapeutic agent for the treatment of CCA. However, future studies are needed to evaluate the clinical applicability of SAHA as a part of the chemotherapeutic regimen for CCA.

FAM196B promotes proliferation and migration via regulating epithelial-mesenchymal transition in esophageal cancer

2021 ◽  
pp. 1-8
Author(s):  
Haifeng Xia ◽  
Fang Hu ◽  
Liangbin Pan ◽  
Chengcheng Xu ◽  
Haitao Huang ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Western Blot ◽  
Cox Regression ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Cox Regression Analysis ◽  
Ec Cells ◽  
And Migration ◽  
Proliferation And Migration

BACKGROUND: EC (esophageal cancer) is a common cancer among people in the world. The molecular mechanism of FAM196B (family with sequence similarity 196 member B) in EC is still unclear. This article aimed to clarify the role of FAM196B in EC. METHODS: The expression of FAM196B in EC tissues was detected using qRT-PCR. The prognosis of FAM196B in EC patients was determined by log-rank kaplan-Meier survival analysis and Cox regression analysis. Furthermore, shRNA was used to knockdown the expression of FAM196B in EC cell lines. MTT, wound healing assays and western blot were used to determine the role of FAM196B in EC cells. RESULTS: In our research, we found that the expression of FAM196B was up-regulated in EC tissues. The increased expression of FAM196B was significantly correlated with differentiation, lymph node metastasis, stage, and poor survival. The proliferation and migration of EC cells were inhibited after FAM196B-shRNA transfection in vitro and vivo. The western blot result showed that FAM196B could regulate EMT. CONCLUSION: These results suggested that FAM196B severs as an oncogene and promotes cell proliferation and migration in EC. In addition, FAM196B may be a potential therapeutic target for EC patients.

scholarly journals MeCP2 inhibits proliferation and migration of breast cancer via suppression of epithelial‐mesenchymal transition

2020 ◽  
Vol 24 (14) ◽  
pp. 7959-7967
Author(s):  
Wei Jiang ◽  
Yan‐Ling Liang ◽  
Yang Liu ◽  
Yu‐Yan Chen ◽  
Shu‐Ting Yang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals TRAF6 Promotes Gastric Cancer Cell Self-Renewal, Proliferation, and Migration

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Mengting Yang ◽  
Meng Jin ◽  
Kailong Li ◽  
Haifeng Liu ◽  
Xiaxia Yang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Tumor Necrosis Factor Receptor ◽  
Gastric Cancer Cells ◽  
Mesenchymal Transition ◽  
In The Wild ◽  
And Migration ◽  
Exact Effect ◽  
Proliferation And Migration

Gastric cancer is the third most common type of tumor associated with death. TRAF6 belongs to the tumor necrosis factor receptor-associated factor family and has been demonstrated to be involved in tumor progression in various cancers. However, the exact effect of TRAF6 on gastric cancer stem cells has not been extensively studied. In this study, abnormal expression of TRAF6 was found in gastric cancer tissues. Overexpression of TRAF6 enhanced proliferation and migration, and TRAF6 knockdown reversed this phenomenon in gastric cancer cells. Moreover, TRAF6 may inhibit differentiation and promote stemness and epithelial-mesenchymal transition (EMT). Transcriptome profiles revealed 701 differentially expressed genes in the wild-type group and the TRAF6 knockout group. Potential molecules associated with cell proliferation and migration were identified, including MAPK, FOXO, and IL-17. In conclusion, TRAF6 is a significant factor promoting proliferation and migration in gastric cancer cells and may provide a new target for the accurate treatment of gastric cancer.

scholarly journals Tumor-Suppressive Function of lncRNA-MEG3 in Glioma Cells by Regulating miR-6088/SMARCB1 Axis

2020 ◽  
Vol 2020 ◽  
pp. 1-15 ◽  
Author(s):  
Xin Gong ◽  
Meng-Yi Huang
Keyword(s):  
Cell Proliferation ◽  
Epithelial Mesenchymal Transition ◽  
Glioma Cells ◽  
Luciferase Reporter ◽  
Favorable Effect ◽  
Mesenchymal Transition ◽  
Gene Assay ◽  
And Migration ◽  
Proliferation And Migration ◽  
Glioma Progression

Objective. Mounting evidence has elaborated the implication of long noncoding RNAs (lncRNAs) in tumorigenesis of several cancers, including glioma. However, little was known about the mechanism of lncRNA maternally expressed gene 3 (MEG3) in the development and progression of glioma. This work is designed to explore the effect of MEG3 on glioma progression and its possible mechanism. Methods. Expressions of lncRNA-MEG3 and SMARCB1 were detected in human glioblastoma U87 and U251 cell lines. Gain and loss of function of MEG3 or/and miR-6088 was performed in U87 and U251 cells to observe its effect on cell proliferation and migration as well as on epithelial-mesenchymal transition (EMT) related markers. Luciferase reporter gene assay was employed to inspect the interactions among MEG3, miR-6088, and SMARCB1. Results. MEG3 and SMARCB1 expressions were downregulated in glioma cells. Transfection of pcDNA3.1-MEG3 or pcDNA3.1-SMARCB1 plasmids could clearly block cell proliferation, migration, and EMT progression. MEG3 functions as a sponge for miR-6088, while SMARCB1 is a downstream protein of miR-6088. Transfection of miR-6088 mimic or si-SMARCB1 could obviously reverse the favorable effect of pcDNA3.1-MEG3 on glioma progression. Conclusion. Collectively, the evidence in this study indicated that MEG3 was downregulated in glioma cells and inhibited proliferation and migration of glioma cells via regulating miR-6088/SMARCB1 axis.

scholarly journals GJA1 promotes hepatocellular carcinoma progression by mediating TGF-β-induced activation and the epithelial–mesenchymal transition of hepatic stellate cells

Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 1459-1471
Author(s):  
Gengming Niu ◽  
Xiaotian Zhang ◽  
Runqi Hong ◽  
Ximin Yang ◽  
Jiawei Gu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Conditioned Medium ◽  
Hepatic Stellate Cells ◽  
Hepatic Cirrhosis ◽  
Epithelial Mesenchymal Transition ◽  
Stellate Cells ◽  
Gene Set Enrichment Analysis ◽  
Mesenchymal Transition ◽  
And Migration ◽  
Proliferation And Migration

Abstract Introduction Gap junction protein, alpha 1 (GJA1), which is correlated with recurrences and unfavorable prognoses in hepatocellular carcinomas (HCCs), is one of the specific proteins expressed by activated hepatic stellate cells (HSCs). Methods Expression of GJA1 was compared between HCCs and nontumor tissues (NTs), between hepatic cirrhosis and NTs, and between primary and metastatic HCCs using transcriptomic datasets from the Gene Expression Omnibus and the Integrative Molecular Database of Hepatocellular Carcinoma. The in vitro activities of GJA1 were investigated in cultured HSCs and HCC cells. The underlying mechanism was characterized using Gene Set Enrichment Analysis and validated by western blotting. Results The expression of GJA1 was significantly increased in HCCs and hepatic cirrhosis compared to that in NTs. GJA1 was also overexpressed in pulmonary metastases from HCCs when compared with HCCs without metastasis. Overexpression of GJA1 promoted while knockdown of GJA1 inhibited proliferation and transforming growth factor (TGF)-β-mediated activation and migration of cultured HSCs. Overexpression of GJA1 by lentivirus infection promoted proliferation and migration, while conditioned medium from HSCs overexpressing GJA1 promoted migration but inhibited proliferation of Hep3B and PLC-PRF-5 cells. Lentivirus infection with shGJA1 or conditioned medium from shGJA1-infected HSCs inhibited the proliferation and migration of HCCLM3 cells that had a high propensity toward lung metastasis. Mechanistically, GJA1 induced the epithelial–mesenchymal transition (EMT) in HSCs and HCCLM3 cells. Conclusion GJA1 promoted HCC progression by inducing HSC activation and the EMT in HSCs. GJA1 is potentially regulated by TGF-β and thus may be a therapeutic target to inhibit HCC progression.

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