scholarly journals Functional genomics identifies novel genes essential for clear cell renal cell carcinoma tumor cell proliferation and migration

Oncotarget ◽  
2014 ◽  
Vol 5 (14) ◽  
pp. 5320-5334 ◽  
Author(s):  
Christina A. von Roemeling ◽  
Laura A. Marlow ◽  
Derek C. Radisky ◽  
Austin Rohl ◽  
Hege E. Larsen ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Tumor Cell ◽  
Clear Cell ◽  
Tumor Cell Proliferation ◽  
Cell Renal Cell Carcinoma ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Carcinoma Tumor ◽  
Proliferation And Migration

scholarly journals Silencing of the TRIM58 Gene by Aberrant Promoter Methylation is Associated with a Poor Patient Outcome and Promotes Cell Proliferation and Migration in Clear Cell Renal Cell Carcinoma

2021 ◽  
Vol 8 ◽  
Author(s):  
Ying Gan ◽  
Congcong Cao ◽  
Aolin Li ◽  
Haifeng Song ◽  
Guanyu Kuang ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Promoter Methylation ◽  
Clear Cell ◽  
Dna Demethylation ◽  
Cell Renal Cell Carcinoma ◽  
Cell Proliferation And Migration ◽  
Poor Patient ◽  
And Migration ◽  
Proliferation And Migration

To investigate the underlying molecular mechanism of tripartite motif-containing 58 (TRIM58) in the development of clear cell renal cell carcinoma (ccRCC), we explored TRIM58 expression and methylation in tumor tissues and the association with clinicopathological features and prognosis of tissue samples; Moreover, we examined the direct gene transcription of TRIM58-specific DNA demethyltransferase (TRIM58-TET1) by the CRISPR-dCas9 fused with the catalytic domain of TET1 and the biological functions in RCC cells. In this study, we demonstrate that TRIM58 is frequently downregulated by promoter methylation in ccRCC tissues, associated significantly with tumor nuclear grade and poor patient survival. TRIM58-TET1 directly induces demethylation of TRIM58 CpG islands, and activates TRIM58 transcription in RCC cell lines. Besides, DNA demethylation of TRIM58 by TRIM58-TET1 significantly inhibits cell proliferation and migration Overall, our results demonstrate that TRIM58 is inactivated by promoter methylation, associates with tumor nuclear grade and poor survival, and TRIM58 DNA demethylation could directly activate TRIM58 transcription and inhibit cell proliferation and migration in RCC cell lines.

scholarly journals Metformin Suppressed CXCL8 Expression and Cell Migration in HEK293/TLR4 Cell Line

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Zhihui Xiao ◽  
Wenjun Wu ◽  
Vladimir Poltoratsky
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Tumor Cell ◽  
Nuclear Translocation ◽  
High Dose ◽  
Dependent Manner ◽  
Tumor Cell Proliferation ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Chronic inflammation is associated with cancer. CXCL8 promotes tumor microenvironment construction through recruiting leukocytes and endothelial progenitor cells that are involved in angiogenesis. It also enhances tumor cell proliferation and migration. Metformin, type II diabetes medication, demonstrates anticancer properties via suppressing inflammation, tumor cell proliferation, angiogenesis, and metastasis. This study intended to address the role of metformin in regulation of CXCL8 expression and cell proliferation and migration. Our data indicated that metformin suppressed LPS-induced CXCL8 expression in a dose-dependent manner through inhibiting NF-κB, but not AP-1 and C/EBP, activities under the conditions we used. This inhibitory effect of metformin is achieved through dampening LPS-induced NF-κB nuclear translocation. Cell migration was inhibited by metformin under high dose (10 mM), but not cell proliferation.

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