scholarly journals Epigenetic Regulation by lncRNAs: An Overview Focused on UCA1 in Colorectal Cancer

Cancers ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 440 ◽  
Author(s):  
Bernadette Neve ◽  
Nicolas Jonckheere ◽  
Audrey Vincent ◽  
Isabelle Van Seuningen
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Regulate Gene Expression ◽  
Metastatic Lesions ◽  
Colorectal Cancer Cells ◽  
Regulation Of Cell Cycle ◽  
Integrate Research

Colorectal cancers have become the second leading cause of cancer-related deaths. In particular, acquired chemoresistance and metastatic lesions occurring in colorectal cancer are a major challenge for chemotherapy treatment. Accumulating evidence shows that long non-coding (lncRNAs) are involved in the initiation, progression, and metastasis of cancer. We here discuss the epigenetic mechanisms through which lncRNAs regulate gene expression in cancer cells. In the second part of this review, we focus on the role of lncRNA Urothelial Cancer Associated 1 (UCA1) to integrate research in different types of cancer in order to decipher its putative function and mechanism of regulation in colorectal cancer cells. UCA1 is highly expressed in cancer cells and mediates transcriptional regulation on an epigenetic level through the interaction with chromatin modifiers, by direct regulation via chromatin looping and/or by sponging the action of a diversity of miRNAs. Furthermore, we discuss the role of UCA1 in the regulation of cell cycle progression and its relation to chemoresistance in colorectal cancer cells.

scholarly journals Pan-Bcl-2 Inhibitor Obatoclax Delays Cell Cycle Progression and Blocks Migration of Colorectal Cancer Cells

PLoS ONE ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. e106571 ◽  
Author(s):  
Bruno Christian Koehler ◽  
Anna-Lena Scherr ◽  
Stephan Lorenz ◽  
Christin Elssner ◽  
Nicole Kautz ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Colorectal Cancer Cells

scholarly journals HNRNPLL stabilizes mRNA for DNA replication proteins and promotes cell cycle progression in colorectal cancer cells

2018 ◽  
Vol 109 (8) ◽  
pp. 2458-2468 ◽  
Author(s):  
Keiichiro Sakuma ◽  
Eiichi Sasaki ◽  
Kenya Kimura ◽  
Koji Komori ◽  
Yasuhiro Shimizu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Dna Replication ◽  
Cancer Cells ◽  
Cell Cycle Progression ◽  
Replication Proteins ◽  
Cycle Progression ◽  
Colorectal Cancer Cells

scholarly journals Cell Cycle Arrest and Autophagy Induced by Compound Kushen Injection in sw620 and sw480 Colorectal Cancer Cells with p53 Mutation

2019 ◽  
Author(s):  
Jie Sun ◽  
Di Wang ◽  
Yu Zhang ◽  
Qing Mu ◽  
Mei Li ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Cell Cycle Progression ◽  
Mutant P53 ◽  
Cycle Progression ◽  
Cycle Arrest ◽  
Colorectal Cancer Cells

Abstract Background Compound Kushen Injection (CKI) has been clinically used in China for 15 years to treat various types of solid tumors, including colorectal cancer. Here we examine cell cycle arrest, induced autophagy, and mutant p53 pathways perturbed by CKI in colorectal cancer cells. We and other groups have shown that CKI alters p53 gene expression patterns and suppresses proliferation in colorectal cancer cells. Methods We measured the effect of CKI on cell proliferation, cell cycle progression and autophagy in sw480 and sw620 colorectal cancer cells in vitro, and carcinogenesis and the progression of azoxymethane/dextran sodium sulfate-induced colorectal cancer in ICR mice in vivo. We also used RNA sequencing to analyze mRNA expression altered by CKI, and further validated the expression of mutant p53 and several genes in the cell cycle pathway using reverse transcriptase-quantitative PCR and western blotting. Using network pharmacology (BATMAN-TCM database), we have also predicted the active ingredients in CKI involved in regulating the expression of mutant p53. Results We show evidence that CKI significantly suppressed proliferation and cell cycle progression, and induced autophagy of sw480 and sw620 cells in vitro; it also inhibited the development of inflammatory colorectal cancer in vivo. We also show that the down-regulated expression of mutant p53 and adjustments in several key genes related closely to cell-cycle progression. Furthermore, N-oxysophocarpine, lupenone, and geranylacetone were predicted to be the active ingredients of CKI involved in the down-regulated expression of mutant p53. Conclusion Our results indicate that CKI likely acts as a potential anti-cancer therapeutic agent that targets the cell cycle pathway, suggesting a key role in the development of a novel subsidiary therapeutic approach against mutant p53 in patients with colorectal cancer.

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