scholarly journals Peer Review #1 of "Coordinative control of G2/M phase of the cell cycle by non-coding RNAs in hepatocellular carcinoma (v0.2)"

2018 ◽  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Peer Review ◽  
M Phase ◽  
Non Coding Rnas

scholarly journals Coordinative control of G2/M phase of the cell cycle by non-coding RNAs in hepatocellular carcinoma

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5787 ◽  
Author(s):  
Jun Shi ◽  
Guangqiang Ye ◽  
Guoliang Zhao ◽  
Xuedong Wang ◽  
Chunhui Ye ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Target Genes ◽  
Expression Profiles ◽  
M Phase ◽  
Non Coding Rnas ◽  
Regulatory Model ◽  
Microarray Analyses ◽  
The Relationship

Objective To investigate the interaction of non-coding RNAs (ncRNAs) in hepatocellular carcinoma. Methods We compared the ncRNAs and mRNAs expression profiles of hepatocellular carcinoma and adjacent tissue by microarray and RT-PCR. The relationship between different ncRNAs and mRNA was analyzed using bioinformatics tools. A regulatory model of ncRNAs in hepatocellular carcinoma cells was developed. Results A total of 1,704 differentially expressed lncRNAs, 57 miRNAs, and 2,093 mRNAs were identified by microarray analyses. There is a co-expression relationship between two ncRNAs (miRNA-125b-2-3p and lncRNA P26302). Bioinformatics analysis demonstrated cyclin-dependent kinases 1 and CyclinA2 as potential targets of miR-125b-2-3p and Polo-like kinase 1 as potential target of lncRNAP26302. All three gene are important components in the G2/M phase of cell cycle. Subsequently real-time polymerase chain reaction (PCR) studies confirmed these microarray results. Conclusion MiR-125b-2-3p and lncRNAP26302 may affect the G2/M phase of the cell cycle through the regulation of their respective target genes. This study shows a role of ncRNAs in pathogenesis of hepatocellular carcinoma at molecular level, providing a basis for the future investigation aiming at early diagnosis and novel treatment of hepatocellular carcinoma.

scholarly journals Novel Hybrid CHC from β-carboline and N-Hydroxyacrylamide Overcomes Drug-Resistant Hepatocellular Carcinoma by Promoting Apoptosis, DNA Damage, and Cell Cycle Arrest

2021 ◽  
Vol 11 ◽  
Author(s):  
Jiefei Miao ◽  
Chi Meng ◽  
Hongmei Wu ◽  
Wenpei Shan ◽  
Haoran Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Dna Damage ◽  
Hdac Inhibitor ◽  
Drug Resistant ◽  
Antiproliferative Effects ◽  
Cycle Arrest ◽  
M Phase ◽  
Cellular Apoptosis ◽  
Related Proteins

A novel hybrid CHC was designed and synthesized by conjugating β-carboline with an important active fragment N-hydroxyacrylamide of histone deacetylase (HDAC) inhibitor by an amide linkage to enhance antitumor efficacy/potency or even block drug resistance. CHC displayed high antiproliferative effects against drug-sensitive SUMM-7721, Bel7402, Huh7, and HCT116 cells and drug-resistant Bel7402/5FU cells with IC50 values ranging from 1.84 to 3.27 μM, which were two-to four-fold lower than those of FDA-approved HDAC inhibitor SAHA. However, CHC had relatively weak effect on non-tumor hepatic LO2 cells. Furthermore, CHC exhibited selective HDAC1/6 inhibitory effects and simultaneously augmented the acetylated histone H3/H4 and α-tubulin, which may make a great contribution to their antiproliferative effects. In addition, CHC also electrostatically interacted with CT-DNA, exerted remarkable cellular apoptosis by regulating the expression of apoptosis-related proteins and DNA damage proteins in Bel7402/5FU cells, and significantly accumulated cancer cells at the G2/M phase of the cell cycle by suppressing CDK1 and cyclin B protein with greater potency than SAHA-treated groups. Finally, CHC displayed strong inhibitory potency to drug-resistant hepatic tumors in mice. Our designed and synthetic hybrid CHC could be further developed as a significant and selective anticancer agent to potentially treat drug-resistant hepatocellular carcinoma.

Involvement of the role of Chk1 in lithium‐induced G2/M phase cell cycle arrest in hepatocellular carcinoma cells

2008 ◽  
Vol 104 (4) ◽  
pp. 1181-1191 ◽  
Author(s):  
Xiao‐Ming Wang ◽  
Jiao Li ◽  
Xiao‐Cheng Feng ◽  
Qiong Wang ◽  
Dong‐Yin Guan ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Carcinoma Cells ◽  
Phase Cell ◽  
Hepatocellular Carcinoma Cells ◽  
Cycle Arrest ◽  
M Phase

scholarly journals α-pinene regulates miR-221 and induces G2/M phase cell cycle arrest in human hepatocellular carcinoma cells

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Qiuxiang Xu ◽  
Ming Li ◽  
Mengdie Yang ◽  
Jiebo Yang ◽  
Jingjing Xie ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Hepg2 Cells ◽  
Carcinoma Cells ◽  
Phase Cell ◽  
Hepatocellular Carcinoma Cells ◽  
Cycle Arrest ◽  
M Phase ◽  
Dependent Growth

The naturally occurring compound α-pinene induces cell cycle arrest and antitumor activity. We examined effects of α-pinene on cell cycle regulation in hepatocellular carcinoma cells (HepG2) cells to establish a foundation for its development as a novel treatment for hepatocellular carcinoma (HCC). HepG2 cells treated with α-pinene exhibited dose-dependent growth inhibition as a result of G2/M-phase cell cycle arrest. Cell cycle arrest was associated with down-regulated cyclin-dependent kinase 1 (CDK1) and miR-221 levels and up-regulated levels of CDKN1B/p27, γ-H2AX, phosphorylated ATM, phosphorylated Chk2 and phosphorylated p53. Our observations are consistent with a model in which α-pinene inhibits miR221 expression, which leads to G2/M-phase arrest and activation of CDKN1B/p27-CDK1 and ATM-p53-Chk2 pathways that suppress human hepatoma tumor progression. Additionally, α-pinene was found to trigger oxidative stress and induce apoptosis of HepG2 cells. α-pinene, therefore, represents a potential chemotherapeutic compound for the treatment of HCC.

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