Identification of Phosphorylated Cyclin-Dependent Kinase 1 Associated with Colorectal Cancer Survival Using Label-Free Quantitative Analyses

Lin, Peng; Yang, Yi; Tyan, Yu‐Chang; Hsiao, Eric S. L.; Chu, Pei Ming; Lee, Jenq Chang; Chen, Yi Ming Arthur; Liao, Pao Chi

doi:10.1371/journal.pone.0158844

Cited by 10 publications

(6 citation statements)

References 63 publications

(66 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Lingling Wu et al revealed that CDK1 is a positive regulator of the IFN signaling pathway and its overexpression may be the primary mechanism of type I IFN signaling that is abnormally amplified in systemic lupus erythematosus [26]. Peng-Chan Lin et al demonstrated that high levels of CDK1 pTyr15 are associated with prolonged disease-free survival in patients with stage II colorectal tumor, and CDK1 pTyr15 protein may be a potential indicator of colorectal tumor advancement [27]. Xingcheng Chen et al verified that ajuba phosphorylation of CDK1 can promote cell proliferation and tumor formation [28].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: LncRNA CASC11 promoted gastric cancer cell proliferation, migration and invasion in vitro by regulating cell cycle pathway

et al. 2018

View full text Add to dashboard Cite

In this study, we aimed to investigate the effects of lncRNA CASC11 on gastric cancer (GC) cell progression through regulating miR-340-5p and cell cycle pathway. Expressions of lncRNA CASC11 in gastric cancer tissues and cell lines were determined by qRT-PCR. Differentially expressed lncRNAs, mRNAs and miRNAs were screened through microarray analysis. The relationship among CASC11, CDK1 and miR-340-5p was predicted by TargetScan and validated through dual luciferase reporter assay. Western blot assay examined the protein level of CDK1 and several cell cycle regulatory proteins. GO functional analysis and KEGG pathway analysis were used to predict the association between functions and related pathways. Cell proliferation was determined by CCK-8 assays. Cell apoptosis and cell cycle were detected by flow cytometry assay. CASC11 was highly expressed in GC tissues and cell lines. Knockdown of CASC11 inhibited GC cell proliferation, promoted cell apoptosis and blocked cell cycle. KEGG further indicated an enriched cell cycle pathway involving CDK1. QRT-PCR showed that miR-340-5p was down-regulated in GC cells tissues, while CDK1 was up-regulated. Furthermore, CASC11 acted as a sponge of miR-340-5p which directly targeted CDK1. Meanwhile, miR-340-5p overexpression promoted GC cell apoptosis and induced cell cycle arrest, while CDK1 overexpression inhibited cell apoptosis and accelerated cell cycle. Our study revealed the mechanism of CASC11/miR-340-5p/CDK1 network in GC cell line, and suggested that CASC11 was a novel facilitator that exerted a biological effect by activating the cell cycle signaling pathway. This finding provides a potential therapeutic target for GC.

show abstract

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: LncRNA CASC11 promoted gastric cancer cell proliferation, migration and invasion in vitro by regulating cell cycle pathway

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Our results support the previous findings on the role of phosphorylation studied by the methods of conventional biology [62][63][64].…”

Section: It Is Evident Fromsupporting

confidence: 93%

Aberrant Protein Phosphorylation in Cancer by Using Raman Biomarkers

Abramczyk

Imiela

Brożek-Płuska

et al. 2019

Cancers

View full text Add to dashboard Cite

1) Background: Novel methods are required for analysing post-translational modifications of protein phosphorylation by visualizing biochemical landscapes of proteins in human normal and cancerous tissues and cells. (2) Methods: A label-free Raman method is presented for detecting spectral changes that arise in proteins due to phosphorylation in the tissue of human breasts, small intestines, and brain tumours, as well as in the normal human astrocytes and primary glioblastoma U-87 MG cell lines. Raman spectroscopy and Raman imaging are effective tools for monitoring and analysing the vibrations of functional groups involved in aberrant phosphorylation in cancer without any phosphorecognition of tag molecules. (3) Results: Our results based on 35 fresh human cancer and normal tissues prove that the aberrant tyrosine phosphorylation monitored by the unique spectral signatures of Raman vibrations is a universal characteristic in the metabolic regulation in different types of cancers. Overexpressed tyrosine phosphorylation in the human breast, small intestine and brain tissues and in the human primary glioblastoma U-87 MG cell line was monitored by using Raman biomarkers. (4) We showed that the bands at 1586 cm −1 and 829 cm −1 , corresponding to phosphorylated tyrosine, play a pivotal role as a Raman biomarker of the phosphorylation status in aggressive cancers. We found that the best Raman biomarker of phosphorylation is the 1586/829 ratio showing the statistical significance at p Values of ≤ 0.05. (5) Conclusions: Raman spectroscopy and imaging have the potential to be used as screening functional assays to detect phosphorylated target proteins and will help researchers to understand the role of phosphorylation in cellular processes and cancer progression. The abnormal and excessive high level of tyrosine phosphorylation in cancer samples compared with normal samples was found in the cancerous human tissue of breasts, small intestines and brain tumours, as well as in the mitochondria and lipid droplets of the glioblastoma U-87 MG cell line. Detailed insights are presented into the intracellular oncogenic metabolic pathways mediated by phosphorylated tyrosine.2 of 25 the abnormalities of many types of cancer, for example, finding over 30,000 mutations in breast cancer cells. Thus, the available evidence appears to suggest that scientific research based solely on cancer genomics cannot continue.Presently, a growing number of reports have led to increased interest in the benefits of metabolic regulation in cancers. While the transformation of oncogenic genes can be directly connected to cancer cell metabolism, mutated metabolic enzymes may also trigger malignant transformations [1][2][3].Understanding the mechanism of the altered energy metabolism that replaces the more efficient oxidative phosphorylation to yield adenosine triphosphate (ATP) by the less efficient process of glycolysis represents the pivotal problem that must be solved to advance the study of cancer. During the past decade, many studies have suggested...

show abstract

“…3D and E) and an elevated number of undifferentiated epithelial cells (Fig. 3F), as evidenced by increased epithelial transcript levels of Cdk1 , a gene encoding a cyclin-dependent kinase involved in cell proliferation (20), and decreased epithelial transcript levels of Angptl4 , a gene activated by (peroxisome proliferator-activated receptor gamma (PPARγ) in terminally differentiated epithelial cells (21, 22). Consistent with reduced epithelial differentiation, alcian blue staining revealed a reduction in the number of goblet cells, a terminally differentiated epithelial cell type, in colonic sections from AOM/DSS-treated mice compared to the level in control animals (Fig.…”

Section: Resultsmentioning

confidence: 99%

Increased Epithelial Oxygenation Links Colitis to an Expansion of Tumorigenic Bacteria

Cevallos

Lee

Tiffany

et al. 2019

mBio

View full text Add to dashboard Cite

Intestinal inflammation is a risk factor for colorectal cancer formation, but the underlying mechanisms remain unknown. Here, we investigated whether colitis alters the colonic microbiota to enhance its cancer-inducing activity. Colitis increased epithelial oxygenation in the colon of mice and drove an expansion of Escherichia coli within the gut-associated microbial community through aerobic respiration. An aerobic expansion of colibactin-producing E. coli was required for the cancer-inducing activity of this pathobiont in a mouse model of colitis-associated colorectal cancer formation. We conclude that increased epithelial oxygenation in the colon is associated with an expansion of a prooncogenic driver species, thereby increasing the cancer-inducing activity of the microbiota. IMPORTANCE One of the environmental factors important for colorectal cancer formation is the gut microbiota, but the habitat filters that control its cancer-inducing activity remain unknown. Here, we show that chemically induced colitis elevates epithelial oxygenation in the colon, thereby driving an expansion of colibactin-producing Escherichia coli, a prooncogenic driver species. These data suggest that elevated epithelial oxygenation is a potential risk factor for colorectal cancer formation because the consequent changes in the gut habitat escalate the cancer-inducing activity of the microbiota.

show abstract

Identification of Phosphorylated Cyclin-Dependent Kinase 1 Associated with Colorectal Cancer Survival Using Label-Free Quantitative Analyses

Cited by 10 publications

References 63 publications

RETRACTED ARTICLE: LncRNA CASC11 promoted gastric cancer cell proliferation, migration and invasion in vitro by regulating cell cycle pathway

RETRACTED ARTICLE: LncRNA CASC11 promoted gastric cancer cell proliferation, migration and invasion in vitro by regulating cell cycle pathway

Aberrant Protein Phosphorylation in Cancer by Using Raman Biomarkers

Increased Epithelial Oxygenation Links Colitis to an Expansion of Tumorigenic Bacteria

Contact Info

Product

Resources

About