The Emerging Role of Cyclin-Dependent Kinases (CDKs) in Pancreatic Ductal Adenocarcinoma

García-Reyes, Balbina; Kretz, Anna-Laura; Ruff, Jan-Philipp; Karstedt, Silvia von; Hillenbrand, Andreas; Knippschild, Uwe; Henne‐Bruns, Doris; Lemke, Johannes

doi:10.3390/ijms19103219

Cited by 70 publications

(54 citation statements)

References 242 publications

(266 reference statements)

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“…In the present study, TBX3 silencing led to an increased number of cells at the S phase of the cell cycle, and a decreased proportion at the G 1 phase, while the cells at the G 2 /M phase remained unchanged. Increasing evidence supports the important role that CDK2, CDK4, cyclin E and p27 serve in cell cycle progression (33–36). AsTBX3 was demonstrated to regulate the cell cycle progression of FaDu cells, the present study then detected whether cell cycle-associated proteins were modulated by TBX3.…”

Section: Discussionmentioning

confidence: 95%

TBX3 knockdown suppresses the proliferation of hypopharyngeal carcinoma FaDu cells by inducing G1/S cell cycle arrest and apoptosis

Huang

Zhu

et al. 2019

Oncol Lett

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The T-box transcription factor family member TBX3 has been demonstrated to participate in the development of various types of cancer, including head and neck squamous cell carcinoma. However, little is currently known about its role in hypopharyngeal carcinoma. In the present study, the involvement of TBX3 in hypopharyngeal carcinoma was investigated. Immunohistochemical assays revealed that TBX3 levels were increased in hypopharyngeal carcinoma compared with normal tissue samples, accompanied by upregulated N-cadherin and downregulated E-cadherin. Lentivirus-mediated TBX3 knockdown efficiently suppressed its expression and inhibited the proliferation of FaDu cells. The opposite was observed in TBX3-overexpressing FaDu cells. These results indicate that TBX3 is essential for FaDu cell proliferation. Furthermore, TBX3 silencing led to a disturbance of the cell cycle, leading to a decrease in the G1 phase and an increase in the S phase. In addition, apoptosis was enhanced following TBX3 knockdown. The present results suggest TBX3 as a potential therapeutic target in hypopharyngeal carcinoma.

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Section: Discussionmentioning

confidence: 95%

TBX3 knockdown suppresses the proliferation of hypopharyngeal carcinoma FaDu cells by inducing G1/S cell cycle arrest and apoptosis

Huang

Zhu

et al. 2019

Oncol Lett

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“…Cell cycle arrest occurs in response to DNA damage (Wenzel and Singh, 2018). Mechanism of cell cycle arrest at G0/G1 is p53-dependent, resulting in inhibition of the synthesis of DNA, cyclin-dependent kinase 4 (CDK4) and cyclin D (García-Reyes et al, 2018, Liu et al, 2003. P53-dependent arrested the transition of cells from G2 to M phase and -independent pathways through inhibition of cyclin B and Cdc2 proteins which are involved in mitosis consequences such as inhibition of mitotic spindle, centromere, or cytokinesis (Stark and Taylor, 2006;Wenzel and Singh, 2018).…”

Section: Discussionmentioning

confidence: 99%

Cytotoxicity, Cell Cycle Arrest, and Apoptosis Induction Activity of Ethyl-p-methoxycinnamate in Cholangiocarcinoma Cell

Muhamad

Panrit

Chai่jaroenkul

et al. 2020

Asian Pac J Cancer Prev

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Objective: To investigate cytotoxic activity of ethyl-p-methoxycinnamate (EPMC) including its effect on p-glycoprotein (multidrug resistance-1: mdr-1 gene) in human cholangiocarcinoma cell. Methods: Cytotoxic activity of EPMC against human cholangiocarcinoma (CL-6), fibroblast (OUMS-36T-1F), and colon cancer (Caco-2) cell lines were assessed using MTT assay. Selectivity index (SI) was determined as the ratio of IC 50 (concentration that inhibits cell growth by 50%) of EPMC in OUMS-36T-1F and that in CL-6 cell. Cell cycle arrest and apoptosis in CL-6 cells were investigated by flow cytometry and fluorescent microscopy. Effect of EPMC on mdr-1 gene expression in CL-6 and Caco-2 was determined by real-time PCR. Results: The median (95% CI) IC 50 values of EPMC in CL-6, OUMS-36T-1F, and Caco-2 were 245.5 (243.1-266.7), 899.60 (855.8-966.3) and 347.0 (340.3-356.9) µg/ml, respectively. The SI value of the compound for the CL-6 cell was 3.70. EPMC at IC 50 inhibited CL-6 cell division and induced apoptosis compared to untreated control. EPMC exposure did not induce mdr-1 gene expression in both CL-6 and Caco-2 cells. Conclusion: The results suggest the potential role of EPMC in cholangiocarcinoma with a low possibility of drug resistance induction.

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“…Cyclin-dependent kinases (CDKs/cyclins) form a family of heterodimeric kinases that serve important roles in regulating cell cycle progression, transcription and other major biological processes (32). Alterations in CDK activity affect the proliferation of cancer cells, and abnormal activities of these proteins have been reported in various types of human cancer, such as pancreatic cancer (32,33). Wnt signaling regulates an evolutionarily conserved pathway that serves an important role in numerous cellular activities, including cell proliferation, calcium homeostasis and cellular polarity (34).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of core serous epithelial ovarian cancer genes as potential prognostic markers and indicators of the underlying molecular mechanisms using an integrated bioinformatics analysis

et al. 2019

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Ovarian cancer is a major cause of mortality in women. However, the molecular events underlying the pathogenesis of the disease are yet to be fully elucidated. In the present study, an integrated bioinformatics analysis was performed to identify core genes involved in serous epithelial ovarian cancer. A total of three expression datasets were downloaded from the Gene Expression Omnibus database, and included 46 serous epithelial ovarian cancer and 30 ovarian surface epithelium samples. The three datasets were merged, and batch normalization was performed. The normalized merged data were subsequently analyzed for differentially expressed genes (DEGs). In total, 2,212 DEGs were identified, including 1,300 upregulated and 912 downregulated genes. Gene Ontology analysis revealed that these DEGs were primarily involved in ‘regulation of cell cycle’, ‘mitosis’, ‘DNA packaging’ and ‘nucleosome assembly’. The main cellular components included ‘extracellular region part’, ‘chromosome’, ‘extracellular matrix’ and ‘condensed chromosome kinetochore’, whereas the molecular functions included ‘Calcium ion binding’, ‘polysaccharide binding’, ‘enzyme inhibitor activity’, ‘growth factor activity’, ‘cyclin-dependent protein kinase regulator activity’, ‘microtubule motor activity’ and ‘Wnt receptor activity’. Kyoto Encyclopedia of Genes and Genomes pathway analysis revealed that these DEGs were predominantly involved in ‘Wnt signaling pathway’, ‘pathways in cancer’, ‘PI3K-Akt signaling pathway’, ‘cell cycle’, ‘ECM-receptor interaction’, ‘p53 signaling pathway’ and ‘focal adhesion’. The 20 most significant DEGs were identified from the protein-protein interaction network, and Oncomine analysis of these core genes revealed that 13 were upregulated and two were downregulated in serous epithelial ovarian cancer. Survival analysis revealed that cyclin B1, polo like kinase 1, G protein subunit γ transducin 1 and G protein subunit γ 12 are key molecules that may be involved in the prognosis of serous epithelial ovarian cancer. These core genes may provide novel treatment targets, although their roles in the carcinogenesis and prognosis of serous epithelial ovarian cancer require further study.

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The Emerging Role of Cyclin-Dependent Kinases (CDKs) in Pancreatic Ductal Adenocarcinoma

Cited by 70 publications

References 242 publications

TBX3 knockdown suppresses the proliferation of hypopharyngeal carcinoma FaDu cells by inducing G1/S cell cycle arrest and apoptosis

TBX3 knockdown suppresses the proliferation of hypopharyngeal carcinoma FaDu cells by inducing G1/S cell cycle arrest and apoptosis

Cytotoxicity, Cell Cycle Arrest, and Apoptosis Induction Activity of Ethyl-p-methoxycinnamate in Cholangiocarcinoma Cell

Evaluation of core serous epithelial ovarian cancer genes as potential prognostic markers and indicators of the underlying molecular mechanisms using an integrated bioinformatics analysis

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