Changes in the transcriptional activity of cell cycle regulator CDK1 and cell proliferation ki67 genes in invasive and non-invasive pancreatic ductal adenocarcinoma

Authors

  • A. V. Evseyev Zaporizhzhya State Medical University,
  • A. M. Kamyshnyi Zaporizhzhya State Medical University,

DOI:

https://doi.org/10.14739/2310-1237.2016.2.81336

Keywords:

pancreas, polymerase chain reaction, carcinoma, proliferation

Abstract

The aim of this work was to determine the levels of mRNA expression of CDK1 and ki67 in pancreatic ductal adenocarcinoma.

Materials and methods. The study was conducted on 20 samples of pancreatic tumor tissue taken at pathomorphological examination of the operational material. To determine the level of investigated genes expression a thermal cycler CFX96 ™ Real-Time PCR Detection Systems («Bio-Rad Laboratories, Inc.», USA) reagent kit and Maxima SYBR Green / ROX qPCR MasterMix (2X) (ThermoScientific, USA) were used. In work using the real time polymerase chain reaction, gene expression levels of CDK1 and ki67 in noninvasive and invasive ductal pancreatic adenocarcinoma cells were identified.

Results. As a result of the study it was found that in ductal carcinoma tissue there is an increase of mRNA levels of the studied genes. Thus there was a significant increase in ki67 mRNA level (from 14.26 to 251.97 times) and increased CDK1 mRNA (from 0.26 to 10.73 times) as compared to normal pancreatic tissue.

Conclusion. Correlation analysis showed that between the growth of the transcriptional activity of cell cycle regulator CDK1 and cell proliferation Ki67 genes there is a strong direct correlation (Pearson's correlation coefficient r=+0,70), that is, increase of the level of CDK1 mRNA is accompanied by the significant increase in levels of ki67 mRNA, resulting in the enhance of tumor cell proliferation index. Unidirectional dynamics of increasing transcriptional activity of both genes was shown (ki67 increased by 54,40±23,82 times in non-invasive and 159,24±66,25 times in invasive carcinoma; CDK1 increased by 2,10±1,47 and 4,16±4,04 times,  respectively) with a strong correlation between these two indicators (Pearson’s coefficient r=+0,74 and +0,75, respectively). Invasive pancreatic carcinoma as compared to adenocarcinoma without invasion is characterized by the significant increase in the mRNA levels of both genes, however, this difference is valid only for the cell proliferation ki67 gene.

References

Evseyev, A. V. (2014). Osoblyvosti protsesiv proliferatsii i apoptozu v invazyvnii protokovii adenokartsynomi pidshlunkovoi zalozy [Features of proliferation and apoptosis of invasive pancreatic ductal adenocarcinoma]. Morfolohiia, 8(3), 23–26.

Tumanskiy, V. A., & Evseyev, A. V. (2014). Sravnitel'naya ocenka e´kspressii rostovykh receptorov semejstva ErbB, Kі-67 i E-kadgerina kletkami protokovoj adenokarcinomy podzheludochnoj zhelezy [Comparative estimation of ErbB family growth receptors, Ki-67 and E-cadherin expression in pancreatic ductal adenocarcinoma cells]. Pathologia, 3(32), 55–59. doi: http://dx.doi.org/10.14739/2310-1237.2014.3.36841.

Cuylen, S., Blaukopf, C., Politi, A. Z., Müller-Reichert, T., Neumann, B., Poser, I., et al. (2016). Ki-67 acts as a biological surfactant to disperse mitotic chromosomes. Nature, 535(7611), 308–312. doi: 10.1038/nature18610.

Hu, H.-Y., Liu, H., Zhang, J.-W., Hu, K., & Lin, Y. (2012). Clinical significance of Smac and Ki-67 expression in pancreatic cancer. Hepato-Gastroenterology, 59, 2640–2643. doi: 10.5754/hge12071.

Qian, J., Beullens, M., Huang, J., De Munter, S., Lesage, B., & Bollen, M. (2015). Cdk1 orders mitotic events through coordination of a chromosome-associated phosphatase switch. Nat Commun., 6, 10215. doi: 10.1038/ncomms10215.

Qin, L., Fan, M., Candas, D., Jiang, G., Papadopoulos, S., Tian, L., et al. (2015). CDK1 Enhances Mitochondrial Bioenergetics for Radiation-Induced DNA Repair. Cell Rep., 13(10), 2056–2063. doi: 10.1016/j.celrep.2015.11.015.

Jeong, S., Lee, D. H., Lee, J. I., Lee, J. W., Kwon, K. S., Kim, P. S., et al. (2005) Expression of Ki-67, p53, and K-ras in chronic pancreatitis and pancreatic ductal adenocarcinoma. World J. Gastroenterol., 11(43), 6765–6769. doi: 10.3748/wjg.v11.i43.6765.

Sobin, L. H., Gospodarowicz, M. K., & Wittekind, C. (eds). TNM Classification of Malignant Tumours. NJ: Wiley-Blackwell.

Downloads

How to Cite

1.
Evseyev AV, Kamyshnyi AM. Changes in the transcriptional activity of cell cycle regulator CDK1 and cell proliferation ki67 genes in invasive and non-invasive pancreatic ductal adenocarcinoma. Pathologia [Internet]. 2016Oct.27 [cited 2024Apr.20];13(2). Available from: http://pat.zsmu.edu.ua/article/view/81336

Issue

No. 2 (2016)

Section

Original research

License

Authors who publish with this journal agree to the following terms:

    1. Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
Лицензия Creative Commons
    1. Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.

  1. Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (SeeThe Effect of Open Access).