Middle East Journal of Cancer

Current Issue

By Issue

By Author

By Subject

Author Index

Keyword Index

About Journal

Aims and Scope

Editorial Board

Publication Ethics

Indexing and Abstracting

Related Links

FAQ

Peer Review Process

News

Forms

Journal Metrics

Hsa-miR-21-mediated Cell Death and Tumor Metastases: A Potential Dual Response During Colorectal Cancer Development

Document Type : Original Article(s)

Authors

1 Department of Molecular Biology, Genetic Engineering and Biotechnology Research Institute, University of Sadat City, Sadat City, Egypt

2 Department of Clinical Biochemistry and Molecular Diagnostic, National Liver Institute, Menofyia University, Sebin El-Kom, Egypt

3 Department of Clinical Pathology, Faculty of Medicine, Menofyia University, Sebin El-Kom, Egypt

4 Industrial Biotechnology Department, Genetic Engineering and Biotechnology Research Institute, University of Sadat City, Sadat City, Egypt

Abstract

Background: Colorectal cancer (CRC), caused by abnormal cells growing in the colon or rectum, has a high mortality rate worldwide. On the other hand, microRNAs are small non-coding RNAs that contain approximately 22 nucleotides in length. They are upregulated in a wide range of human cancers such as CRC. MiRNA-21 post-transcriptionally regulates the expression of many tumor suppressor genes such as P53 gene. This indicates that miRNA-21 interacts like oncogenes and is required for CRC development.
Method: The current original study was conducted in the National Liver Institute, Menofyia University, Egypt. We collected a total of 40 blood samples from CRC patients 40 samples from healthy individuals who served as controls. Quantitative real-time PCR detected the levels of miRNA-21 and the fold changes of phosphates-tensin homology (PTEN) gene expression, as a tumor suppressor gene, in blood samples.
Results: The expression levels of miR-21 were upregulated in all obtained samples from patients with CRC in association with aging, gender, and tumor-node-metastasis staging. Furthermore, patients with poor and well-differentiated CRC revealed reduced levels of PTEN gene expression. We observed a putative binding site of miR-21 in PTEN gene sequences. This indicates the direct cleavage between miR-21 and PTEN coding sequence. Prediction analysis for other potential targets identified several malignancy factors and tumor suppressor genes with putative seeding regions for miR-21 such as STAT3, transforming growth factor-beta, tumor necrosis factor-α (TNF-α), and programmed cell death CD4.
Conclusion: The current data exhibited the potential dual role of hsa-miR-21 in regulating cancer progression and showed that hsa-miR-21 is an efficacious biomarker for CRC d evelopment and an attractive candidate for CRC treatment during early transformation.

Keywords

Full Text

How to cite this article:

Maher E, Gedawy G, Fathy W, Farouk S, Maksoud AA, Guirgis AA, et al. Hsa-miR-21-mediated cell death and tumor metastases: A potential dual response during colorectal cancer development. Middle East J Cancer. 2020;11(4): 483-92. doi: 10.30476/mejc.2020. 83146.1139.

References
1.        Durko L, Malecka-Panas E. Lifestyle modifications and colorectal cancer. Curr Colorectal Cancer Rep. 2014;10:45-54.
2.        Simonian M, Khosravi S, Mortazavi D, Bagheri H, Salehi R, Hassanzadeh A, et al. Environmental risk factors associated with sporadic colorectal cancer in Isfahan, Iran. Middle East J Cancer. 2018;9(4), 318-22.
3.        Gandomani H, Yousefi SM, Aghajani M, Mohammadian-Hafshejani A, Tarazoj A, Pouyesh V, et al. Colorectal cancer in the world: incidence, mortality and risk factors. Biomed Res Ther. 2017,4(10):1656–75.
4.        Lorestani S,  Hashemy SI, Mojarad M, Keyvanloo Shahrestanaki M, Bahari A, Asadi M, et al. Increased glutathione reductase expression and activity in colorectal cancer tissue samples: An investigational study in Mashhad, Iran. Middle East J Cancer. 2018;9(2), 99-104.
5.        Ibrahim AS, Khaled HM, Mikhail NN, Baraka H, Kamel H. Cancer incidence in Egypt: results of the national population-based cancer registry program. J Cancer Epidemiol. 2014;2014:437971.
6.        Kim ER, Chang DK. Colorectal cancer in inflammatory bowel disease: the risk, pathogenesis, prevention and diagnosis. World J Gastroenterol. 2014;20(29):9872-81. doi: 10.3748/wjg.v20.i29.9872.
7.        Stracci F, Zorzi M, Grazzini G. Colorectal cancer screening: Tests, strategies, and perspectives. Front Public Heal. 2014;2: 210.
8.        Zygulska AL, Furgala A, Krzemieniecki K, Wlodarczyk B,Thor P. Autonomic dysregulation in colon cancer patients. Cancer Invest. 2018;36:255–63.
9.        Islam SMA, Patel R, Acevedo-Duncan M. Protein Kinase C-ζ stimulates colorectal cancer cell carcinogenesis via PKC-ζ/Rac1/Pak1/β-Catenin signaling cascade. Biochim Biophys Acta Mol Cell Res. 2018;1865(4):650-664. doi:10.1016/j.bbamcr.2018.02.002.
10.      Asho KP, Thomas D, Kalaviani K, Vadivel D, Bakthavatchalam V, Ganapasam S. Colorectal carcinogenesis: Insights into the cell death and signal transduction pathways: A review. World J Gastrointest Oncol. 2018;10(9),244-59.
11.      Buhmeida A, Assidi M, Al-Maghrabi J, Dallol A, Sibiany A, Al-Ahwal M, et al. Membranous or Cytoplasmic HER2 Expression in Colorectal Carcinoma: Evaluation of Prognostic Value Using Both IHC & BDISH. Cancer Invest. 2018;36(2):129-140. doi:10.1080/07357907.2018.1439054.
12.   MaksoudAI, Taher RF, Gaara AH, Abdelrazik E, Gaara AH,  et al. Selective regulation of B- Raf dependent K-Ras/mitogen-activated protein by natural occurring multi-kinase inhibitors in cancer cells. Front Oncol. 2019; 01220. doi: 10.3389/fonc.2019.01220.
13.      Mehlen P, Fearon ER. Role of the dependence receptor DCC in colorectal cancer pathogenesis. J Clin Oncol. 2004;22(16):3420-8.
14.      Grady WM. Transforming growth factor -β signaling in colorectal cancer. Curr. Colorectal Cancer Rep. 2007;3:65-70.
15.      Kaufman EJ, Miska EA. The microRNAs of Caenorhabditis elegans. Semin Cell Dev Biol. 2010;21(7):728-37. doi: 10.1016/j.semcdb.2010.07.001.
16.      Volinia S, Calin GA, Liu CG, Ambs S, Cimmino A, Petrocca F, et al. A microRNA expression signature of human solid tumors defines cancer gene targets. Proc Natl Acad Sci U S A. 2006;103(7):2257-61.
17.      Zhu S, Wu H, Wu F, Nile D, Sheng S, Mo YY. MicroRNA-21 targets tumor suppressor genes in invasion and metastasis. Cell Res.2008;18(3),350-9.
18.      Khalil H, Abd El Maksoud AI, Alian A, El-Hamady WA, Daif AA, Awad AM, et al. Interruption of autophagosome formation in cardiovascular disease, an evidence for protective response of autophagy. Immunol Invest. 2019:1-15.doi: 10.1080/08820139.2019.1635619.
19.      Khalil H, Arfa M, El-Masrey S, El-Sherbini SM, Abd-Elaziz AA. Single nucleotide polymorphisms of interleukins associated with hepatitis C virus infection in Egypt. J Infect Dev Ctries. 2017;11(3):261-268. doi:10.3855/jidc.8127.
20.      Khalil H, Abd El Maksoud AI, Roshdey T, El-Masry S. Guava flavonoid glycosides prevent influenza A virus infection via rescue of P53 activity. J Med Virol. 2019;91(1):45-55. doi: 10.1002/jmv.25295.
21.      Farghaly H., Guirgis A, Khalil H. Heat shock reduces HCV replication via regulation of ribosomal L22 in Alu-RNA molecule dependent manner. Hepatoma Res. 2018;4:41.
22.      Salehi Z, Akrami H, Sisakhtnezhad S. The effect of placenta growth factor knockdown on hsa-miR-22-3p, hsa-let-7b-3p, hsa-miR-451b, and hsa-mir-4290 expressions in MKN-45- derived gastric cancer stem-like cells. Middle East J Cancer. 2018; 9:113-22.
23.      Khalil H. Influenza A virus stimulates autophagy to undermine host cell IFN-β production. Egypt J Biochem Mol Biol. 2012;30: 283-99.
24.      Khalil H, El Malah T, El Maksoud AIA, El Halfawy I, El Rashedy AA, El Hefnawy M. identification of novel and efficacious chemical compounds that disturb influenza a virus entry in vitro. Front Cell Infect Microbiol. 2017;7:304.doi: 10.3389/fcimb.2017.00304.
25.  Abd El Maksoud AI, Elebedeey D, Abass NH, Awad AM, Naser GM, Roshdy T et al. Methylomic changes of autophagy-related genes by Legionella effector Lpg2936 in infected macrophages. Front Cell Dev Biol. 2019; 7(390):1-16. doi: 10.3389/fcell.2019.00390.
26.      Levy DE, Lee CK. What does Stat3 do? J Clin Invest. 2002;109(9):1143-8.
27.       Tscherner A, Brown AC, Stalker L, Kao J, Dufort I, Sirard MA, et al. STAT3 signaling stimulates miR-21 expression in bovine cumulus cells during in vitro oocyte maturation. Sci Rep. 2018;8(1):11527. doi:10.1038/s41598-018-29874-w.
28.      Cao Q, Li YY, He WF, Zhang ZZ, Zhou Q, Liu X, et al. Interplay between microRNAs and the STAT3 signaling pathway in human cancers. Physiol Genomics. 2013;45(24):1206-14. doi: 10.1152/physiolgenomics.00122.2013.
29.      Zhang C, Liu K, Li T, Fang J, Ding Y, Sun L, et al. miR-21: A gene of dual regulation in breast cancer. Int J Oncol. 2016;48(1):161-72.
Middle East Journal of Cancer
Volume 11, Issue 4 - Serial Number 44
October 2020
Pages 483-492
Files
Share
How to cite
Statistics