Evaluating Gelsolin Gene Expression Among Iranian Breast Cancer Patients

  • Sara Tutunchi Department of Medical Genetics, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
  • Mojtaba Saffari Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran. I.R Iran.
  • Mahta Mazaheri Department of Medical Genetics, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
  • Parisa Nourmohammadi Department of Medical Genetics, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
  • Fereidoon Memari Iran National Tumor Bank, Cancer Research Center, Cancer Institute of Iran, Tehran University of Medical Sciences, Tehran, Iran.
  • Reza Shirkoohi Cancer Biology Research Center, Cancer Institute of Iran, Tehran University of Medical Science, Tehran, Iran.
  • Nasrin Ghasemi Recurrent Abortion Research Centre, Reproductive Sciences Institute, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Keywords: Breast cancer, Gelsolin expression, Iranian population, Tumor grade, Tumor size


Background: Breast cancer is the most common type of cancer among women, and is among the five most prevalent cancer types among Iranian women. Advanced-stage breast cancer is often correlated with distant metastases. Alterations in gene expression affect general cytoskeleton changes during differentiation and oncogenesis, and can be considered an important factor in tumor progression. Gelsolin plays a significant role in actin assembly and has been introduced as a tumor activator. The aim of this study was to evaluate the expression of Gelsolin in breast cancer as well as its correlation with patients’ clinical parameters.Methods: In this study, 70 breast cancer patients, who had been referred to Imam Khomeini Complex Cancer Institute for surgery were randomly selected. Normal and tumor tissues were prepared and stored at -80°C. Gelsolin gene expression was measured using real-time polymerase chain reaction (PCR). Results: The results showed that Gelsolin gene expression had increased in 68.6% of the tumor samples. In addition, there was a significant association between increased levels of gene expression and tumor progression stages (P < 0.05). However, there was no significant association between increased levels of gene expression and other clinical findings, such as tumor grade, tumor size or patient age.Conclusion: The results revealed that Gelsolin gene expression had increased in the tumor samples. Gelsolin overexpression also resulted in increased lymph node involvement in breast cancer. The expression of this gene also increased significantly during advanced stages of breast cancer; however, there was no significant relation between Gelsolin expression and tumor grade or tumor size.


1.Banin Hirata BK, Oda JMM, Losi Guembarovski R, ArizaCB, Oliveira CECd, Watanabe MAE. Molecular markers for
breast cancer: prediction on tumor behavior. Disease markers.2014;2014.
2.Hanahan D, Weinberg RA. Hallmarks of cancer: the nextgeneration. cell. 2011;144(5):646-74.
3.Bray F, Ren JS, Masuyer E, Ferlay J. Global estimates ofcancer prevalence for 27 sites in the adult population in
2008. International Journal of Cancer. 2013;132(5):1133-45.
4.Ghodsi Z, Salehi A, Hojjatoleslami S. Knowledge of Iranianomen about Warning Signs and Risk Factors for
Breast Cancer. Procedia-Social and Behavioral Sciences.2013;93:343-8.
5.Sun X, Sandhu R, Figueroa JD, Gierach GL, Sherman ME,Troester MA. Benign breast tissue composition in breast
cancer patients: association with risk factors, clinical variables,and gene expression. Cancer Epidemiology Biomarkers
& Prevention. 2014;23(12):2810-8.
6.Sgroi DC. Preinvasive Breast Cancer. Annual review of pathology.2010;5:193-221.
7.Saleh MS. Reproductive factors and common genetic mutationsassociated with breast cancer risk in Gaza Strip: Islamic
University–Gaza; 2011.
8.Herbein G, Kumar A. The oncogenic potential of human cytomegalovirusand breast cancer. Frontiers in oncology. 2014;4.
9.Jazayeri SB, Saadat S, Ramezani R, Kaviani A. Incidenceof primary breast cancer in Iran: Ten-year national cancer
registry data report. Cancer Epidemiol. 2015;39(4):519-27.
10.Tan G, Bhoo-Pathy N, Taib N, See M, Jamaris S, Yip C. TheWill Rogers phenomenon in the staging of breast cancer–
Does it matter? Cancer epidemiology. 2015;39(1):115-7.
11.Ludwig JA, Weinstein JN. Biomarkers in cancer staging,prognosis and treatment selection. Nature Reviews Cancer.
12.Dos Remedios C, Chhabra D, Kekic M, Dedova I, Tsub-akihara M, Berry D, et al. Actin binding proteins: regulation
of cytoskeletal microfilaments. Physiological reviews.2003;83(2):433-73.
13.Cross A, Wilson A, Guerrero M, Thomas K, Bachir A,Kubow K, et al. Breast cancer antiestrogen resistance 3–
p130Cas interactions promote adhesion disassembly andinvasion in breast cancer cells. Oncogene. 2016.
14.Menhofer MH, Kubisch R, Schreiner L, Zorn M, FoersterF, Mueller R, et al. The actin targeting compound Chondramide
inhibits breast cancer metastasis via reduction of cellularcontractility. PloS one. 2014;9(11):e112542.
15.Shirkoohi R, Fujita H, Darmanin S, Takimoto M. GelsolinInduces Promonocytic Leukemia Differentiation Accompanied
by Upregulation of p21CIP1. Asian Pacific Journal ofCancer Prevention. 2012;13(9):4827-34.
16.Simoneau M, Aboulkassim TO, LaRue H, Rousseau F, FradetY. Four tumor suppressor loci on chromosome 9q in
bladder cancer: evidence for two novel candidate regions at9q22. 3 and 9q31. Oncogene. 1999;18(1):157-63.
17.Li GH, Arora PD, Chen Y, McCulloch CA, Liu P. Multifunctionalroles of gelsolin in health and diseases. Medicinal
research reviews. 2012;32(5):999-1025.
18.Narayan K, Chumnarnsilpa S, Choe H, Irobi E, Urosev D,Lindberg U, et al. Activation in isolation: exposure of the
actin-binding site in the C-terminal half of gelsolin does notrequire actin1. FEBS letters. 2003;552(2-3):82-5.
19.Baig RM, Mahjabeen I, Sabir M, Masood N, Ali K, MalikFA, et al. Mutational spectrum of Gelsolin and its down
regulation is associated with breast cancer. Disease markers.2013;34(2):71-80.
20.Deng R, Hao J, Han W, Ni Y, Huang X, Hu Q. Gelsolin regulatesproliferation, apoptosis, migration and invasion in humanoral carcinoma cells. Oncology letters. 2015;9(5):2129-34.
21.Abedini MR, Wang P-W, Huang Y-F, Cao M, Chou C-Y,Shieh D-B, et al. Cell fate regulation by gelsolin in human
gynecologic cancers. Proceedings of the National Academyof Sciences. 2014;111(40):14442-7.
22.Stock A-M, Klee F, Edlund K, Grinberg M, Hammad S,Marchan R, et al. Gelsolin is associated with longer metastasis-
free survival and reduced cell migration in estrogenreceptor-positive breast cancer. Anticancer research.2015;35(10):5277-85.
23.Zhuo J, Tan EH, Yan B, Tochhawng L, Jayapal M, Koh S, etal. Gelsolin induces colorectal tumor cell invasion via modulationof the urokinase-type plasminogen activator cascade.PloS one. 2012;7(8):e43594.
24.Zhu WY, Hunag YY, Liu XG, He JY, Chen DD, Zeng F, etal. Prognostic Evaluation of CapG, Gelsolin, P-gp, GSTP1,
and Topo-II Proteins in Non-Small Cell Lung Cancer. TheAnatomical Record. 2012;295(2):208-14.
25.Shieh D-B, Chen I-W, Wei T-Y, Shao C-Y, Chang H-J,Chung C-H, et al. Tissue expression of gelsolin in oral carcinogenesisprogression and its clinicopathological implications.Oral oncology. 2006;42(6):599-606.
How to Cite
Tutunchi S, Saffari M, Mazaheri M, Nourmohammadi P, Memari F, Shirkoohi R, Ghasemi N. Evaluating Gelsolin Gene Expression Among Iranian Breast Cancer Patients. Basic Clin Cancer Res. 10(4):16-25.