Clusterin mRNA silencing reduces cell proliferation, inhibits cell migration, and increases CCL5 expression in SW480, SW620, and Caco2 cells
Author:
Rui Fan1ORCID, Abdalkareem Eshtiyag Abdalla23ORCID, Huat Lim Boon4ORCID, Yin Khoo Boon2ORCID
Affiliation:
1. Department of Anorectal , Harbin Hospital of Traditional Chinese Medicine , Harbin , Heilongjiang , China 2. Institute for Research in Molecular Medicine (INFORMM) , Universiti Sains Malaysia , Penang , Malaysia 3. Tropical Medicine Research Institute (TMRI) , Khartoum , Sudan 4. School of Health Sciences , Universiti Sains Malaysia , Kubang Kerian , Kelantan , Malaysia
Abstract
Abstract
Objectives
This study aimed to investigate the effects of specific gene silencing in colorectal cancer cells. Clusterin protein was found in the serum samples of colorectal cancer patients infected with Schistosoma mansoni previously.
Methods
For this reason, silencing clusterin mRNA in colorectal cancer cells was first performed to study the cytotoxic effect by lactate dehydrogenase assay. Next, propidium iodide staining and flow cytometry were performed to investigate the cell cycle profile in clusterin-silenced cells. A wound-healing assay was also used to examine the migration rate of clusterin-silenced cells. The mRNA expression of cell proliferation- and migration-related genes was then assessed by real-time PCR.
Results
Clusterin mRNA silencing caused a significant reduction in cell growth but induced no cell cycle arrest or potential apoptosis in all cells. It was found in this study that cell migration rate was inhibited in clusterin-silenced cells. Surprisingly, significantly induced chemokine (C–C motif) ligand 5 (CCL5) mRNA expression was detected in clusterin-silenced Caco2, which indicated that the cell proliferation and migration of clusterin-silenced Caco2 were likely associated with CCL5 mRNA expression.
Conclusions
Clusterin may be a potential target for regulation, staging, surveillance, and developing a cost-effective therapeutic agent for treating parasite-infected Caco2 type of colorectal cancer patients.
Publisher
Walter de Gruyter GmbH
Subject
Biochemistry (medical),Clinical Biochemistry,Molecular Biology,Biochemistry
Reference40 articles.
1. Shu, F, Zou, X, Tuo, H, She, S, Huang, J, Ren, H, et al.. Stathmin gene silencing suppresses proliferation, migration and invasion of gastric cancer cells via AKT/sCLU and STAT3 signaling. Int J Oncol 2019;54:1086–98, https://doi.org/10.3892/ijo.2019.4674. 2. Wang, Q, Cao, W, Su, Q, Liu, Z, Zhang, L. Clusterin silencing inhibits proliferation and reduces invasion in human laryngeal squamous carcinoma cells. World J Surg Oncol 2014;12:124, https://doi.org/10.1186/1477-7819-12-124. 3. Trougakos, IP, Gonos, ES. Clusterin/apolipoprotein J in human aging and cancer. Int J Biochem Cell Biol 2002;34:1430–48, https://doi.org/10.1016/s1357-2725(02)00041-9. 4. Shannan, B, Seifert, M, Leskov, K, Willis, J, Boothman, D, Tilgen, W, et al.. Challenge and promise: roles for clusterin in pathogenesis, progression and therapy of cancer. Cell Death Differ 2006;13:12–9, https://doi.org/10.1038/sj.cdd.4401779. 5. Chen, XD, Halberg, RB, Ehrhardt, WM, Torrealba, J, Dove, WF. Clusterin as a biomarker in murine and human intestinal neoplasia. Proc Natl Acad Sci USA 2003;100:9530–5, https://doi.org/10.1073/pnas.1233633100.
Cited by
1 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献
|
|