title: CCL21/CCR7 enhances the proliferation, migration, and invasion of human bladder cancer T24 cells.
abstract: OBJECTIVE
  To investigate the effects of CCL21/CCR7 on the proliferation, migration, and invasion of T24 cells and the possible associated mechanisms: expression of MMP-2 and MMP-9, and regulation of BCL-2 and BAX proteins.
  
  
  METHODS
  T24 cells received corresponding treatments including vehicle control, antibody (20 ng/mL CCR7 antibody and 50 ng/ml CCL21), and 50, 100, and 200 ng/ml CCL21. Proliferation was evaluated by MTT assay; cell migration and invasion were assayed using a transwell chamber. Cell apoptosis was induced by Adriamycin (ADM). The rate of cell apoptosis was examined by flow cytometry using annexin V-FITC/PI staining. Western-blot was used to analyze MMP-2 and MMP-9 and BCL-2 and BAX proteins.
  
  
  RESULTS
  CCL21 promoted T24 cell proliferation in concentration-dependent manner with that 200 ng/mL induced the largest amount of proliferation. Significant differences of cell migration were found between CCL21treatment groups and the control group in both the migration and invasion studies (P < 0.001 for all). The expressions of MMP-2 and MMP-9 proteins were significantly increased after CCL21 treatment (p < 0.05 for all). Protein expression of Bcl-21 follows an ascending trend while the expression of Bax follows a descending trend as the concentration of CCL21 increases. No difference was found between the control group and antibody group for all assessments.
  
  
  CONCLUSIONS
  CCL21/CCR7 promoted T24 cell proliferation and enhanced its migration and invasion via the increased expression of MMP-2 and MMP-9. CCL21/CCR7 had antiapoptotic activities on T24 cells via regulation of Bcl-2 and Bax proteins. CCL21/CCR7 may promote bladder cancer development and metastasis.
authors: Department of Urology, Xiangya Hospital, Central South University, Changsha 410008, Hunan, P.R. China.
authors: Miao
authors: M
authors: Mo
authors: Department of Urology, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang 310014, P.R. China.
authors: Mi
authors: M
authors: Zhou
authors: Health Management Center, Xiangya Hospital, Central South University, Changsha 410008, Hunan, P.R. China.
authors: Lu
authors: L
authors: Wang
authors: Department of Urology, Xiangya Hospital, Central South University, Changsha 410008, Hunan, P.R. China.
authors: Lin
authors: L
authors: Qi
authors: Department of Health Care Studies, Daemen College, 4380 Main Street, Amherst, NY 14226, United States of America.
authors: Kehua
authors: K
authors: Zhou
authors: Department of Urology, Xiangya Hospital, Central South University, Changsha 410008, Hunan, P.R. China.
authors: Long-Fei
authors: LF
authors: Liu
authors: Department of Urology, Xiangya Hospital, Central South University, Changsha 410008, Hunan, P.R. China.
authors: Zhi
authors: Z
authors: Chen
authors: Department of Urology, Xiangya Hospital, Central South University, Changsha 410008, Hunan, P.R. China.
authors: Xiong-Bing
authors: XB
authors: Zu
mesh_terms: D017209:Apoptosis; D015153:Blotting, Western; D002448:Cell Adhesion; D002465:Cell Movement; D049109:Cell Proliferation; D054421:Chemokine CCL21 / Q000378:metabolism*; D005434:Flow Cytometry; D006801:Humans; D009361:Neoplasm Invasiveness; D054400:Receptors, CCR7 / Q000378:metabolism*; D014407:Tumor Cells, Cultured; D001749:Urinary Bladder Neoplasms / Q000378:metabolism* / Q000473:pathology*
chemical_list: C515478:CCL21 protein, human; D054421:Chemokine CCL21; D054400:Receptors, CCR7