CLASP2 is involved in the EMT and early progression after transurethral resection of the bladder tumor

Bisong Zhu,Wentao Liu,Lin Qi,Sulai Liu,Minfeng Chen,Jun Wang,Longfei Liu,Xiongbing Zu,Zhenyu Ou,Yuan Li

doi:10.1186/s12885-017-3101-3

Abstract

BackgroundCytoplasmic linker-associated protein 2 (CLASP2) belongs to a family of microtubule plus-end tracking proteins that localizes to the distal ends of microtubules and regulate microtubule dynamics. We speculated that it might be involved in the epithelial-mesenchymal transition (EMT) and progression of bladder cancer (BC).MethodsWestern blotting and RT-PCR were used to detect the changes at protein and mRNA levels in BC cell lines. Cell proliferation, clonogenic formation, wound healing and chamber invasion assay were used to investigate the abilities of cellular proliferation, migration and invasion. The data of BC patients treated with transurethral resection of the bladder tumor (TURBT) was collected and analyzed. The levels of mRNA of CLASP2 and EMT-related markers in tumor and urine samples were tested by RT-PCR.ResultsExpressions of CLASP2 varied in four BC cell lines. Manipulation of CLASP2 expression changed EMT-related markers. CLASP2 could promote proliferation, migration and invasion in BC cell lines. The combination (CLASP2 + E-cadherin mRNA in urine) could better discriminate the patients with or without 2-years progression compared with tumor grade after TURBT.ConclusionCLASP2 is involved in the EMT and progression of bladder urothelial cancer. Simultaneous urine-based detection of CLASP2 and E-cadherin mRNA can efficiently discriminate patients with or without 2-years progression after TURBT.

Highlights

Cytoplasmic linker-associated protein 2 (CLASP2) belongs to a family of microtubule plus-end tracking proteins that localizes to the distal ends of microtubules and regulates microtubule dynamics
Expressions of CLASP2 varied in four BC cell lines Four bladder cancer cell lines including J82, HTB 9, CRL1749 and T24 were tested the expression of CLASP2 at protein level
Knockdown of CLASP2 by shRNA inhibited these abilities in CRL1749 cells (Fig. 3a-c). These results vividly demonstrated that CLASP2 mediated the migration and invasiveness of BC cells in vitro. These results suggested that overexpression of CLASP2 could facilitate the growth and aggressive phenotype of BC cells in vitro

Summary

Introduction

Cytoplasmic linker-associated protein 2 (CLASP2) belongs to a family of microtubule plus-end tracking proteins that localizes to the distal ends of microtubules and regulate microtubule dynamics We speculated that it might be involved in the epithelial-mesenchymal transition (EMT) and progression of bladder cancer (BC). BC are classified as non-muscle-invasive bladder cancer (non-MIBC) (pTa, pT1 or carcinoma in situ [CIS]) or invasive cancer (pT2, pT3 or pT4) with the latter carrying a worse prognosis [2, 3]. CLASP2 functions in various microtubule-dependent processes, including cell division, cytoskeletal remodeling for cell migration, podosome regulation, and stabilization of adherens junctions [6,7,8,9] These studies suggested CLASP2 might be implemented in cancer progression

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