Limits...
CC chemokine ligand 18 correlates with malignant progression of prostate cancer.

Chen G, Liang YX, Zhu JG, Fu X, Chen YF, Mo RJ, Zhou L, Fu H, Bi XC, He HC, Yang SB, Wu YD, Jiang FN, Zhong WD - Biomed Res Int (2014)

Bottom Line: However, its involvement in human prostate cancer has not been fully elucidated.The effects of PCa cell migration, invasion, and apoptosis were tested.CCL18 upregulation was correlated with high Gleason score (P = 0.034) of patients with PCa. rCCL18 stimulation in PCa cells promoted cell migration and invasion but decreased DU145 cells apoptosis rate.

View Article: PubMed Central - PubMed

Affiliation: Department of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine and Diagnostics, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou 510180, China.

ABSTRACT

Background and aim: CC chemokine ligand 18 (CCL18) promotes malignant behaviors of various human cancer types. However, its involvement in human prostate cancer has not been fully elucidated. The aim of this study was to investigate the role of CCL18 in PCa.

Methods: Expression of CCL18 at mRNA and protein levels was detected using real-time qRT-PCR and immunohistochemistry analysis. We analyzed the associations of CCL18 expression with clinical features of human PCa. The effects of PCa cell migration, invasion, and apoptosis were tested. The efficiency of CCL18 on prostate tumor growth was assessed in a subcutaneous xenograft model.

Results: CCL18 expression was upregulated (both P < 0.01) in PCa tissues compared with those in noncancerous prostate tissues. CCL18 upregulation was correlated with high Gleason score (P = 0.034) of patients with PCa. rCCL18 stimulation in PCa cells promoted cell migration and invasion but decreased DU145 cells apoptosis rate. Furthermore, subcutaneous homografts models showed the increased tumor growth and tumor vascularization with the CCL18 stimulation, and the expression of Ki67, PCNA, and CD31 in CCL18 stimulation mice was also significantly increased.

Conclusions: Our data offer the convincing evidence that the upregulation of CCL18 may be involved in the malignant progression of PCa.

Show MeSH

Related in: MedlinePlus

Expression level of PITPNM3 in DU145 cells was higher than that in LNCaP cells (a), which was in line with the data of GEO profiles (GDS1699/28324/PITPNM3, (b)).
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4150478&req=5

fig6: Expression level of PITPNM3 in DU145 cells was higher than that in LNCaP cells (a), which was in line with the data of GEO profiles (GDS1699/28324/PITPNM3, (b)).

Mentions: We observed the mRNA and protein levels of CCL18 expression in PCa tissues were both higher than those in noncancerous prostate tissues. In our cohorts, CCL18 upregulation was associated with high Gleason score. Moreover, we found that rCCL18 stimulation in the in vitro system could significantly enhance the metastatic and the invasive potentials while reducing the apoptosis rate of DU145 but not LNCaP. In order to find out the reasons for this phenomenon, we detected the expression levels of CCL18 receptor PITPNM3 in LNCaP and DU145 cells. As a result, the expression level of PITPNM3 in DU145 cells was higher than that in LNCaP cells (Figure 6(a)), which was in line with the data of GEO profiles (GDS1699/28324/PITPNM3, Figure 6(b)). These data imply that DU145 may be more sensitive to CCL18 than LNCaP. Furthermore, the in vitro results were also supported by in vivo study using a subcutaneous homograft mouse model. We found that CCL18 could promote tumor growth in vivo by enhancing angiogenesis and expression of cell proliferation markers PCNA and Ki67.


CC chemokine ligand 18 correlates with malignant progression of prostate cancer.

Chen G, Liang YX, Zhu JG, Fu X, Chen YF, Mo RJ, Zhou L, Fu H, Bi XC, He HC, Yang SB, Wu YD, Jiang FN, Zhong WD - Biomed Res Int (2014)

Expression level of PITPNM3 in DU145 cells was higher than that in LNCaP cells (a), which was in line with the data of GEO profiles (GDS1699/28324/PITPNM3, (b)).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4150478&req=5

fig6: Expression level of PITPNM3 in DU145 cells was higher than that in LNCaP cells (a), which was in line with the data of GEO profiles (GDS1699/28324/PITPNM3, (b)).
Mentions: We observed the mRNA and protein levels of CCL18 expression in PCa tissues were both higher than those in noncancerous prostate tissues. In our cohorts, CCL18 upregulation was associated with high Gleason score. Moreover, we found that rCCL18 stimulation in the in vitro system could significantly enhance the metastatic and the invasive potentials while reducing the apoptosis rate of DU145 but not LNCaP. In order to find out the reasons for this phenomenon, we detected the expression levels of CCL18 receptor PITPNM3 in LNCaP and DU145 cells. As a result, the expression level of PITPNM3 in DU145 cells was higher than that in LNCaP cells (Figure 6(a)), which was in line with the data of GEO profiles (GDS1699/28324/PITPNM3, Figure 6(b)). These data imply that DU145 may be more sensitive to CCL18 than LNCaP. Furthermore, the in vitro results were also supported by in vivo study using a subcutaneous homograft mouse model. We found that CCL18 could promote tumor growth in vivo by enhancing angiogenesis and expression of cell proliferation markers PCNA and Ki67.

Bottom Line: However, its involvement in human prostate cancer has not been fully elucidated.The effects of PCa cell migration, invasion, and apoptosis were tested.CCL18 upregulation was correlated with high Gleason score (P = 0.034) of patients with PCa. rCCL18 stimulation in PCa cells promoted cell migration and invasion but decreased DU145 cells apoptosis rate.

View Article: PubMed Central - PubMed

Affiliation: Department of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine and Diagnostics, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou 510180, China.

ABSTRACT

Background and aim: CC chemokine ligand 18 (CCL18) promotes malignant behaviors of various human cancer types. However, its involvement in human prostate cancer has not been fully elucidated. The aim of this study was to investigate the role of CCL18 in PCa.

Methods: Expression of CCL18 at mRNA and protein levels was detected using real-time qRT-PCR and immunohistochemistry analysis. We analyzed the associations of CCL18 expression with clinical features of human PCa. The effects of PCa cell migration, invasion, and apoptosis were tested. The efficiency of CCL18 on prostate tumor growth was assessed in a subcutaneous xenograft model.

Results: CCL18 expression was upregulated (both P < 0.01) in PCa tissues compared with those in noncancerous prostate tissues. CCL18 upregulation was correlated with high Gleason score (P = 0.034) of patients with PCa. rCCL18 stimulation in PCa cells promoted cell migration and invasion but decreased DU145 cells apoptosis rate. Furthermore, subcutaneous homografts models showed the increased tumor growth and tumor vascularization with the CCL18 stimulation, and the expression of Ki67, PCNA, and CD31 in CCL18 stimulation mice was also significantly increased.

Conclusions: Our data offer the convincing evidence that the upregulation of CCL18 may be involved in the malignant progression of PCa.

Show MeSH
Related in: MedlinePlus