TY - JOUR
T1 - Silencing Id-1 inhibits lymphangiogenesis through down-regulation of VEGF-C in oral squamous cell carcinoma
AU - Dong, Zuoqing
AU - Wei, Fengcai
AU - Zhou, Chengjun
AU - Sumida, Tomoki
AU - Hamakawa, Hiroyuki
AU - Hu, Yingwei
AU - Liu, Shaohua
N1 - Funding Information:
This work was supported by the National Natural Science Foundation of China (No. 30672339 ) and the Project of Shandong Medical Science and Technological Development (No. 2009HZ044 ).
PY - 2011/1
Y1 - 2011/1
N2 - Our previous study demonstrated that overexpression of Id-1 (inhibitor of differentiation/DNA binding) was associated with lymphatic metastasis in human oral squamous cell carcinoma (OSCC). In this study, we further unveiled the association of Id-1 with vascular endothelial growth factor-C (VEGF-C) and peritumoral lymphatic vessel density (PLVD), and the effect of silencing Id-1 on inhibiting lymphangiogenesis in OSCC. We found that Id-1 was associated with VEGF-C (r = 0.569, p < 0.001) and PLVD (r = 0.240, p < 0.001) in OSCC. Lentivirus-mediated RNA interference targeting Id-1 in an OSCC cell line Tca8113 resulted in down-regulation of VEGF-C (p = 0.003, 0.007). Moreover, when Id-1 was suppressed by injecting Id-1-siRNA-lentivirus into the transplanted tumors in nude mice, VEGF-C was down-regulated (p = 0.018) and the PLVD decreased (p = 0.001). Our results suggest that Id-1 was correlated with lymphangiogenesis in OSCC. Silencing Id-1 could inhibit lymphangiogenesis through down-regulation of VEGF-C and it might be a promising treatment modality for the lymphatic metastasis of OSCC.
AB - Our previous study demonstrated that overexpression of Id-1 (inhibitor of differentiation/DNA binding) was associated with lymphatic metastasis in human oral squamous cell carcinoma (OSCC). In this study, we further unveiled the association of Id-1 with vascular endothelial growth factor-C (VEGF-C) and peritumoral lymphatic vessel density (PLVD), and the effect of silencing Id-1 on inhibiting lymphangiogenesis in OSCC. We found that Id-1 was associated with VEGF-C (r = 0.569, p < 0.001) and PLVD (r = 0.240, p < 0.001) in OSCC. Lentivirus-mediated RNA interference targeting Id-1 in an OSCC cell line Tca8113 resulted in down-regulation of VEGF-C (p = 0.003, 0.007). Moreover, when Id-1 was suppressed by injecting Id-1-siRNA-lentivirus into the transplanted tumors in nude mice, VEGF-C was down-regulated (p = 0.018) and the PLVD decreased (p = 0.001). Our results suggest that Id-1 was correlated with lymphangiogenesis in OSCC. Silencing Id-1 could inhibit lymphangiogenesis through down-regulation of VEGF-C and it might be a promising treatment modality for the lymphatic metastasis of OSCC.
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U2 - 10.1016/j.oraloncology.2010.10.012
DO - 10.1016/j.oraloncology.2010.10.012
M3 - Article
C2 - 21111670
AN - SCOPUS:79551514772
SN - 1368-8375
VL - 47
SP - 27
EP - 32
JO - Oral Oncology
JF - Oral Oncology
IS - 1
ER -
