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[Effect of platelet derived growth factor-B and its receptor expression on the proliferation of renal cell carcinoma ACHN cells].
Wang, Wenling; Zhang, Zhenting; Wang, Shuhua; Du, Jun; Yao, Xin.
Afiliação
  • Wang W; Department of Genitourinary Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China.
  • Zhang Z; Department of Genitourinary Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China.
  • Wang S; Department of Genitourinary Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China.
  • Du J; Department of Genitourinary Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China.
  • Yao X; Department of Genitourinary Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China; Email: yaoxin1969@hotmail.com.
Zhonghua Zhong Liu Za Zhi ; 37(3): 170-4, 2015 Mar.
Article em Zh | MEDLINE | ID: mdl-25975783
ABSTRACT

OBJECTIVE:

To study the effect of platelet derived growth factor-B and its receptor expression on the proliferation of renal cell carcinoma ACHN cells in vitro and in vivo.

METHODS:

PDGF-B gene was transfected into human renal carcinoma cell line ACHN cells, and the proliferation capability of ACHN cells transfected with or without PDGF-B was assessed by MTT assay. The effect of PDGF-B on the expression of p-PDGFR-ß in endothelial cells and vascular smooth muscle cells (VSMC) was detected by Western blot. ACHN cells transfected with PDGF-B were injected into mice (untransfected ACHN as control) to induce tumor formation. Immunohistochemical staining was used to detect the expression of Ki-67 in tumor cells and the tumor volume was measured to compare the tumor growth in the two groups.

RESULTS:

The PDGF-B expression of ACHN cells in transfected group was significantly increased than that in the untransfected group. MTT assay showed that the proliferation capability of ACHN cells in the transfected and untransfected groups had no significant differences at different time points (P>0.05). The expression of p-PDGFR-ß in VSMC was significantly increased when cultured with PDGF-B overexpression culture medium. The mean tumor size of the PDGF-B group and control group was (0.305±0.108) cm(3) and (0.577±0.218) cm(3), respectively (P=0.007). Ki-67-positive tumor cells were (41.00±5.34)/HPF in the PDGF-B-transfected group and (55.80±2.95)/HPF in the untransfected group (P=0.001).

CONCLUSION:

PDGF-B overexpression may up-regulate p-PDGFR-ß expression of VSMC in renal cell carcinoma, and inhibit the tumor cell proliferation and tumor growth through paracrine signaling.
Assuntos
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Carcinoma de Células Renais / Receptor beta de Fator de Crescimento Derivado de Plaquetas / Neoplasias Renais Limite: Animals / Humans Idioma: Zh Ano de publicação: 2015 Tipo de documento: Article
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Carcinoma de Células Renais / Receptor beta de Fator de Crescimento Derivado de Plaquetas / Neoplasias Renais Limite: Animals / Humans Idioma: Zh Ano de publicação: 2015 Tipo de documento: Article