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[1]楊風(fēng)光,許清江,魏永寶,等.羅格列酮對(duì)舒尼替尼耐藥腎癌細(xì)胞血管生成的影響[J].福建醫(yī)藥雜志,2023,45(03):106-109.
　YANG Fengguang,XU Qingjiang,WEI Yongbao,et al.Effect of peroxisome on angiogenesis in sunitinib-resistant renal carcinoma cells[J].FUJIAN MEDICAL JOURNAL,2023,45(03):106-109.
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羅格列酮對(duì)舒尼替尼耐藥腎癌細(xì)胞血管生成的影響()
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《福建醫(yī)藥雜志》[ISSN:1002-2600/CN:35-1071/R]

卷:
45
期數(shù):
2023年03期
頁碼:
106-109
欄目:
基礎(chǔ)研究
出版日期:
2023-06-15

文章信息/Info

Title:
Effect of peroxisome on angiogenesis in sunitinib-resistant renal carcinoma cells
文章編號(hào):
1002-2600(2023)03-0106-04
作者:
楊風(fēng)光; 許清江; 魏永寶; 彭俊銘; 張弛; 陳平舟; 阮君山1
福建醫(yī)科大學(xué)省立臨床醫(yī)學(xué)院 福建省立醫(yī)院泌尿外科(福州 350001)
Author(s):
YANG Fengguang;  XU Qingjiang;  WEI Yongbao;  PENG Junming;  ZHANG Chi;  CHEN Pingzhou;  RUAN Junshan
Department of Urology Surgery, Fujian Provincial Hospital, Provincial Clinical Medical College of Fujian Medical University, Fuzhou, Fujian 350001, China
關(guān)鍵詞:
腎細(xì)胞癌;  過氧化物酶體增殖物激活受體γ;  血管生成;  舒尼替尼耐藥
Keywords:
renal cell carcinoma;  peroxisome proliferator activated receptorγ;  angiogenesis;  sunitinib resistance
分類號(hào):
R737.11
文獻(xiàn)標(biāo)志碼:
A
摘要:
目的 探討過氧化物酶體增殖物激活受體γ(PPARγ)配體羅格列酮(RG)對(duì)舒尼替尼(SU)耐藥的腎癌細(xì)胞血管生成的影響及其作用機(jī)制。方法 通過濃度梯度培養(yǎng)建立SU耐藥的腎癌細(xì)胞株(786-O/SR和A498/SR),構(gòu)建并轉(zhuǎn)染短發(fā)夾PPARγ(shPPARγ)慢病毒載體靜默PPARγ的表達(dá)。細(xì)胞生長曲線觀察RG對(duì)耐藥腎癌細(xì)胞生長的影響。人臍靜脈血管內(nèi)皮細(xì)胞(HUVEC)小管形成實(shí)驗(yàn)觀察RG對(duì)血管生成的作用,以及與PPARγ表達(dá)的關(guān)系。Western blot檢測血管內(nèi)皮生長因子(VEGF)和蛋白激酶B/信號(hào)傳導(dǎo)轉(zhuǎn)錄激活因子3(AKT/STAT3)通路蛋白表達(dá)的變化。結(jié)果 RG抑制SU耐藥腎癌細(xì)胞的生長。30 μmol/L RG抑制786-O/SR和A498/SR細(xì)胞生成HUVEC小管的能力,Western blot結(jié)果顯示VEGF、p-AKT、AKT、p-STAT3、STAT3的表達(dá)降低,靜默PPARγ可以逆轉(zhuǎn)RG的抑制作用。結(jié)論 RG通過激活PPARγ抑制SU耐藥腎癌細(xì)胞的生長和血管生成,PPARγ配體有可能成為耐藥腎癌細(xì)胞的治療藥物。
Abstract:
Objective To investigate the effect of PPARγ ligand rosiglitazone(RG)on angiogenesis of sunitinib-resistant renal carcinoma cells and explore its mechanism. Methods Renal cancer cell lines 786-O and A498 were cultured in concentration gradient sunitinib to construct drug resistant cells.Sunitinib resistant cells 786-O/SR and A498/SR were transfected with shPPARγ lentivirus vector to silence PPARγ expression. The effect of rosiglitazone on the growth of drug-resistant cells was detected by cell growth curve. The ability of angiogenesis induced by drug-resistant renal carcinoma cells treated with rosiglitazone were observed by HUVEC tubule formation assay. The expression levels of pathway proteins were detected by Western blot. Results Rosiglitazone inhibited the growth of sunitinib resistant renal carcinoma cells. 30 μmol/L rosiglitazone inhibited the ability of 786-O/SR and A498/SR cells to generate HUVEC tubules. Western blot results showed that the expressions of VEGF, p-AKT, AKT, p-STAT3 and STAT3 were decreased. Silent PPARγ reversed the inhibitory effect of rosiglitazone. Conclusion Rosiglitazone inhibits cell growth and angiogenesis in sunitinib-resistant renal carcinoma cells through activating PPARγ,and may be a potential therapeutic agent for sunitinib-resistance.

參考文獻(xiàn)/References:

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備注/Memo

備注/Memo:
基金項(xiàng)目:福建省自然科學(xué)基金面上項(xiàng)目(2019J01181)
1 福建省立醫(yī)院中醫(yī)藥分子生物學(xué)實(shí)驗(yàn)室,通信作者,Email: [email protected]
更新日期/Last Update: 2023-06-15