中国肺癌杂志
中國肺癌雜誌
중국폐암잡지
CHINESE JOURNAL OF LUNG CANCER
2001年
2期
83-87
,共5页
吴晓%郑杰%朱建健%付坚%马春树%由江峰%崔湘琳%王洁良%方伟岗%周爱儒%汤健%吴秉铨
吳曉%鄭傑%硃建健%付堅%馬春樹%由江峰%崔湘琳%王潔良%方偉崗%週愛儒%湯健%吳秉銓
오효%정걸%주건건%부견%마춘수%유강봉%최상림%왕길량%방위강%주애유%탕건%오병전
肺肿瘤%血管内皮生长因子%内皮抑素%基因转染
肺腫瘤%血管內皮生長因子%內皮抑素%基因轉染
폐종류%혈관내피생장인자%내피억소%기인전염
目的 探讨反义VEGF基因和内皮抑素基因联合转染在抑制肿瘤血管生成和肿瘤生长转移中的作用。方法 反义VEGF121cDNA脂质体法转染人肺巨细胞癌细胞（PG-AS-VEGF），先行转基因细胞裸鼠异种移植，之后电脉冲介导PsectagA-内皮抑素基因转染，观察反义VEGF基因和内皮抑素转染对肿瘤血管生成和肿瘤生长转移的调节作用。结果 肿瘤内微血管密度在PG-AS-VEGF、转染空载体组分别为40.67±9.35和58.34±10.52(P＜0.05)；裸鼠体内接种PG-AS-VEGF细胞后18天，PG-AS-VEGF、转染空载体组肿瘤体积分别为(0.9779±0.2421)和(1.5210±0.4150)cm3(P＜0.05)；PG-AS-VEGF、转染空载体组淋巴结转移率分别为16.7％(2／12)和50％(6／12)(P＜0.05)。在肿瘤局部行PsectagA-内皮抑素基因转染的PG-AS-VEGF瘤，当肿瘤生长到21天时，肿瘤生长受到明显抑制，PsectagA-内皮抑素基因转染组与PsectagA空载体转染组肿瘤体积分别为(1.5889±1.1396)和(3.398±2.642)cm3(P＜0.05)；两者肿瘤淋巴结转移率分别为12.5％(1／8)和75％(6／8)(P＜0.05)。结论 内皮抑素基因转染对反义VEGF基因转染的PG细胞裸鼠体内生长和淋巴结自发性转移有协同抑制作用。
目的 探討反義VEGF基因和內皮抑素基因聯閤轉染在抑製腫瘤血管生成和腫瘤生長轉移中的作用。方法 反義VEGF121cDNA脂質體法轉染人肺巨細胞癌細胞（PG-AS-VEGF），先行轉基因細胞裸鼠異種移植，之後電脈遲介導PsectagA-內皮抑素基因轉染，觀察反義VEGF基因和內皮抑素轉染對腫瘤血管生成和腫瘤生長轉移的調節作用。結果 腫瘤內微血管密度在PG-AS-VEGF、轉染空載體組分彆為40.67±9.35和58.34±10.52(P＜0.05)；裸鼠體內接種PG-AS-VEGF細胞後18天，PG-AS-VEGF、轉染空載體組腫瘤體積分彆為(0.9779±0.2421)和(1.5210±0.4150)cm3(P＜0.05)；PG-AS-VEGF、轉染空載體組淋巴結轉移率分彆為16.7％(2／12)和50％(6／12)(P＜0.05)。在腫瘤跼部行PsectagA-內皮抑素基因轉染的PG-AS-VEGF瘤，噹腫瘤生長到21天時，腫瘤生長受到明顯抑製，PsectagA-內皮抑素基因轉染組與PsectagA空載體轉染組腫瘤體積分彆為(1.5889±1.1396)和(3.398±2.642)cm3(P＜0.05)；兩者腫瘤淋巴結轉移率分彆為12.5％(1／8)和75％(6／8)(P＜0.05)。結論 內皮抑素基因轉染對反義VEGF基因轉染的PG細胞裸鼠體內生長和淋巴結自髮性轉移有協同抑製作用。
목적 탐토반의VEGF기인화내피억소기인연합전염재억제종류혈관생성화종류생장전이중적작용。방법 반의VEGF121cDNA지질체법전염인폐거세포암세포（PG-AS-VEGF），선행전기인세포라서이충이식，지후전맥충개도PsectagA-내피억소기인전염，관찰반의VEGF기인화내피억소전염대종류혈관생성화종류생장전이적조절작용。결과 종류내미혈관밀도재PG-AS-VEGF、전염공재체조분별위40.67±9.35화58.34±10.52(P＜0.05)；라서체내접충PG-AS-VEGF세포후18천，PG-AS-VEGF、전염공재체조종류체적분별위(0.9779±0.2421)화(1.5210±0.4150)cm3(P＜0.05)；PG-AS-VEGF、전염공재체조림파결전이솔분별위16.7％(2／12)화50％(6／12)(P＜0.05)。재종류국부행PsectagA-내피억소기인전염적PG-AS-VEGF류，당종류생장도21천시，종류생장수도명현억제，PsectagA-내피억소기인전염조여PsectagA공재체전염조종류체적분별위(1.5889±1.1396)화(3.398±2.642)cm3(P＜0.05)；량자종류림파결전이솔분별위12.5％(1／8)화75％(6／8)(P＜0.05)。결론 내피억소기인전염대반의VEGF기인전염적PG세포라서체내생장화림파결자발성전이유협동억제작용。
bjective To explore the co-operative inhibitory effect ofantisense VEGF gene and endostatin gene transfection on tumor angiogenesis, tumor growth and metastasis of lung cancer. Methods Antisense VEGF121 cDNA was transfected into PG cells(PG-AS-VEGF) by lipofectin. After PG-AS-VEGF cells were xenografted to nude mice, PsectagA-endostatin gene was transfected into nude mice by electric pulse mediation. The MVDs in tumors and tumor biological characteristics were observed. Results ①The MVD in PG-AS-VEGF tumor in nude mice was significantly lower than that in PG-vector tumor (PG-AS-VEGF and PG-vector: 40.67±9.35 and 58.34±10.52, respectively) in nude mice. ②There was no significant difference between the PG-vector tumor and PG-AS-VEGF tumor in early stage of the tumor growth in vivo. However, PG-AS-VEGF tumor grew significantly more slowly than PG-vector tumor after 18 days (P＜0.05). ③PG-AS-VEGF tumor could lead to regional and／or distant lymph node metastases (16.7％, 2／12）, which was much more infrequent than that in PG-vector group (50％, 6／12). ④ PG-AS-VEGF tumor growth was remarkably inhibited by endostatin gene transfected at site of the tumor inoculation as compared with the control group in nude mice (P＜0.05). ⑤The PG-AS-VEGF tumors transfected with the endostatin gene at site of the tumor inoculation(AST) could also produce much lower regional and／or distant lymph node metastases rate (12.5％, 1／8） than that in the PG-AS-VEGF tumor transfected with the PsectagA vector (ASP)(75％, 6／8). Conclusion Endostatin gene transfection could cooperatively inhibit the growth and spontaneous lymph node metastasis of antisense VEGF gene transfected PG cells in nude mice.
