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中华结直肠疾病电子杂志 ›› 2013, Vol. 02 ›› Issue (02) : 63 -67. doi: 10.3877/cma.j.issn.2095-3224.2013.02.04

所属专题: 文献

论著

细胞自噬与结肠癌Lovo细胞迁移和侵袭的相关性研究
王天宝1,(), 石汉平1, 韩方海1, 董文广1   
  1. 1. 510080 广州,中山大学附属第一医院外科
  • 收稿日期:2013-01-06 出版日期:2013-04-25
  • 通信作者: 王天宝
  • 基金资助:
    广东省科技计划资助项目(2012B060900100)

The relationship of cell autophagy and Lovo cell migration and invasion

Tian-bao WANG1,(), Han-ping SHI1, Fang-hai HAN1, Wen-guang DONG1   

  1. 1. Department of Surgery, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, China
  • Received:2013-01-06 Published:2013-04-25
  • Corresponding author: Tian-bao WANG
  • About author:
    Corresponding author: WANG Tian-bao, Email:
引用本文:

王天宝, 石汉平, 韩方海, 董文广. 细胞自噬与结肠癌Lovo细胞迁移和侵袭的相关性研究[J/OL]. 中华结直肠疾病电子杂志, 2013, 02(02): 63-67.

Tian-bao WANG, Han-ping SHI, Fang-hai HAN, Wen-guang DONG. The relationship of cell autophagy and Lovo cell migration and invasion[J/OL]. Chinese Journal of Colorectal Diseases(Electronic Edition), 2013, 02(02): 63-67.

目的

探讨不同自噬状态对结直肠癌Lovo细胞迁移和侵袭能力的影响。

方法

将Lovo细胞分为自噬增强组、正常细胞组和3-甲基嘌呤自噬抑制组。用激光共聚焦显微镜观察绿色荧光颗粒,用Q-PCR检测Beclin1 mRNA表达水平,透射电镜观察自噬溶酶体,Transwell实验评价Lovo细胞迁移与侵袭能力。

结果

绿色荧光颗粒数以自噬增强组最多,其次为正常细胞组,而自噬抑制组最少。Beclin1 mRNA表达量自噬增强组为(1.23±0.12)个,正常细胞组为(1±0.13)个,自噬抑制组为(0.98±0.1)个。自噬增强组可见大量的自噬溶酶体,明显多于正常细胞组和自噬抑制组。迁移实验细胞计数:自噬增强组高于正常细胞组(138.0±16.7与90.7±12.9,P=0.026)和自噬抑制组(138.0±16.7与92.7±26.7,P=0.030)。侵袭实验细胞计数:自噬增强组高于正常细胞组(147.0±13.0与99.0±20.5,P=0.028)和自噬抑制组(147.0±13.0与95.7±25.6,P=0.021)。

结论

结肠癌Lovo细胞自噬增强促进肿瘤细胞迁移和浸润,可能是局部浸润和远处转移的机制之一。

Objective

To investigate the influence of autophagy on migration and invasion in colon cancer cells.

Methods

The Lovo cells of colon cancer were classified as autophagy-enhanced group, normal cell group, and 3-Methyladenine autophagy-inhibited group.Laser canning confocal microscope was used to identify the green fluorescence particles.Beclin1 mRNA expressive level was measured with Q-PCR.Transmission electron microscope was employed to observe the autolysosome.Transwell chamber was applied to evaluate the migration and invasion of Lovo cell.

Results

There were more green fluorescence particles in the autophagy-enhanced group than the normal cell group and the autophagy-inhibited group.The Beclin 1 mRNA expressive level was 1.23±0.12 in the autophagy-enhanced group, while 1±0.13 in the normal cell group and 0.98±0.1 in the autophagy-inhibited group.There were the most autolysosomes in autophagy-enhanced group of all groups.The migration experiment showed the mean number of Lovo cell in the autophagy-enhanced group(138.0±16.7)were more than the normal Lovo cell group(90.7±12.9, P=0.026)and the autophagy-inhibited group(92.7±26.7, P=0.030). The invasion experiment found the mean number of Lovo cell in autophagy-enhanced group(147.0±13.0)were also more than the normal Lovo cell group(99.0±20.5, P=0.028)and the autophagy-inhibited group(95.7±25.6, P=0.021).

Conclusions

Autophagy enhancement could promote the migrating and invasive ability of Lovo cell.And that might be an important mechanism of invasion and metastasis in malignant tumors.

图1 激光共聚焦显微镜镜下观察自噬增强组、正常细胞组和自噬抑制组Lovo细胞内荧光颗粒图像
图2 透视电镜下观察自噬增强组细胞、正常细胞组和3-MA自噬抑制组Lovo细胞的自噬溶酶体图像
[1]
Parsons HM,Tuttle TM,Kuntz KM,et al.Association between lymph node evaluation for colon cancer and node positivity over the past 20 years.JAMA,2011,306(10):1089-1097.
[2]
Rice J.Metastasis:The rude awakening.Nature,2012,485(7400):55-57.
[3]
Behrends C,Sowa ME,Gygi SP,et al.Network organization of the human autophagy system.Nature,2010,466(7302):68-76.
[4]
Buchser WJ,Laskow TC,Pavlik PJ,et al.Cell-mediated autophagy promotes cancer cell survival.Cancer Res,2012,72(12):2970-2979.
[5]
Yoshioka A,Miyata H,Doki Y,et al.LC3,an autophagosome marker,is highly expressed in gastrointestinal cancers.Int J Oncol,2008,33(3):461-468.
[6]
Habeeb BS,Kitayama J,Nagawa H.Adiponectin supports cell survival in glucose deprivation through enhancement of autophagic response in colorectal cancer cells.Cancer Sci,2011,102(5):999-1006.
[7]
Sancak Y,Bar-Peled L,Zoncu R,et al.Ragulator-Rag complex targets mTORC1 to the lysosomal surface and is necessary for its activation by amino acids.Cell,2010,141(2):290-303.
[8]
Groulx JF,Khalfaoui T,Benoit YD,et al.Autophagy is active in normal colon mucosa.Autophagy,2012,8(6):893-902.
[9]
Giatromanolaki A,Koukourakis MI,Harris AL,et al.Prognostic relevance of light chain 3(LC3A)autophagy patterns in colorectal adenocarcinomas.J Clin Pathol,2010,63(10):867-872.
[10]
Chen F,Wang CC,Kim E,et al.Hyperthermia in combination with oxidative stress induces autophagic cell death in HT-29 colon cancer cells.Cell Biol Int,2008,32(7):715-723.
[11]
Scherz-Shouval R,Weidberg H,Gonen C,et al.p53-dependent regulation of autophagy protein LC3 supports cancer cell survival under prolonged starvation.Proc Natl Acad Sci USA,2010,107(43):18511-1856.
[12]
Li J,Hou N,Faried A,et al.Inhibition of autophagy augments 5-fluorouracil chemotherapy in human colon cancer in vitro and in vivo model.Eur J Cancer,2010,46(10):1900-1909.
[13]
Sasaki K,Tsuno NH,Sunami E,et al.Resistance of colon cancer to 5-fluorouracil may be overcome by combination with chloroquine,an in vivo study.Anticancer Drugs,2012,23(7):675-782.
[14]
王天宝,石汉平,韩方海,等.SDF-1/CXCR4系统和结直肠癌转移的相关性研究进展.中华结直肠疾病电子杂志,2012,1(1):31-33.
[15]
Teicher BA,Fricker SP.CXCL12(SDF-1)/CXCR4 pathway in cancer.Clin Cancer Res,2010,16(11):2927-2931.
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