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人核糖体蛋白 S13 通过下调 p27(Kip1) 促进胃癌生长。

Human ribosomal protein S13 promotes gastric cancer growth through down-regulating p27(Kip1).

机构信息

State Key Laboratory of Cancer Biology and Institute of Digestive Diseases, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi, China.

出版信息

J Cell Mol Med. 2011 Feb;15(2):296-306. doi: 10.1111/j.1582-4934.2009.00969.x.

DOI:10.1111/j.1582-4934.2009.00969.x
PMID:19912438
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3822796/
Abstract

Our previous works revealed that human ribosomal protein S13 (RPS13) was up-regulated in multidrug-resistant gastric cancer cells and overexpression of RPS13 could protect gastric cancer cells from drug-induced apoptosis. The present study was designed to explore the role of RPS13 in tumorigenesis and development of gastric cancer. The expression of RPS13 in gastric cancer tissues and normal gastric mucosa was evaluated by immunohistochemical staining and Western blot analysis. It was found RPS13 was expressed at a higher level in gastric cancer tissues than that in normal gastric mucosa. RPS13 was then genetically overexpressed in gastric cancer cells or knocked down by RNA interference. It was demonstrated that up-regulation of RPS13 accelerated the growth, enhanced in vitro colony forming and soft agar cologenic ability and promoted in vivo tumour formation potential of gastric cancer cells. Meanwhile, down-regulation of RPS13 in gastric cancer cells resulted in complete opposite effects. Moreover, overexpression of RPS13 could promote G1 to S phase transition whereas knocking down of RPS13 led to G1 arrest of gastric cancer cells. It was further demonstrated that RPS13 down-regulated p27(kip1) expression and CDK2 kinase activity but did not change the expression of cyclin D, cyclin E, CDK2, CDK4 and p16(INK4A). Taken together, these data indicate that RPS13 could promote the growth and cell cycle progression of gastric cancer cells at least through inhibiting p27(kip1) expression.

摘要

我们之前的工作表明，人类核糖体蛋白 S13（RPS13）在多药耐药性胃癌细胞中上调，并且 RPS13 的过表达可以保护胃癌细胞免受药物诱导的凋亡。本研究旨在探讨 RPS13 在胃癌发生发展中的作用。通过免疫组织化学染色和 Western blot 分析评估 RPS13 在胃癌组织和正常胃黏膜中的表达。结果发现，RPS13 在胃癌组织中的表达水平高于正常胃黏膜。然后通过基因过表达或 RNA 干扰敲低 RPS13 在胃癌细胞中的表达。结果表明，上调 RPS13 加速了胃癌细胞的生长，增强了体外集落形成和软琼脂集落形成能力，并促进了体内胃癌细胞的成瘤潜能。同时，下调胃癌细胞中的 RPS13 则产生完全相反的效果。此外，RPS13 的过表达可促进 G1 期向 S 期转变，而敲低 RPS13 则导致胃癌细胞 G1 期停滞。进一步研究表明，RPS13 下调了 p27(kip1)的表达和 CDK2 激酶活性，但不改变 cyclin D、cyclin E、CDK2、CDK4 和 p16(INK4A)的表达。综上所述，这些数据表明 RPS13 至少通过抑制 p27(kip1)的表达促进胃癌细胞的生长和细胞周期进程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfae/3822796/a0469c64c891/jcmm0015-0296-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfae/3822796/c5929c926405/jcmm0015-0296-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfae/3822796/4f235313598d/jcmm0015-0296-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfae/3822796/482a0054d1aa/jcmm0015-0296-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfae/3822796/d46e9b4f4048/jcmm0015-0296-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfae/3822796/c8f30a9f2c54/jcmm0015-0296-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfae/3822796/b3c6422159da/jcmm0015-0296-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfae/3822796/a0469c64c891/jcmm0015-0296-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfae/3822796/c5929c926405/jcmm0015-0296-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfae/3822796/4f235313598d/jcmm0015-0296-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfae/3822796/482a0054d1aa/jcmm0015-0296-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfae/3822796/d46e9b4f4048/jcmm0015-0296-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfae/3822796/c8f30a9f2c54/jcmm0015-0296-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfae/3822796/b3c6422159da/jcmm0015-0296-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfae/3822796/a0469c64c891/jcmm0015-0296-f7.jpg

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