中文摘要：

化疗是为 colorectal 腺癌癌症的重要治疗；然而， colorectal 腺癌房间经常开发抵抗到化学疗法的药，导致恶化和差的耐心的预后。药抵抗的发展经常是一个 multifactor 过程，它包含了几基因和细胞的机制。microRNAs 是否定地在 post-transcriptional 水平调整基因表示的内长的小非编码的 RNA。在现在的学习，我们在调整 colorectal 腺癌房间 SW620 和 SW480 的药敏感调查了 microRNAs 的可能的角色。使用 microRNA 表达式数组和我们发现了房间展出了的那 SW620 的量的反向的 transcriptase (RT )-PCR, 与 SW480 房间相比提高了 miR-20a 表示。另外，这二房间行显示了不同敏感到化学疗法的药氟尿嘧啶， oxaliplatin，和 teniposide。miR-20a 的调整改变了 SW620 和 SW480 房间的敏感到这些药；miR-20a 击倒敏化的 SW620 房间到化学疗法的代理人，而在 SW480 房间的 miR-20a 的 overexpression 导致了 chemoresistance。内长的 BNIP2 mRNA 和 BNIP2 蛋白质层次是相反地由量的 RT-PCR 和西方的污点分析与是的 miR-20a 层次有关检测了。荧光记者试金显示出在 miR-20a 和 BNIP2 3UTR 之间的一个直接相互作用。一起拿，我们的调查结果建议 miR-20a 可以在 colorectal 腺癌癌症房间药抵抗起一个作用并且可以是对在 colorectal 腺癌的化疗药抵抗的一个治疗学的目标。

英文摘要：

Chemotherapy is an important treatment for colorectal adenocarcinoma cancer; however, colorectal adenocarci- noma cells often develop resistance to chemotherapeutic drugs, leading to relapse and poor patient prognosis. The development of drug resistance is often a multifactor process, which involved several genes and cellular mechanisms, microRNAs are endogenous small non- coding RNAs that negatively regulate gene expression at the post-transcriptional level. In the present study, we investigated the possible role of microRNAs in regulating drug sensitivity of colorectal adenocarcinoma cells SW620 and SW480. Using microRNA expression arrays and quantitative reverse transcriptase （RT）-PCR, we found that SW620 cells exhibited elevated miR-20a expression compared with SW480 cells. In addition, these two cell lines displayed different sensitivities to the chemotherapeutic drugs fluorouracil, oxaliplatin, and teniposide. Modulation of miR-20a altered the sen- sitivity of SW620 and SW480 cells to these drugs; knockdown of miR-20a sensitized SW620 cells to chemotherapeutic agents, whereas overexpression of miR- 20a in SW480 cells resulted in chemoresistance. Endogenous BNIP2 mRNA and BNIP2 protein levels were inversely related to miR-20a levels as detected by quantitative RT-PCR and western blot analysis. Fluorescence reporter assays showed a direct interaction between miR-20a and the BNIP2 3tUTR. Taken together, our findings suggested that miR-20a may play a role in colorectal adenocarcinoma cancer cell drug resistance and may be a therapeutic target against chemotherapy drug resistance in colorectal adenocarcinoma.