**3.20 miR-26a**

miR-26a is an miRNA that plays role of tumor suppressor gene. Lu (Lu *et al,* 2011) found that miR-26a could down-regulate the level of EZH2 expression in nasopharyngeal cancer cells, inhibit cell proliferation significantly, and block cell division at G1. Kota *et al* (Kota *et al,* 2009) used miR-26a to intervene HCC, and found that miR-26a could down-regulate the level of cyclin CCND2 and CCNE2 expression, inhibit the proliferation of HCC cells in vitro, and inhibit tumor progression in vivo, indicating that miR-26a could be used as a strategy for tumor treatment by down-regulating cancer genes.

#### **3.21 Specific mutation ectopic gene**

1. Ras: Ras is the gene that is most likely to undergo mutation in human malignant tumors. A single-point mutation is enough to transform normal protein into cancer protein. Therefore, there is mild difference in DNA sequence between the wild-type Ras

similar between the two groups, indicating that EPOR plays a role in regulating cell

miR-221 and miR-222 are miRNA in cluster distribution with high homogeneity. Studies have shown that tumor suppressor gene p27 (Fornari *et al,* 2008), p57(Fornari *et al,* 2008), pro-apoptotic factor Bim and Bmf (Gramantieri *et al,* 2009) are all target genes of mir-222/mir-221. studies in recent years have shown that miR-221and miR-222 participate in the development of bladder cancer, HCC, prostate cancer and melanoma. Artificially synthesized small RNA precisely compensatory with miRNA can be used as an miRNA inhibitor to silence endogenous miRNA. Mercatelli *et al* (Mercatelli *et al,* 2008) used anti miR-221 and anti miR-222 inhibitors and a negative control inhibitor to intervene transplanted prostate cancer in nude mice for 33 days, and found that the means tumor size of the intervention group and the control group was 197.2mm3 and 276.82mm3 respectively, indicating that regulation of miR221/222 via RNAi could be used as the target of tumor

miR-16 can target Oncogene BCL-2. By regulating BCL-2 expression with miR-16, tumor cell proliferation can be inhibited. Schaefer *et al* (Schaefer *et al,* 2010) found that miR-16 can down-regulate BCL-2 expression in prostate cancer cells. Takeshita *et al* (Takeshita *et al,*  2010) used chemically synthesized miR-16 to transfect prostate cancer cell line 22Rv1, Du145, PPC-1 and PC-3M-luc, and found that the proliferation of these cells was inhibited. They administered miR-16 and atelocollagen to prevent bone metastasis from transplanted prostate cancer tumor in nude mice via tail vein injection. The results showed that, compared to i.v. injection of atelocollagen as a positive control, miR-16 halted the progression of the transplanted tumors and metastatic lesions, and that miR-16 could regulate the expression of CDK1 and CDK2 that participate in cell cycle and proliferation. Therefore, intravenous administration of miR-16 could be applied as a strategy for the

miR-26a is an miRNA that plays role of tumor suppressor gene. Lu (Lu *et al,* 2011) found that miR-26a could down-regulate the level of EZH2 expression in nasopharyngeal cancer cells, inhibit cell proliferation significantly, and block cell division at G1. Kota *et al* (Kota *et al,* 2009) used miR-26a to intervene HCC, and found that miR-26a could down-regulate the level of cyclin CCND2 and CCNE2 expression, inhibit the proliferation of HCC cells in vitro, and inhibit tumor progression in vivo, indicating that miR-26a could be used as a strategy

1. Ras: Ras is the gene that is most likely to undergo mutation in human malignant tumors. A single-point mutation is enough to transform normal protein into cancer protein. Therefore, there is mild difference in DNA sequence between the wild-type Ras

proliferation, and this effect is independent of EPO.

**3.18 miR-221 and miR-222** 

treatment.

**3.19 miR-16** 

**3.20 miR-26a** 

treatment of advanced prostate cancer.

**3.21 Specific mutation ectopic gene** 

for tumor treatment by down-regulating cancer genes.

and mutated-type Ras. Previous methods of gene therapy were unable to inhibit the expression of mutated-type Ras effectively. Researchers have succeeded in using retrovirus-mediated RNA intervention technique to inhibit the expression of mutant KrasV12 without affecting the other Ras subtypes (Brummelkamp *et al,* 2002). It not only inhibited neoplastic growth and transformation in experiments in vitro but obtained the same result in animal models.

