分析甲基胞嘧啶加双氧酶3（TET3）在肾透明细胞癌中的表达变化，验证TET3在肾透明细胞癌中的作用并探讨其机制。

利用Fire Browse数据库分析TET3在肾透明细胞癌和正常癌旁组织中的表达差异，利用TCGA数据库分析TET3在肾透明细胞癌中的表达，人肾腺癌细胞（ACHN）细胞稳定转染shRNA-NC、shRNA-TET3，CCK8检测转染细胞24、48、72 h的增殖，克隆形成实验计数转染细胞克隆个数，Transwell共培养迁移实验检测转染细胞的迁移情况，Western blot检测蛋白TET3、聚腺苷二磷酸核糖聚合酶（PARP）、p-P38、P38、p-ERK和ERK的表达。两组间比较采用独立样本t检验，多组间比较采用单因素方差分析，多重比较采用Dunnett's-t检验。

数据库分析发现TET3在肾透明细胞癌中高表达。与转染shRNA-NC相比，转染shRNA-TET3后ACHN细胞吸光度值在24 h（0.2501±0.0065比0.2500±0.0073）和48 h（0.3964±0.01402比0.3711±0.011）时差异无统计学意义（P > 0.05），在72 h时吸光度值（0.4303±0.0287比0.3641±0.0230）降低，差异有统计学意义（P < 0.05）。与转染shRNA-NC相比，转染shRNA-TET3后克隆形成个数[（60.00±6.00）个比（37.00±9.00）个]减少，差异有统计学意义（P < 0.01）。与转染shRNA-NC相比，转染shRNA-TET3后迁移细胞个数[（49.00±4.00）个比（50.00±3.00）个]差异无统计学意义（P > 0.05）。与转染shRNA-NC相比，转染shRNA-TET3后PARP、ERK、P38蛋白表达差异无统计学意义，p-ERK、p-P38蛋白表达降低。

TET3在肾透明细胞癌中高表达，敲低TET3可以抑制p-ERK、p-P38蛋白表达从而抑制肿瘤细胞增殖，为TET3成为肾透明细胞癌诊断标志物提供了线索和依据。

To analyze TET3 expression in renal clear cell carcinoma, verify the role of TET3 in renal clear cell carcinoma cells and explore its mechanism.

The expression of TET3 gene in normal tissues and their corresponding tumor tissues was analyzed by Fire Browse. The expression of TET3 in renal clear cell carcinoma and normal tissues was analyzed by TCGA database. Human renal carcinoma cells (ACHN) cells were stably transfected with shRNA-NC, shRNA-TET3. Cell proliferation was detected on 24, 48 and 72 hours by the Cell Counting Kit-8 (CCK-8) assay. The number of clones in transfected cell was counted by clone formation experiment. The migration of transfected cells was detected by transwell co-culture migration test. The expression of protein TET3, PARP, p-P38, P38, p-ERK, and ERK was determined by Western blot. Independent sample t test was used for comparison between two groups. Dunnett's-t test was used to compare multiple experimental groups with the same control group.

Based on the data excavation, the expression of TET3 inrenal clear cell carcinoma was higher than that in the normal tissues. Compared with transfected shRNA-NC, the absorbance of ACHN cells after shRNA-TET3 transfection was not significantly different at 24 h (0.2501±0.0065 vs 0.2500±0.0073) and 48 h (0.3964±0.01402 vs 0.3711±0.011) , the difference was not statistically significant (P > 0.05) ,the absorbance value at 72 h (0.4303±0.0287 vs 0.3641±0.0230) is significantly reduced, the difference is statistically significant (P < 0.05) . Compared with transfection of shRNA-NC, the number of cell clones formed after transfection of shRNA-TET3 [ (60.00±6.00) vs (37.00±9.00) ] was significantly reduced, the difference is statistically significant (P < 0.01) . Compared with transfected shRNA-NC, there is no significant difference in the number of migrating cells after transfection of shRNA-TET3 [(49.00±4.00) vs (50.00±3.00) ], the difference was not statistically significant (P > 0.05) . Compared with transfected shRNA-NC, there is no significant difference in PARP, ERK, and P38 protein molecules after transfection of shRNA-TET3, the expression of p-ERK and p-P38 protein molecules is significantly reduced.

TET3 is highly expressed in renal clear cell carcinoma, Knockdown of TET3 can inhibit the expression of p-ERK and p-P38 protein to restrain tumor cell proliferation in vitro. These results provide clues and basis for TET3 as a marker for diagnosis of renal clear cell carcinoma.