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16q23.1 肿瘤抑制基因 ADAMTS18 的异常甲基化促进透明细胞肾细胞癌的发生和进展。

Aberrant methylation of the 16q23.1 tumor suppressor gene ADAMTS18 promotes tumorigenesis and progression of clear cell renal cell carcinoma.

机构信息

Department of Urology, National Urological Cancer Center, Peking University First Hospital and Institute of Urology, Peking University, 8 Xishiku Street, Xicheng District, Beijing, 100034, China.

出版信息

Genes Genomics. 2021 Feb;43(2):123-131. doi: 10.1007/s13258-021-01036-9. Epub 2021 Jan 19.

Abstract

BACKGROUND

The 16q23.1 tumor suppressor gene (TSG) of ADAMTS18 has been identified to be aberrant methylated in clear cell renal cell carcinoma (ccRCC), and there still exists an unclear situation between its methylation and the progression of ccRCC.

OBJECTIVE

To analyze the biological function and mechanism of ADAMTS18 gene in the tumorigenesis and progression of ccRCC.

METHODS

We examined ADAMTS18 gene methylation using methylation- specific polymerase chain reaction (MSP) in 92 ccRCC primary tumors from September 2017 to May 2018. Using reverse transcriptase PCR (RT-PCR) and immunohistochemical (IHC) assay, the relative expression level of ADAMTS18 was measured in the representative tumor samples with their adjacent normal tissues. Meanwhile, colony formation, cell viability, wound healing, transwell chamber, flow cytometry, and PI staining were performed to confirm the tumor-suppressive function and mechanism of ADAMTS18 gene.

RESULTS

Aberrant methylation was further detected in 47 of the 92 (51.1%) primary tumors and in 8 of the 92 (8.7%) adjacent normal tissues (p < 0.05). Due to the phenomenon of aberrant methylation, ectopic low-level expression of ADAMTS18 gene could result in the promotion of tumorigenesis and progression in ccRCC.

CONCLUSION

The aberrantly methylated ADAMTS18 gene may be involved in the tumorigenesis and progression of ccRCC.

摘要

背景

ADAMTS18 的 16q23.1 肿瘤抑制基因(TSG)已被确定在肾透明细胞癌(ccRCC)中出现异常甲基化,但其甲基化与 ccRCC 的进展之间仍存在不清楚的情况。

目的

分析 ADAMTS18 基因在 ccRCC 发生和发展中的生物学功能和机制。

方法

我们使用甲基化特异性聚合酶链反应(MSP)在 2017 年 9 月至 2018 年 5 月的 92 例 ccRCC 原发性肿瘤中检测 ADAMTS18 基因甲基化。使用逆转录聚合酶链反应(RT-PCR)和免疫组织化学(IHC)检测,在具有代表性的肿瘤样本及其相邻正常组织中测量 ADAMTS18 的相对表达水平。同时,进行集落形成、细胞活力、划痕愈合、Transwell 室、流式细胞术和 PI 染色,以证实 ADAMTS18 基因的肿瘤抑制功能和机制。

结果

在 92 例原发性肿瘤中的 47 例(51.1%)和 92 例相邻正常组织中的 8 例(8.7%)中进一步检测到异常甲基化(p<0.05)。由于异常甲基化的现象,ADAMTS18 基因的异位低水平表达可能导致 ccRCC 的肿瘤发生和进展。

结论

异常甲基化的 ADAMTS18 基因可能参与 ccRCC 的发生和发展。

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