Laboratory Animal Center, College of Animal Science, Jilin University, Changchun, China.
Department of Hand Surgery, The First Hospital of Jilin University, Changchun, China.
DNA Cell Biol. 2022 Feb;41(2):169-178. doi: 10.1089/dna.2021.0418. Epub 2021 Dec 27.
extract (GBE) has antitumor and antioxidant properties, which play a role in regulating gene and protein expression. The ten-eleven translocation (TET) proteins have the ability to regulate epigenetic modifications. However, the abnormal expression of TET2 protein has also been demonstrated in cancer development. In the present study, we analyzed the effects of GBE administration on TET2 expression in human colorectal cancer (CRC). The Cancer Genome Atlas database suggested that the expression of was lost in CRC. To investigate the expression profiles of TET2, GBE was used to treat CRC cells. The results showed that GBE could increase the expression of TET2 and 5-hydroxymethylcytosine (5hmC). In addition, GBE inhibited cell growth and invasion in SW480 cells. Moreover, to confirm whether TET2 expression affected cell proliferation, apoptosis, migration, and invasion, was knocked down and a overexpressing vector was constructed in human CRC cells. The results showed that overexpression of TET2 induced cell proliferation and invasion. Bioinformatic analyses showed that is a target gene of microRNA-29a (miR-29a). Moreover, reduced expression of miR-29a and increased TET2 expression in CRC cells. GBE was also used to treat a tumor model in nude mice. Compared to the control group, tumor growth was inhibited, and there was increased expression of TET2 in the GBE-treatment group . In conclusion, these results indicated that GBE inhibited cell proliferation and invasion through TET2 protein expression regulated by miR-29a in the development of CRC.
GBE 具有抗肿瘤和抗氧化特性，可调节基因和蛋白质表达。十号染色体缺失的磷酸酶及张力蛋白同源物（TET）蛋白具有调节表观遗传修饰的能力。然而，TET2 蛋白的异常表达也已被证实与癌症的发展有关。在本研究中，我们分析了 GBE 给药对人结直肠癌（CRC）中 TET2 表达的影响。癌症基因组图谱数据库表明，在 CRC 中 丢失。为了研究 TET2 的表达谱，我们用 GBE 处理 CRC 细胞。结果表明，GBE 可增加 TET2 和 5-羟甲基胞嘧啶（5hmC）的表达。此外，GBE 抑制 SW480 细胞的生长和侵袭。此外，为了证实 TET2 表达是否影响细胞增殖、凋亡、迁移和侵袭，我们敲低了 TET2，并在人 CRC 细胞中构建了一个过表达载体。结果表明，TET2 的过表达诱导了细胞增殖和侵袭。生物信息学分析表明 是 microRNA-29a（miR-29a）的靶基因。此外，CRC 细胞中 miR-29a 的表达降低和 TET2 表达增加。我们还用 GBE 处理裸鼠肿瘤模型。与对照组相比，GBE 治疗组肿瘤生长受到抑制，TET2 表达增加。综上所述，这些结果表明，GBE 通过 miR-29a 调控的 TET2 蛋白表达抑制 CRC 发展中的细胞增殖和侵袭。
