MED30调节胃癌细胞的增殖和运动能力。
MED30 Regulates the Proliferation and Motility of Gastric Cancer Cells.
作者信息
Lee Yong Joo, Han Myoung-Eun, Baek Su-Jin, Kim Seon-Young, Oh Sae-Ock
机构信息
Department of Anatomy, School of Medicine, Pusan National University, Busan, Republic of Korea.
Department of Anatomy, School of Medicine, Pusan National University, Busan, Republic of Korea; Medical Research Center for Ischemic Tissue Regeneration, Pusan National University, Busan, Republic of Korea.
出版信息
PLoS One. 2015 Jun 25;10(6):e0130826. doi: 10.1371/journal.pone.0130826. eCollection 2015.
MED30 is an essential member of the mediator complex that forms a hub between transcriptional activators and RNA polymerase II. However, the expressions and roles of MED30 have been poorly characterized in cancer. In this study, we examined the functional roles of MED30 during gastric cancer progression. It was found that MED30 was overexpressed in gastric cancer tissues and cell lines. Moreover, MED30 overexpression increased the proliferation, migration, and invasion of gastric cancer cells, whereas MED30 knockdown inhibited these effects. Furthermore the knockdown significantly inhibited tumorigenicity in SCID mice. MED30 also promoted the expressions of genes related to epithelial-mesenchymal transition and induced a fibroblast-like morphology. This study shows MED30 has pathophysiological roles in the proliferation, migration, and invasion of gastric cancer cells and suggests that MED30 should be viewed as a potent therapeutic target for malignant gastric carcinoma.
MED30是中介体复合物的一个重要成员，该复合物在转录激活因子和RNA聚合酶II之间形成一个枢纽。然而，MED30在癌症中的表达和作用尚未得到充分表征。在本研究中，我们研究了MED30在胃癌进展过程中的功能作用。结果发现，MED30在胃癌组织和细胞系中过表达。此外，MED30过表达增加了胃癌细胞的增殖、迁移和侵袭，而MED30基因敲低则抑制了这些作用。此外，基因敲低显著抑制了SCID小鼠的致瘤性。MED30还促进了与上皮-间质转化相关的基因表达，并诱导了成纤维细胞样形态。本研究表明，MED30在胃癌细胞的增殖、迁移和侵袭中具有病理生理作用，并提示MED30应被视为恶性胃癌的一个有效治疗靶点。
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