Department of Biotechnology, Institute of Science and High Technology and Environmental Sciences, Graduate University of Advanced Technology, Kerman, Iran.
J Cell Biochem. 2018 Aug;119(8):6470-6481. doi: 10.1002/jcb.26678. Epub 2018 May 8.
Long non-coding RNAs are known as key regulators in the progression and metastasis of breast cancer. MIAT originally has been considered as an lncRNA to be associated with a susceptibility to myocardial infarction. Here, we have detected the expression of MIAT in different cancer cells and a series of breast tumor tissue. MIAT expression was much higher in high-grade tumors compared to low-grade ones. Unlike P53 positive tumors, MIAT expression was upregulated in ER, PR, Her2 positive tumor tissues. Knockdown MIAT suppressed breast cancer cell proliferation and caused G1 arrest in cell cycle. Furthermore, downregulation of MIAT promoted apoptosis and significantly decreased migration of breast cancer cells. An increase in the expression of mir-302, mir-150, and a decrease in the expression of mir-29c were detected following MIAT silencing. More importantly, knockdown MIAT significantly elevated the expression of p16 and Cox2, which commitment cellular senescence in breast cancer cells. Altogether, our results suggest that MIAT involved in breast cancer progression and could be candidate as a novel tumor marker for diagnosis and treatment of breast cancer.
长非编码 RNA 被认为是乳腺癌发生和转移的关键调节因子。MIAT 最初被认为是一种与心肌梗死易感性相关的 lncRNA。在这里，我们检测了不同癌细胞和一系列乳腺癌组织中 MIAT 的表达。与低级别肿瘤相比，高级别肿瘤中 MIAT 的表达明显更高。与 P53 阳性肿瘤不同，MIAT 在 ER、PR、Her2 阳性肿瘤组织中上调表达。下调 MIAT 抑制乳腺癌细胞增殖，并导致细胞周期 G1 期停滞。此外，下调 MIAT 促进细胞凋亡，并显著减少乳腺癌细胞的迁移。沉默 MIAT 后，检测到 mir-302、mir-150 的表达增加，mir-29c 的表达降低。更重要的是，下调 MIAT 显著增加了 p16 和 Cox2 的表达，从而使乳腺癌细胞发生细胞衰老。总之，我们的研究结果表明，MIAT 参与了乳腺癌的进展，可能成为乳腺癌诊断和治疗的新型肿瘤标志物。
