Abstract
Breast cancer, the most prevalent cancer type among women worldwide, remains incurable once metastatic. Long noncoding RNA (lncRNA) and microRNA (miRNA) play important roles in breast cancer by regulating specific genes or proteins. In this study, we found miR-133b was silenced in breast cancer cell lines and in breast cancer tissues, which predicted poor prognosis in breast cancer patients. We also confirmed that lncRNA NEAT1 was up-regulated in breast cancer and inhibited the expression of miR-133b, and identified the mitochondrial protein translocase of inner mitochondrial membrane 17 homolog A (TIMM17A) that serves as the target of miR-133b. Both miR-133b knockdown and TIMM17A overexpression in breast cancer cells promoted cell migration and invasion both in vitro and in vivo. In summary, our findings reveal that miR-133b plays a critical role in breast cancer cell metastasis by targeting TIMM17A. These findings may provide new insights into novel molecular therapeutic targets for breast cancer.
Highlights
Breast cancer is the most frequently diagnosed cancer causing woman death
Our study firstly revealed that the NEAT1/miR-133b/TIMM17A axis was involved in breast cancer metastasis and might provide a potential target for breast cancer therapy
We found miR-133b levels were down-regulated in all the 14 types of common cancer tissues compared to their normal counterparts (Figure 1A), and remarkably lower in 1085 breast cancer tissues compared to 104 normal breast tissues according to the TCGA database (Figure 1B)
Summary
Breast cancer is the most frequently diagnosed cancer causing woman death. Thanks to improved diagnostic tools and treatment, breast cancer-caused deaths have decreased since the early 1990s. High miR-133b expression levels were found to be associated with poor prognosis for progression-free survival with bladder cancer, whereas its low expression levels in tumor tissues were found to be related to poor prognosis for overall survival and positive lymph node metastasis in colorectal cancer [16], and promote cell apoptosis, repress cell proliferation, tumor angiogenesis, drug-resistant and radioresistant, cell migration and invasion in lung cancer [17]. Despite these studies, whether miR-133b is involved in the development of breast cancer remains largely elusive. Our study firstly revealed that the NEAT1/miR-133b/TIMM17A axis was involved in breast cancer metastasis and might provide a potential target for breast cancer therapy
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