Triple-negative breast cancer (TNBC), defined by a lack of expression of estrogen receptor (ER), progesterone receptor (PR) expression, and human epidermal growth factor receptor 2 (HER2), is the most aggressive subtype among breast cancers 2, 3. Conclusively, our findings provided novel insights into the anti-oncogenic mechanism of MCPIP1, suggesting that MCPIP1 could serve as an alternative treatment target in TNBC.īreast cancer is the most common malignancy and the fourth leading cause of cancer-related deaths among women in China, accounting for 19.9% of all cancer diagnosed and 9.9% of all cancer-associated deaths in females in 2020 1. Subsequently, we showed that CTF5 participated in MCPIP1-mediated antiproliferative effect by transcriptionally repressing cyclin D1 expression, as well as downregulating its downstream signaling targets p-Rb and E2F1. Furthermore, we demonstrated that MCPIP1 modulated NFIC AS to promote CTF5 synthesis, which acted as a negative regulator in TNBC cells. Mechanistically, MCPIP1 was first demonstrated to act as a splicing factor to regulate AS in TNBC cells. We demonstrated that MCPIP1 overexpression dramatically suppressed cell cycle progression and proliferation of TNBC cells in vitro and repressed tumor growth in vivo. Here, we showed that MCPIP1 was downregulated in 80 TNBC tissues and five TNBC cell lines compared to adjacent paracancerous tissues and one human immortalized breast epithelial cell line, while its high expression levels were associated with increased overall survival in TNBC patients. Monocyte chemotactic protein induced protein 1 (MCPIP1), a zinc finger RBP, functions as a tumor suppressor in many cancers. AS is generally controlled by AS-associated RNA binding proteins (RBPs). Recently, emerging evidence suggested that aberrant alternative splicing (AS) plays a crucial role in tumorigenesis and progression. Simple and fuss-free solution to recovering content from your iPod to your Mac or PC.Triple-negative breast cancer (TNBC) is the most aggressive subtype with the worst prognosis and the highest metastatic and recurrence potential, which represents 15–20% of all breast cancers in Chinese females, and the 5-year overall survival rate is about 80% in Chinese women. The trial version will allow you to copy 50 tracks off your iPod, iPhone or iPad before you'll be forced to register to continue using it. Alternatively, you can copy selected items to iTunes or a pre-selected folder – perfect if the bulk of your library is present, but you're missing a handful of items.Īnd that's it: it really is that simple. The simplest way to restore anything to your computer is to select your chosen category, then click the Transfer button and choose the Sync option. Mac users get the best deal here - version 2 now supports videos, podcasts, ringtones, books and photos too PC users must make do with audio and video content. Once done, it's just a case of plugging in your iPod – after a short pause a list of all your music will be displayed, with options to view other content too. Download and launch the program without plugging in your iPod – the first thing it'll do is check to see if auto-sync is enabled in iTunes if it is, you'll be warned about switching it off before you go any further. iRip aims – like most Little App Factory products – to make this process as simple as possible. This is a problem third-party vendors have fallen over themselves to provide a solution for. First, iTunes is automatically set to synchronise your iPod with your computer's contents, which means if you fire it up expecting to transfer your iPod's content back you'll not only be disappointed, you may even end up wiping the content from your iPod! Getting music from your computer to your iPod, iPhone and iPad is easy thanks to iTunes, but the reverse isn’t always true: if you want to transfer your media collection back from your iPod to a new computer or your existing computer as part of a data recovery exercise, it’s less straightforward.
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