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Membrane-type 1 matrix metalloproteinase (MT1-MMP) is a multifunctional protease implicated in cancer aggressiveness for its ability to promote proliferation, migration, and invasion, particularly at low expression levels. Due to its multidomain structure and cell signalling abilities, MT1-MMP may act as a key regulatory node enhancing ATP production, which may confer further advantages in cell proliferation and motility. Low levels of MT1-MMP that enhance cell growth/movement were examined with respect to cell metabolism. Cells expressing different levels or forms of MT1-MMP were cultured in media containing different metabolites to assess viability, proliferation, and metabolic gene transcript levels. While cells with a cytoplasmic domain deletion in MT1-MMP demonstrated more transcript level changes than cells that differed in MT1-MMP levels, there were no metabolically relevant differences in metabolic gene transcript levels, suggesting MT1-MMP does not modulate key metabolic pathways to confer proliferative advantages.

Effective Research Data Management (RDM) is a key component of research integrity and reproducible research, and its importance is increasingly emphasised by funding bodies, governments, and research institutions around the world. However, many researchers are unfamiliar with RDM best practices, and research support staff are faced with the diffi cult task of delivering support to researchers across diff erent disciplines and career stages. What strategies can institutions use to solve these problems? Engaging Researchers with Data Management is an invaluable collection of 24 case studies, drawn from institutions across the globe, that demonstrate clearly and practically how to engage the research community with RDM. These case studies together illustrate the variety of innovative strategies research institutions have developed to engage with their researchers about managing research data. Each study is presented concisely and clearly, highlighting the essential ingredients that led to its success and challenges encountered along the way. By interviewing key staff about their experiences and the organisational context, the authors of this book have created an essential resource for organisations looking to increase engagement with their research communities. This handbook is a collaboration by research institutions, for research institutions. It aims not only to inspire and engage, but also to help drive cultural change towards betier data management. It has been writien for anyone interested in RDM, or simply, good research practice.

We are all familiar with what a data management lifecycle looks like: you start with the idea or the concept for your research journey, then move on to collecting a dataset and analysing it, then cleaning and tidying it up to prepare it for sharing, before finally preserving or archiving it for perpetuity. That is the ideal Research Data Management (RDM) scenario, but most of the time the final archiving step never happens. Instead, data remains with the original researchers and moves around ...

Figure S4. Flow cytometric analysis of PDX tumor shows obASCs promote EMT and increase classically activated macrophages and alternatively activated macrophages. (A) Representative images of metastases are shown all and were acquired at the same magnification (scale bar = 100 μm). Image of lung section with annotation metastases are shown. Black arrows point to annotations on lung sections. (B) PDX tumors were digested using 0.01% collagenase to a single-cell suspension, and cells were analyzed using flow cytometry. Tumors had no significant change in cancer stem cell enrichment marker CD44+CD24−, but tumors from the obASC group showed decreased expression of CD326 (epithelial cell adhesion molecule). Analysis of myeloid cells in circulation revealed that obASCs increase the circulating myeloid cells (CD11b+). obASCs significantly increase classically activated macrophages (CD11b+CD86+) and alternatively activated macrophages (CD11b+CD206+) cells. Mean values are represented (n = 5 mice/group) Bars, ± SEM. *p

Figure S5. shRNA knockdown of leptin in obASCs. (A) Representative images of metastases are shown and were acquired at identical magnification (scale bar = 100 μm). (B) Leptin expression in control shRNA obASCs versus leptin shRNA obASCs was compared to evaluate knockdown efficiency. Leptin knockdown was confirmed via Western blot. Values reported are the mean of three independent experiments each performed in triplicate. Bars, ± SEM. *p

Figure S2. TNBC xenograft growth is unaffected by ASCs. (A) Histologic analysis of tumors at end point revealed that stem cells had no effect on proliferation (ki67+ cells) or angiogenesis (CD31+ blood vessels). All images in panel were acquired at the same magnification. Scale bar represents 100 μm. (B) Representative images of metastases are shown. Image of lung section with annotation metastases are shown. Black arrows point to annotations on lung sections. All images in this panel were acquired at the same magnification. Scale bar represents 100 μm. Values reported are the mean (n = 5 mice per group). Bars, ± SEM. *p

Figure S3. Patient-derived xenograft. (A) Primary human TNBC was surgically removed and implanted with Matrigel into SCID/Beige female mice (n = 5 per group). SCID/Beige mice lack B cells, T cells, and functional natural killer cells. At passage seven, tumors pieces were implanted with lnASCs, obASCs, or PDX alone. (B) Analysis of immunostaining of tumors at end point revealed that ASCs had no effect on proliferation (ki67+ cells) or angiogenesis (CD31+ blood vessels). All images in panel acquired at the same magnification. Scale bar represents 200 μm. (C) Histologic analysis CD44+ is shown. Scale bar in upper row represents 60 μm and 20 μm in the lower panel. (D) Histologic analysis CD44+, CD36+, and CPT1 is shown. All images were acquired at the same magnification. Scale bar represents 10 μm. Values reported are the mean (n = 5 mice/group). Bars, ± SEM. *p

Figure S6. shRNA knockdown of leptin in obASCs decreases pro-metastatic gene expression in breast cancer cells. RT-qPCR of breast cancer cells after 3 days of transwell co-culture with control shRNA obASCs or leptin shRNA obASCs shows an increase in expression of CCL5, CD90, PTGS2, and IL-6 after co-culture with obASCs that is abrogated by leptin shRNA in the obASCs. Values reported are the mean of three independent experiments each performed in triplicate. Bars, ± SEM. *p