Breast cancer is the most frequently diagnosed malignancy and the leading cause of cancer‐related deaths in women worldwide. Cancer‐associated fibroblasts (CAFs) are one of the fundamental cellular components of the tumor microenvironment and play a critical role in the initiation, progression, and therapy resistance of breast cancer. However, the detailed molecular mechanisms of CAFs activation from normal fibroblasts (NFs) are still not well understood. In the present study, we reported that ZNF32 expression in breast cancer cells was negatively correlated with CAF‐related markers (FSP1, α‐SMA, and FAP) in stromal fibroblasts, and loss of ZNF32 promoted the activation of CAFs, as evidenced by the enhanced proliferation and contractility of CAFs. ZNF32 deficiency‐mediated fibroblast activation promoted the growth and metastasis of breast cancer cells in vitro and in vivo. Mechanistically, we demonstrated that ZNF32 inhibited TGFB1 transcription by directly binding to the −1968/−1962 region of the TGFB1 promoter, leading to the prevention of fibroblast activation. Altogether, our findings reveal an important mechanism by which ZNF32 suppression increases the transcription of the TGFB1 gene in breast cancer cells, and subsequently, elevated levels of secretory TGF‐β stimulate NFs transformation into CAFs, which in turn facilitates the malignant progression of breast cancer. Our data implicated ZNF32 as a potential therapeutic strategy against breast cancer.

Background There is commonly a discrepancy between conference abstracts and published article abstracts in prosthodontic randomized controlled trials (RCTs), which may mislead the scholars those attend conferences. Objective To identify the characteristics predicting inconsistency between conference abstracts and published article abstracts in prosthodontic RCTs. Methods The conference abstracts of prosthodontic RCTs presented at the IADR general sessions from 2002 to 2015 were searched. Electronic searches of MEDLINE, EMBASE, the Cochrane Library, and Google Scholar databases were conducted to match full-text publications for conference abstracts. Two investigators extracted basic characteristics and assessed the consistency and reporting quality independently and in duplicate. The linear regression model was used to analyze the predictors of inconsistency. Results A total of 147 conference abstracts were matched with published articles. Results for the secondary outcome measure, Statistical analysis, and precision measure were less than 50% consistent, and even nearly 5% of the studies had opposite conclusions. Multiple linear regression analysis showed that three factors were correlated with lower inconsistency, including continent of origin (p = 0.011), presentation type (p = 0.017), and difference in reporting quality (p = 0.013). Conclusion Conference attendees should cautiously treat the findings of the conference abstracts. Researchers should improve the precision of the information delivered at conferences. We recommend the authors of RCTs to explain the primary difference between conference abstracts and article abstracts.

Tissue factor (TF) has been confirmed to be specifically expressed by vascular endothelial cells (VECs) in solid tumors and certain types of malignant tumor cells. Coagulation factor VII (FVII) can specifically bind to TF with high affinity, so the FVII-TF interaction provides an ideal target for tumor therapy. Expression of proteins in skeletal muscles is a simple and economical avenue for continuous production of therapeutic molecules. However, it is difficult to treat solid tumors till now due to the limited number of therapeutic proteins produced by the intramuscular gene expression system. Herein, we strived to explore whether anti-tumor effects can be achieved via intramuscular delivery of a plasmid encoding a FVII-guided immunoconjugate (Icon) molecule by a previously established Pluronic L64/electropulse (L/E) technique. Our study exhibited several interesting outcomes. 1) The mouse light chain of FVII (mLFVII) molecule could guide red fluorescent protein (RFP) to accumulate predominantly at tumor sites in a TF-dependent manner. 2) Intramuscular expression of mLFVII-hFc (human IgG1 Fc) Icon could significantly inhibit the growth of both liver and lung cancers in nude mice, and the inhibition extent was proportional to the level of tumor-expressed TF. 3) The number of blood vessels and the amount of blood flow in tumors were significantly decreased in mLFVII-hFc Icon-treated mice. 4) This immunotherapy system did not display obvious side effects. Our study provided an efficient and economical system for tumor immunotherapy by targeting both blood vessels and tumor cells. It is also an open system for synergistic therapy by conveniently integrating other anticancer regimens.