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COL17A1 (collagen type XVII alpha 1 chain) is known to be upregulated and has a prognostic role in many malignancies, as well as contributing to cell proliferation, apoptosis, and invasion. However, little knowledge is available on the expression and prognostic value of COL17A1 in pancreatic adenocarcinoma (PDAC). In our study, we searched the public database and found that mRNA and protein levels of COL17A1 are commonly upregulated in PDAC tissues. The immunohistochemical analysis conducted by us revealed enhanced expression of COL17A1 protein in 169 PDAC samples compared with that in 67 adjacent normal tissues. We also observed a significantly positive correlation between COL17A1 expression and lymph node metastasis ( p < 0.0001), TNM clinical stage ( p < 0.0001), and pathology differentiation ( p < 0.01). The KM-plot results indicated that PDAC patients with a high COL17A1 expression have a poorer overall survival ( p < 0.001) than those with a low COL17A1 expression. The result of the Cox regression analysis of multivariate data suggested COL17A1 is an independent prognostic indicator of PDAC patients' overall survival. CCK-8, wound healing, and transwell assays suggested that COL17A1 knockdown markedly inhibited tumor proliferation and invasion in PDAC cells, and cells with COL17A1 overexpression had a prominently higher proliferative and invasive capacity. Knockdown of COL17A1 significantly upregulated the apoptosis rate. We deduce that upregulated COL17A1 activated the NF- κ B pathway in PDAC cells. In summary, our studies showed the prognostic value of COL17A1 in PDAC and that COL17A1 may act as a molecular therapeutic target for PDAC treatment., Competing Interests: The authors declare that they have no conflicts of interest., (Copyright © 2020 Feiyu Mao et al.)

When the skin barrier is damaged, surgical dressings are often used to cover wounds, sustain skin barrier, protect the injured area, prevent bacterial infection, and promote wound healing. However, at present, traditional dressings will be come stiffing as it absorbs the exudates of wound and sometimes cause secondary injury to the wound during the application process, which aggravate the pain of patients without analgesic effect. For this reason, the medical staff from Northern Jiangsu People's Hospital designed a new antibacterial analgesic dressing that can reduce the pain and increase the antibacterial ability. The dressings provide a sterile, moist environment to facilitate wound healing. Meanwhile, this dressing has the advantages of low cost, safeness and effectiveness, which can reduce the frequency of dressing changes, the possibility of wound infection, the pain and the medical expenses, which is worthy of clinical promotion.

The fluctuating CDK-CYCLIN complex plays a general role in cell-cycle control. Many types of stem cells use unique features of the cell cycle to facilitate asymmetric division. However, the manner in which these features are established remains poorly understood. The cell cycle of Drosophila female germline stem cells (GSCs) is characterized by short G 1 and very long G 2 phases, making it an excellent model for the study of cell cycle control in stem cell fate determination. Using a Drosophila female GSC model, we found Gcn5, the first discovered histone acetyltransferase, to maintain germline stem cells in Drosophila ovaries. Results showed that Gcn5 is dispensable for the transcriptional silencing of bam , but interacts with Cyclin A to facilitate proper turnover in GSCs. Results also showed that Gcn5 promotes Cyclin A ubiquitination, which is dependent on its acetylating activity. Finally, results showed that knockdown of Cyclin A rescued the GSC-loss phenotype caused by lack of Gcn5. Collectively, these findings support the conclusion that Gcn5 acts through acetylation to facilitate Cyclin A ubiquitination and proper turnover, thereby determining the fate of GSCs.-Liu, T., Wang, Q., Li, W., Mao, F., Yue, S., Liu, S., Liu, X., Xiao, S., Xia, L. Gcn5 determines the fate of Drosophila germline stem cells through degradation of Cyclin A., (© FASEB.)