ABSTRACT
The toughening modification of epoxy resin has received widespread attention. The addition of the second-phase resin has a good toughening effect on epoxy resin. In order to investigate the effect of the second-phase resin on the interphase of composites, in this work the interfacial properties of carbon fiber (CF)/epoxy resin with the second-phase resin structure were investigated. Methodologies including surface structure observation, chemical characteristics, surface energy of the CF, and micro-phase structure characterization of resin were tested, followed by the micro-interfacial performance of CF/epoxy composites before and after hygrothermal treatment. The results revealed that the sizing process has the positive effect of increasing the interfacial bonding properties of CF/epoxy. From the interfacial shear strength (IFSS) test, the introduction of the second phase in the resin reduced the interfacial bonding performance between the CF and epoxy. After the hygrothermal treatment, water molecules diffused along the interfacial paths between the two resins, which in turn created defects and consequently brought about a reduction in the IFSS.
ABSTRACT
BACKGROUND: Long non-coding RNA (lncRNA) LINC01125 is an anti-tumor factor in a variety of tumors, and regulates cancer cell function. However, its function and mechanism of N6-methyladenosine (m6A) modification in papillary thyroid cancer (PTC) tumorigenesis remain unclear. AIMS: This study aimed to reveal the function and m6A modification of LINC01125 in PTC tumorigenesis. METHODS: The LINC01125 and methyltransferase-like 3 (METTL3) levels in PTC cells and tissues was assessed by qRT-PCR. The binding relationship among LINC01125 and METTL3 was determined by MeRIP, Pearson, bioinformatics, and RNA stabilization analysis. Transwell assays were performed to confirm the changes of PTC cell migration and invasion. Cell proliferation was revealed by CCK-8 as well as colony formation assays. RESULTS: Low expression of LINC01125 and METTL3 was identified in PTC. LINC01125 was a downstream target of METTL3-mediated m6A modification and was stably upregulated via METTL3. Cell invasion, migration, viability, and colony formation levels were decreased when LINC01125 or METTL3 was upregulated. Inhibition of LINC01125 had the opposite impact, promoting cell proliferation and metastasis, and reversing METTL3 overexpression-resulted cell malignancy suppression. CONCLUSIONS: Overall, this study proved that the m6A modification of LINC01125 was mediated by METTL3 and LINC01125 inhibited cell invasion, migration and proliferation, thereby suppressing the development of PTC. This points to the LINC01125-m6A-METTL3 axis as a possible prospective target for future treatment of PTC.
