Core–shell structured nanoparticles for near-infrared (NIR) photocatalysis were synthesized by a two-step wet-chemical route. The core is composed of upconversion luminescence NaYF4:Yb,Tm prepared by a solvothermal process, and the shell is anatase TiO2 nanocrystals around NaYF4 particles formed via a method similar to a Stöber process. Methylene blue compound as a model pollutant was used to investigate the photocatalytic activity of NaYF4:Yb,Tm@TiO2 composites under NIR irradiation. To understand the nature of NIR-responsive photocatalysis of NaYF4:Yb,Tm@TiO2, we investigated the energy transfer process between NaYF4:Yb,Tm and TiO2 and the origin of the degradation of organic pollutants under NIR radiation. Results indicate that the energy transfer route between NaYF4:Yb,Tm and TiO2 is an important factor that influences the photocatalytic activity significantly and that the degradation of organic pollutants under NIR irradiation is caused mostly by the oxidation of reactive oxygen species generated in the photocatalytic reaction, rather than by the thermal energy generated by NIR irradiation. The understanding of NIR-responsive photocatalytic mechanism helps to improve the structural design and functionality of this new type of catalytic material.

BackgroundMETTL3 is an RNA methyltransferase that mediates m6A modification and is implicated in mRNA biogenesis, decay, and translation. However, the biomechanism through which METTL3 regulates MALAT1-miR-1914-3p-YAP axis activity to induce NSCLC drug resistance and metastasis is not very clear.MethodsThe expression of mRNA was analyzed by qPCR assays. Protein levels were analyzed by western blotting and immunofluorescent staining. Cellular proliferation was detected by CCK8 assays. Cell migration and invasion were analyzed by wound healing and transwell assays, respectively. Promoter activities and gene transcription were analyzed by luciferase reporter assays. Finally, m6A modification was analyzed by MeRIP.ResultsMETTL3 increased the m6A modification of YAP. METTL3, YTHDF3, YTHDF1, and eIF3b directly promoted YAP translation through an interaction with the translation initiation machinery. Moreover, the RNA level of MALAT1 was increased due to a higher level of m6A modification mediated by METTL3. Meanwhile, the stability of MALAT1 was increased by METTL3/YTHDF3 complex. Additionally, MALAT1 functions as a competing endogenous RNA that sponges miR-1914-3p to promote the invasion and metastasis of NSCLC via YAP. Furthermore, the reduction of YAP m6A modification by METTL3 knockdown inhibits tumor growth and enhances sensitivity to DDP in vivo.ConclusionResults indicated that the m6A mRNA methylation initiated by METTL3 promotes YAP mRNA translation via recruiting YTHDF1/3 and eIF3b to the translation initiation complex and increases YAP mRNA stability through regulating the MALAT1-miR-1914-3p-YAP axis. The increased YAP expression and activity induce NSCLC drug resistance and metastasis.

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