NIR-Responsive Photocatalytic Activity and Mechanism of NaYF₄:Yb,Tm@TiO₂ Core–Shell Nanoparticles

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

Inhibition of TMEM16A Expression Suppresses Growth and Invasion in Human Colorectal Cancer Cells

<div><p>Metastasis leads to poor prognosis in colorectal cancer patients, and there is a growing need for new therapeutic targets. TMEM16A (ANO1, DOG1 or TAOS2) has recently been identified as a calcium-activated chloride channel (CaCC) and is reported to be overexpressed in several malignancies; however, its expression and function in colorectal cancer (CRC) remains unclear. In this study, we found expression of TMEM16A mRNA and protein in high-metastatic-potential SW620, HCT116 and LS174T cells, but not in primary HCT8 and SW480 cells, using RT-PCR, western blotting and immunofluorescence labeling. Patch-clamp recordings detected CaCC currents regulated by intracellular Ca²⁺ and voltage in SW620 cells. Knockdown of TMEM16A by short hairpin RNAs (shRNA) resulted in the suppression of growth, migration and invasion of SW620 cells as detected by MTT, wound-healing and transwell assays. Mechanistically, TMEM16A depletion was accompanied by the dysregulation of phospho-MEK, phospho-ERK1/2 and cyclin D1 expression. Flow cytometry analysis showed that SW620 cells were inhibited from the G1 to S phase of the cell cycle in the TMEM16A shRNA group compared with the control group. In conclusion, our results indicate that TMEM16A CaCC is involved in growth, migration and invasion of metastatic CRC cells and provide evidence for TMEM16A as a potential drug target for treating metastatic colorectal carcinoma.</p></div

Effect of T16Ainh-A01 on growth of SW480 and SW620 cells.

<p>Cells were treated with different concentrations of T16Ainh-A01 for 24 h and cell viability was measured by MTT assay. Data are expressed as Mean ± SD (n = 3).</p

Expression of TMEM16A in CRC cell lines, HCT8, SW480, SW620, HCT116 and LS174T cells.

<p>A, RT-PCR reveals TMEM16A mRNA expression in SW620, HCT116 and LS174T cells, but not in HCT8 and SW480 cells. B, TMEM16A protein expression in HCT8 and SW480, SW620, HCT116 and LS174T cells was detected by Western blotting. Null FRT cells acts as negative control. FRT cells transfected with human TMEM16A serve as positive control.</p

Scratch wound assay of TMEM16A shRNA on SW620 cells.

<p>A, Migration of SW620 cells was assessed by a wound-healing assay in the presence of TMEM16A shRNA #1 and shRNA #2, compared with control shRNA. Representative images of wound closure were taken at 0 h, 24 h, 48 h and 72 h after wounding under 100× magnification. B, Bar graphs of panel A are shown. Values are the means ± SD; n = 3; ** P<0.01. Ctrl, control.</p

TMEM16A knockdown induced a decrease in proliferation of SW620 cells.

<p>A, The growth of SW620 cells was inhibited by TMEM16A shRNA #1 and #2 compared to the control group (Mean ± SD; n = 3; * P<0.05). B, Representative immunoblots confirming knockdown of TMEM16A. Ctrl, control.</p

TMEM16A knockdown decreased activation of the MEK-ERK1/2 pathway and expression of cyclin D1.

<p>Western blot results show inhibition of TMEM16A led to a decrease in phospho-MEK, phospho-ERK1/2 and cyclin D1. Ctrl, control.</p

Flow cytometric analysis of the cell cycle distribution in SW620 cells.

<p>A, B and C, Flow cytometric analysis of the cell cycle distribution of SW620 cells transfected with control shRNA,TMEM16A shRNA #1 and #2 respectively for 72 h. D, Bar graphs showing the relative percentage of cells in the indicated phases of the cell cycle after knockdown of TMEM16A. Data are expressed as the mean ± SD; n = 3; * P<0.05.</p

Immunofluorescence labeling of TMEM16A in CRC cell lines.

<p>Cells were grown on coverslips and stained with anti-TMEM16A antibodies. Left column, anti-TMEM16A immunofluorescence (Cy3, red). Middle column, DAPI staining to visualize nuclei. Right column, merged images are composites of anti-TMEM16A immunofluorescence and DAPI staining (200×).</p

Inhibition of TMEM16A decreased SW620 cell migration and invasion.

<p>A, Migration (without Matrigel) and invasion (with Matrigel) of SW620 cells are significantly suppressed by knockdown of TMEM16A compared with the control group through transwell penetration assays. Non-migrated cells were scraped with a cotton swab. Cells that penetrated the transwell filters were stained with Coomassie blue. Representative images are shown. B and C, Bar graphs of panel A are shown. Values are the means ± SD; n = 3; ** P<0.01. Ctrl, control.</p