Taurine (Tau), the most abundant free amino acid in humans has numerous potential health benefits through its antioxidant and anti‑inflammatory properties. However, limited studies have assessed its effect on tumors and the antitumor mechanism remains unknown. The present study investigated the cellular and molecular changes induced by Tau, leading to the induction of apoptosis in human breast cancer cell lines MCF‑7 and MDA‑MB‑231. MCF‑7 is p53 proficient (p53+/+) and MDA‑MB‑231 is a p53 null mutant (p53-/-). Cell proliferation and viability were assessed by MTT. Flow cytometry and hoechst33342 fluorescent staining were employed to detect apoptosis. Spectrophotometry was used to detect caspase‑3 activity. Reverse transcription‑polymerase chain reaction and western blot analysis were used to detect the levels of mRNA and proteins of p53‑upregulated modulator of apoptosis (PUMA), Bax and Bcl‑2. Finally, the affect of Tau on the growth of MDA‑MB‑231‑cell‑nude mice xenografts was examined. In the study, Tau inhibited growth and induced apoptosis of the two cell lines in a concentration‑ and time‑dependent manner. Notably, the inhibitory effect of Tau on p53-/- cancer cells was clearly significant compared to the p53+/+ cancer cells. Further studies showed that Tau promoted apoptosis in human breast cancer cells and inhibited the growth of tumor in nude mice by inducing the expression of PUMA, which further up‑ and downregulated the expression of Bax and Bcl‑2 protein, giving rise to increased activation of caspase‑3. Collectively, these results indicate that Tau is a potent candidate for the chemotherapy of breast cancer through increasing the PUMA expression independent of p53 status.
Two-dimensional molecular crystals (2DMCs) open a new door for the controllable growth of 2D materials by molecular design with a energy gap and solution processability. However, the growth of 2DMCs with defined molecular layers remains full of challenges. Herein, we report a novel method to produce various 2DMCs with a defined number of molecular layers. When the surface tension and viscosity are tuned to control the spreading of the solution on the liquid surface, large-area quasi-freestanding 2DMCs from bulk size down to the monolayer limit are obtained, which makes it possible to probe the intrinsic layer-dependent optoelectronic properties of organic semiconductors down to the physical limit, and paves the way for the application of 2DMCs in new optoelectronic devices and technologies.
Abstract Organic single crystals with low defect density are key functional materials for next‐generation electronics. Classical crystallization commonly results in a high density of molecular steps, which are defects that can trap charge carriers and reduce the mobility of organic semiconductors. Herein, a novel nonclassical crystallization mechanism involving nucleation, fusion, and growth is designed. The introduction of the fusion stage changes the crystal growth mode from three‐dimensional island growth to two‐dimensional layer‐by‐layer growth and leads to large‐area two‐dimensional molecular crystals with almost no molecular steps. Therefore, the average mobility is observed to improve from 1.26 to 2.07 cm 2 V −1 s −1 . The nonclassical crystallization mechanism paves the way for atomically flat single crystals to probe the intrinsic optoelectronic properties of organic semiconductors.
A uniform and smooth Dif-TES-ADT film with thickness of ∼4.62 nm is achieved within 50 s in 2-inch size through the use of a mixed solvent system. The ultrathin Dif-TES-ADT film-based transistors exhibit a maximum mobility up to 5.54 cm2 V−1 s−1.
The aim of this study was to observe the impact of the mammalian sterile 20-like kinase 1-c-Jun N-terminal kinase (MST1-JNK) signaling pathway on apoptosis in colorectal cancer (CRC) cells induced by Taurine (Tau). Caco-2 and SW620 cells transfected with p-enhanced green fluorescent protein (EGFP)-MST1 or short interfering RNA (siRNA)-MST1 were treated with Tau for 48 h. Apoptosis was detected by flow cytometry, and the levels of MST1 and JNK were detected by western blotting. Compared with the control group, 80 mM Tau could significantly induce apoptosis of CRC cells, and the apoptotic rate increased with increasing Tau concentration (P < 0.01). Meanwhile, the protein levels of MST1 and phosphorylated (p)-JNK in Caco-2 cells increased significantly (P < 0.01). The apoptotic rate of the p-EGFP-MST1 plasmid-transfected cancer cells was significantly higher than that of the control group (P < 0.05); however, the apoptotic rate of the p-EGFP-MST1+Tau group was increased further (P < 0.01). Silencing the MST1 gene could decrease the apoptotic rate of cancer cells, and Tau treatment could reverse this decrease. Blocking the JNK signaling pathway significantly reduced the Tau-induced apoptotic rate of CRC cells. Thus, the MST1-JNK pathway plays an important role in Tau-induced apoptosis of CRC cells.
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