Chemoresistance is an inevitable occurrence in lung adenocarcinoma, which has been associated with decreased expression of the phosphatase and tensin homolog deleted on chromosome ten (PTEN). Therefore, it is important to identify novel molecular mechanisms to suppress chemoresistance in lung adenocarcinoma cells. Paclitaxel- and cisplatin-resistant A549 lung carcinoma cell derivatives were developed by long-term serial culture. The metastatic properties of the cells were assessed using wound-healing assays, migration assays, invasion assays, morphological examination, and western blot analysis/RT-PCR of genes associated with the epithelial-mesenchymal transition (EMT). To identify novel regulators of EMT in A549 cells, differentially expressed miRNAs in drug-resistant cells were identified by microarray analysis. The role of miR-181a was established by transfection with specific mimic and inhibitor followed by functional assays. Luciferase assays were performed to assess the ability of miR-181a to target the PTEN promoter, and regulation of PTEN expression by miR-181a was assessed by western blot analysis and RT-PCR. Paclitaxel- and cisplatin-resistant A549 cells acquired metastatic properties and EMT phenotype and had reduced PTEN expression as compared to sensitive cells. miR‑181a was identified as a differentially expressed miRNA in drug-resistant A549 cells, and miR-181a mimic and inhibitor were shown to affect migration, invasion, morphology and expression of EMT-associated genes. PTEN was identified as a direct target of miR-181a. Our findings demonstrate that miR-181a expression in lung adenocarcinoma is associated with EMT progression, potentially through targeting of PTEN. Regulation of miR-181a may provide a novel strategy for overcoming resistance to paclitaxel and cisplatin in lung adenocarcinoma.

A facile and clean strategy for synthesizing unimodal polymethacrylates with narrow dispersity (Đ < 1.10) is successfully developed by a near‐infrared (NIR) light‐emitting diode (LED) light (λmax = 740 nm)‐controlled in situ bromine–iodine transformation reversible‐deactivation radical polymerization system without the use of NIR dyes and expensive catalysts. In this system, alkyl iodide ethyl α‐iodophenylacetate (EIPA) initiator is generated in situ by the nucleophilic substitution reaction between an alkyl bromide compound ethyl α‐bromophenylacetate and sodium iodide (NaI). At the same time, excessive NaI is also acted as a highly active catalyst by forming halogen bonds with terminal iodine of the polymer chains in this system to make it capable of precisely synthesizing polymethacrylates with narrow dispersities (Đ = 1.03–1.10). In addition, the strong penetration ability of NIR LED light is illustrated by the successful polymerization even through 11 pieces of A4 paper.

Flexible metal electrodes are essential for flexible electronics, where the main challenge is to obtain mask-free patterned metals directly on substrates such as poly­(dimethylsiloxane) (PDMS) at low cost. This work highlights a feasible strategy named femtosecond laser-activated metal deposition for electroless deposition of metals (Cu, Ni, Ag, and Au) on PDMS, which is suitable for maskless and low-cost fabrication of metal layers on PDMS and even on other materials of different natures including polyethylene terephthalate, paper, Si, and glass. The electrical conductivity of the PDMS/Cu electrode is comparable to that of bulk Cu. Moreover, robust bonding at the PDMS/Cu interface is evidenced by a scotch tape test and bending test of more than 20,000 cycles. Compared with previous studies using a nanosecond laser, the restriction on absorbing sensitizers could be alleviated, and catalysts could originate from precursors without polymer substrates under a femtosecond laser, which may be attributed to nonlinear absorption and ultrashort heating time with the femtosecond laser. Implementing a human–machine interface task is demonstrated by recognizing hand gestures via a multichannel electrode array with high fidelity to control a robot hand.

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Tanshinone IIA is a lipophilic diterpene extracted from the Salvia miltiorrhiza bunge, possessing antiapoptotic and antioxidant activities. The purpose of this study was to explore the effects of Tanshinone IIA on age‐related nuclear cataract. Human lens epithelial cell line SRA01/04 was subjected to H 2O 2 to mimic a cell model of cataract. Cell Counting Kit‐8 assay, flow cytometer, and reactive oxygen species (ROS) detection were performed to evaluate the effect of Tanshinone IIA pretreatment on SRA01/04 cells injured by H 2O 2. Besides, the real‐time quantitative polymerase chain reaction was used to assess the expression of long noncoding RNA (lncRNA) antisense noncoding RNA in the INK4 locus (ANRIL). Western blot analysis was performed to detect the expression of core proteins involved in cell survival and nuclear factor‐κB (NF‐κB) pathway. H 2O 2 significantly decreased SRA01/04 cells viability, whereas increased apoptosis and ROS generation. This phenomenon was coupled with the upregulated p53, p21, Bax, cleaved caspase‐3, and the downregulated cyclinD1, CDK4, and Bcl‐2. Tanshinone IIA pretreatment protected SRA01/04 cells against H 2O 2‐induced injury. In the meantime, the expression of lncRNA ANRIL was upregulated by Tanshinone IIA. And, the protective effects of Tanshinone IIA on H 2O 2‐stimulated SRA01/04 cells were abolished when lncRNA ANRIL was silenced. Moreover, the elevated expression of lncRNA ANRIL induced by Tanshinone IIA was abolished by BAY 11‐7082 (an inhibitor of NF‐κB). To conclude, Tanshinone IIA protects SRA01/04 cells from apoptosis triggered by H 2O 2. Tanshinone IIA confers its protective effects possibly via modulation of NF‐κB signaling and thereby elevating the expression of lncRNA ANRIL.

The ideal particle size and high stability of unimolecular micelles (UIM) formed from star copolymers make them less susceptible to microenvironment changes in vivo, giving them unique advantages in many...

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