Wnt/ß-catenin signaling in the development and therapeutic resistance of non-small cell lung cancer.

Wnt/ß-catenin signaling is a critical pathway that influences development and therapeutic response of non-small cell lung cancer (NSCLC). In recent years, many Wnt regulators, including proteins, miRNAs, lncRNAs, and circRNAs, have been found to promote or inhibit signaling by acting on Wnt proteins, receptors, signal transducers and transcriptional effectors. The identification of these regulators and their underlying molecular mechanisms provides important implications for how to target this pathway therapeutically. In this review, we summarize recent studies of Wnt regulators in the development and therapeutic response of NSCLC.

Computational study on mechanisms and kinetics of the atmospheric CFCl2CH2O2 with Cl reaction.

Ab initio BMC-CCSD//B3LYP calculations of the potential energy surfaces (PESs) are associated with the rate constants and branch ratio of products by means of RRKM theories to research the mechanism and product distribution of the CFCl2CH2O2 with Cl reaction. The singlet and triplet PESs of this reaction have been calculated. Addition/elimination and SN2 displacement mechanisms are located on the singlet PES, and SN2 displacement and H-abstraction are located on the triplet PES. P1 (CFCl2CHO + HClO) are expected to the primary products at T ≤ 2400 K, which is by original barrierless Cl addition to the terminal-O atom in CFCl2CH2O2 and then eliminate HClO molecule, and the branch ratio of products rely on collision energy. The H-abstraction products on the triplet PES are the dominant products at higher temperatures. At 298 and 500 K, the total rate constants are not subject to pressure, conversely, the total rate constants presented typical falloff behavior at 1000 and 3000 K. The atmospheric lifetime of CFCl2CH2O2 in Cl is around one day. TD-DFT computations imply that IM1 (CFCl2CH2OOCl) and IM2 (CFCl2CH2OClO) will photolyze under the sunlight.