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Our data suggest that the anti-apoptosis property of A549/Taxol cells originates from a defect in activation of the mitochondrial apoptotic pathway, and autophagy inhibitors can potentiate BZML-induced MC to overcome resistance to mitochondrial apoptosis.

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Hydrocracking of 1-methylnaphthalene to benzene (B), toluene (T), and xylene (X) was performed over a series of bi-functional catalysts (W/Beta) at 420 °C and 6 MPa. The reaction results and kinetic study indicated that metal–acid balance (metal–acid interaction and metal–acid ratio) and metal dispersion had a great impact on the cracking, hydrogenation, and selective hydrogenation activity, which directly determine the BTX yield. An inappropriate metal–acid ratio would lead to producing plenty of intermediates or by-products, and poor metal dispersion would result in low hydrogenation activity. However, good metal dispersion usually accompanies the strong metal–acid interaction, which reduces the sulfidation of metal. In this work, a new tungsten precursor, W-complex, was used to prepare the catalysts with good dispersion of metal oxides and high hydrogenation activity. The external surface acidity of zeolite was modified to regulate the metal–acid interaction by forming a layer of SiO2 on acid sites through chemical liquid deposition.

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Aberrant activation of TGF-β signaling plays a pivotal role in cancer metastasis and progression. However, molecular mechanisms underlying the dysregulation of TGF-β pathway remain to be understood. Here, we found that SMAD7, a direct downstream transcriptional target and also a key antagonist of TGF-β signaling, is transcriptionally suppressed in lung adenocarcinoma (LAD) due to DNA hypermethylation. We further identified that PHF14 binds DNMT3B and serves as a DNA CpG motif reader, recruiting DNMT3B to the SMAD7 gene locus, resulting in DNA methylation and transcriptional suppression of SMAD7. Our in vitro and in vivo experiments showed that PHF14 promotes metastasis through binding DNMT3B to suppress SMAD7 expression. Moreover, our data revealed that PHF14 expression correlates with lowered SMAD7 level and shorter survival of LAD patients, and importantly that SMAD7 methylation level of circulating tumor DNA (ctDNA) can potentially be used for prognosis prediction. Together, our present study illustrates a new epigenetic mechanism, mediated by PHF14 and DNMT3B, in the regulation of SMAD7 transcription and TGF-β-driven LAD metastasis, and suggests potential opportunities for LAD prognosis.