BackgroundEpithelial-mesenchymal transition (EMT) is an early event in tumour invasion and metastasis, and widespread and distant metastasis at early stages is the typical biological behaviour in small cell lung cancer (SCLC). Our previous reports showed that high expression of the transcription factor E2F1 was involved in the invasion and metastasis of SCLC, but the role of E2F1 in the process of EMT in SCLC is unknown.MethodsImmunohistochemistry was performed to evaluate the expressions of EMT related markers. Immunofluorescence was used to detect the expressions of cytoskeletal proteins and EMT related markers when E2F1 was silenced in SCLC cell lines. Adenovirus containing shRNA against E2F1 was used to knock down the E2F1 expression, and the dual luciferase reporter system was employed to clarify the regulatory relationship between E2F1 and ZEB2.ResultsIn this study, we observed the remodelling of cytoskeletal proteins when E2F1 was silenced in SCLC cell lines, indicating that E2F1 was involved in the EMT in SCLC. Depletion of E2F1 promoted the expression of epithelial markers (CDH1 and CTNNB1) and inhibited the expression of mesenchymal markers (VIM and CDH2) in SCLC cell lines, verifying that E2F1 promotes EMT occurrence. Next, the mechanism by which E2F1 promoted EMT was explored. Among the CDH1 related inhibitory transcriptional regulators ZEB1, ZEB2, SNAI1 and SNAI2, the expression of ZEB2 was the highest in SCLC tissue samples and was highly consistent with E2F1 expression. ChIP-seq data and dual luciferase reporter system analysis confirmed that E2F1 could regulate ZEB2 gene expression.ConclusionOur data supports that E2F1 promotes EMT by regulating ZEB2 gene expression in SCLC.Electronic supplementary materialThe online version of this article (10.1186/s12885-017-3701-y) contains supplementary material, which is available to authorized users.

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A soluble (E)-poly(p-phenylenephosphaalkene) having sterically encumbering ligands has been prepared by a phospha-Wittig reaction. This material exhibits a bathochromic shift with respect to E-PPV and with respect to representative model oligomers. We also report the first fluorescence study of a poly(p-phenylenephosphaalkene) and find that this material exhibits fluorescence, though with modest intensity relative to similarly sized carbon-based analogues.

Hematite nanoparticles have been functionalized with a self-assembled monolayer of undecanoic acid (UA) by covalent attachment via siloxane groups. The number density of carboxylic/carboxylate groups on the surface was determined by titration, yielding values on the order of 10(14) UA molecules/cm(2) and thus consistent with a closed-packed monolayer. The ability of these functionalized particles to adsorb Cd(2+) in the ppm range was demonstrated using in situ anodic stripping voltammetry.

An expedient tandem deprotonation-trapping protocol was employed to prepare a tris(difluoroboronyl) complex of a triferrocenyl ligand that is geometrically analogous to substituted triphenylenes. A triple Schiff base condensation reaction between 1,3,5-triformylphloroglucinol and aminoferrocene afforded the tris(N-salicylideneamine) adducts 5a + 5b in ca. 1:1 ratio. The keto-enamine tautomeric core of this isomeric mixture could be converted to a common enolate-imine intermediate. Subsequent trapping with BF3.Et2O cleanly afforded the tris(difluoroboronyl) adduct 6 in essentially quantitative yield. The electronic and structural properties of this new class of ferrocene compounds were investigated using various methods including UV-vis, cyclic voltammetry (CV), differential pulse voltammetry (DPV), and X-ray crystallography. In CH2Cl2-CH3CN, 6 displayed a reversible three-electron oxidation process at E1/2ox = +210 mV (vs Fc/Fc+). Despite the sharing of a common [pi,pi]/[n,pi]-conjugated core, no significant electronic communication was observed among the three ferrocenyl units in 6 under either CV or DPV conditions. On the other hand, the broad oxidation wave of 5a + 5b at E1/2ox = +60 mV in CH2Cl2-CH3CN was comprised of at least two major components at +20 and +90 mV, which collapsed to become a single peak in DMF electrolyte, despite that the ratios between the two isomers 5a,b remained essentially invariant to the change in solvent.

Our previous study reported that ADAM12 was highly expressed in small cell lung cancer (SCLC) and could be an effective marker for diagnosis and prognosis. Yet, the reason for the high expression of ADAM12 in SCLC requires further elucidation. Transcription factor E2F1 has been receiving increasing attention due to the complexity and diversity of its function in cancer. In the present study, the expression of ADAM12 was significantly decreased following silencing of E2F1 expression by siRNA, thus indicating that E2F1 may regulate the expression of ADAM12 at the level of transcription. Chromatin immunoprecipitation-to-sequence analysis identified three binding sites for E2F1 in the locus for ADAM12. They were Chr10: 128010444-128011026, located in the intron of ADAM12, named seq0; Chr10: 128076927‑128078127, located in the promoter of ADAM12, named seq1; and Chr10: 128086195‑128086876, located in the upstream 20 kb from the transcription start site of ADAM12, named: seq2. Dual‑luciferase reporter experiments revealed that seq1 not seq0 and seq2 was able to promote the expression of luciferase. Notably, co-transfection of E2F1 significantly increased the activity of seq1 not seq0 and seq2, but quantitative polymerase chain reaction results showed that seq0, seq1 and seq2 could recruit E2F1, indicating that the influence of E2F1 in regulating the expression of ADAM12 was complex. Sequence analysis clarified that seq1 was a part of the ADAM12 promoter, yet the functions of seq0 and seq2 were unknown. Fusion fragments containing seq0-seq1 or seq2-seq1 were analyzed in luciferase constructs. Compared with seq1 alone, the activities of these fusion fragments were non-significantly reduced. The activities of fusion fragments were significantly decreased following co-transfection with E2F1. Thus, the present findings support the conclusion that the E2F1 transcription factor regulates the expression of ADAM12 by binding differential cis-acting elements.

The reaction of phosphanylidene-[sigma](4)-phosphoranes ArP=PMe(3)(Ar = 2,6-Mes(2)C(6)H(3) or 2,4,6-t-Bu(3)C(6)H(2)) with select ortho-quinones yields 1,3,2-dioxophospholanes, one of which shows interesting [small pi]-stacking of the aromatic groups in the solid state.

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