Regularly Tuning Quantum Interference in Single-Molecule Junctions through Systematic Substitution of Side Groups with Varied Electron Effects

Investigating the quantum interference effect in single molecules is essential to comprehensively understand the underlying mechanism of single-molecule charge transport.In this study,we employed the mother molecule m-OPE and introduced a series of side groups with various electronic effects at the 2-position of the central phenyl ring,creating four daughter m-OPE derivatives.The single molecular conductivities of these molecule wires were measured using the scanning tunneling microscope breaking junction technique.Our findings demonstrate that the substitutions regularly modulate the destructive quantum interference occurring within the m-OPE molecules.By combining optical and electrochemical investigations,along with density functional theory computations,we discover that the conductivity of the molecules corresponds to the electron-donating/withdrawing ability of the substituents.Specifically,by adjusting the electron structures of the molecular backbone,we can systematically tailor the destructive quantum interference in the m-OPE molecules.

Expression and function of long non-coding RNA DLX6-AS1 in endometrial cancer

Background:LncRNA DLX6-AS1 has been uncovered to exert effects on various cancers.Nevertheless,the impacts of DLX6-AS1 on endometrial cancer(EC)development remained obscure.The study explored the influence of DLX6-AS1 on EC progression via the microRNA(miR)-374a-3p/zinc-finger protein(ZFX)axis.Methods:EC cell lines were collected and DLX6-AS1,miR-374a-3p,and ZFX levels in EC cell lines were detected.The EC cells were transfected with DLX6-AS1,miR-374a-3p,and ZFX constructs to examine the biological functions of EC cells.The xenograft model was established for detecting tumor growth.Rescue experiments were conducted to verify the interaction of DLX6-AS1,miR-374a-3p,and ZFX in EC cells.Results:DLX6-AS1 and ZFX levels were elevated,while miR-374a-3p exhibited a reduced level in EC cells.Silencing DLX6-AS1 and elevated miR-374a-3p expressions repressed the biological activities of EC cells.Reduced DLX6-AS1 repressed tumor development.MiR-374a-3p silencing reversed the impacts of DLX6-AS1 silencing,while ZFX overexpression abrogated the impacts of miR-374a-3p elevation on EC cell growth.Mechanically,DLX6-AS1 was found to bind to miR-374a-3p,and miR-374a-3p targeted ZFX.Conclusion:DLX6-AS1 depletion restricts the malignant phenotype of EC cells.The study might provide novel therapeutic biomarkers for EC treatment.