Objective To investigate the effects of leptin on proliferation of the breast carcinoma MCF-7 cells in terms of protein and nRNA of Rab-25 and C-myc.Methods MCF-7 cells were treated with leptin and normal saline (NS) as control.The 490 nm OD values of cells were read by MTT and the protein and mRNA expressions of Rab-25 and C-myc were measured by western blot and RT-PCR methods in two groups.Results Compared with control group,leptin can promote the proliferation of MCF-7 cells in a dose and time dependent manner within certain limit and up-regulate the protein expressions of Rab-25 and C-myc in the breast carcinoma MCF-7 cells (P ＜ 0.05).However,leptin also can up-regulate the mRNA expressions of Rab-25 but without significance (P =0.05).On the contrary,leptin can also up-regulate the mRNA expressions of C-myc (P ＜ 0.05).Conclusion Leptin promotes breast cancer cells proliferation,which may be related to up-regulate the protein and mRNA expressions of Rab-25 and C-myc.It could provide theoretical foundation and new target of gene therapy in the clinical treatment of breast cancer.

N6-methyladenosine(m6A)denotes the addition of a methyl group to the sixth nitrogen atom of ade-nosine,a common occurrence in eukaryotic RNA.The m6A modifications govern RNA splicing,translocation,stability,and translation into proteins.The RNA methyltransferases,like methyltransferase-like protein 3(METTL3),METTL14,and Wilms'tumor 1-associated protein(WTAP),are responsible for these modifications,while the removal process in-volves demethylases,specifically fat mass and obesity-associated protein(FTO)and ALKB homolog 5(ALKBH5).Recog-nition of these modifications is facilitated by m6A-binding proteins,such as YTH family proteins and insulin-like growth factor 2 mRNA-binding proteins(IGF2BPs).The m6A modification regulators are involved in the onset and progression of non-small-cell lung cancer through multiple mechanisms.This review concentrates on the biological functions and molecu-lar mechanisms of m6A modification-related regulatory factors in the malignant progression of non-small-cell lung cancer.

Bacitracin is a broad-spectrum cyclic peptide antibiotic, and mainly produced by Bacillus. Energy metabolism plays as a critical role in high-level production of target metabolites. In this study, Bacillus licheniformis DW2, an industrial strain for bacitracin production, was served as the original strain. First, our results confirmed that elimination of cytochrome bd oxidase branch via deleting gene cydB benefited bacitracin synthesis. Bacitracin titer and ATP content were increased by 10.97% and 22.96%, compared with those of original strain, respectively. Then, strengthening cytochrome aa3 oxidase branch via overexpressing gene qoxA was conducive to bacitracin production. Bacitracin titer and ATP content were increased by 18.97% and 34.00%, respectively. In addition, strengthening ADP synthesis supply is also proven as an effective strategy to promote intracellular ATP accumulation, overexpression of adenosine kinase DcK and adenylate kinase AdK could all improve bacitracin titers, among which, dck overexpression strain showed the better performance, and bacitracin titer was increased by 16.78%. Based on the above individual methods, a method of combining the deletion of gene cydB and overexpression of genes qoxA, dck were used to enhance ATP content of cells to 39.54 nmol/L, increased by 49.32% compared to original strain, and bacitracin titer produced by the final strain DW2-CQD (DW2ΔcydB::qoxA::dck) was 954.25 U/mL, increased by 21.66%. The bacitracin titer produced per cell was 2.11 U/CFU, increased by 11.05%. Collectively, this study demonstrates that improving ATP content was an efficient strategy to improve bacitracin production, and a promising strain B. licheniformis DW2-CQD was attained for industrial production of bacitracin.
Bacillus licheniformis ; metabolism ; Bacitracin ; biosynthesis ; Energy Metabolism ; genetics ; Industrial Microbiology ; methods