No abstract

Lung cancer is one of the leading causes of cancer-related death in the world. MicroRNA- (miR-) 628-3p plays critical roles in many cancers, including lung cancer. We investigated how miR-628-3p affected migration and apoptosis in A549 cells. We used bioinformatics algorithms to predict the miR-628-3p target gene to study the molecular mechanism by which miR-628-3p contributes to lung cancer. Then, we used the luciferase reporter assay to identify whether heat shock protein 90a (HSP90) is a direct target of miR-628-3p. Western blotting and quantitative real-time PCR showed that miR-628-3p downregulated HSP90a protein expression via a posttranscriptional mechanism. We confirm that miR-628-3p promotes apoptosis and inhibits migration in A549 cells by negatively regulating HSP90. Our results may reveal a novel strategy for lung cancer treatment.

Objective. To evaluate the therapeutic effect of epigallocatechin gallate (EGCG) on precancerous lesions of gastric carcinoma (PLGC) and to determine whether EGCG protects against PLGC by regulating PI3K/Akt/mTOR pathway. Methods. Twenty-four male Wistar rats were randomly divided into 3 groups: normal control group (NC), PLGC model group (MC), and group of PLGC rats treated with EGCG (MC + EGCG). 1-Methyl-3-nitro-1-nitrosoguanidine (MNNG) and sodium salicylate were combined and used to establish the PLGC rat animal model. The therapeutic effect of EGCG on PLGC was evaluated by body weight and pathological lesions of gastric mucosa in PLGC rats. Quantitative polymerase chain reaction (qPCR) was applied to measure the mRNA expressions of PI3K, Akt, and mTOR. The protein expressions of cleaved caspase-3, PTEN, PI3K, p-PI3K, Akt, p-Akt, p-mTOR, and mTOR were determined by automated western immunoblotting. Results. The body weight decreased in PLGC rats while EGCG significantly increased body weight. The gastric mucosa of PLGC rats exhibited the pathological lesions of atrophy, intestinal metaplasia, and atypical hyperplasia while EGCG could ameliorate the pathological lesions. EGCG could upregulate the expressions of cleaved caspase-3 and PTEN and reduce the expressions of PI3K, Akt, and mTOR. Conclusions. EGCG ameliorated pathological lesions of PLGC and exerted the effect of apoptosis promotion in PLGC rats. The apoptotic pathway triggered by EGCG may be related to inhibition of PI3K/Akt/mTOR pathway. It provided a theoretical basis for the PLGC treatment and gastric cancer prevention.

Bletilla striata (Thunb.), an ornamental and medicinal plant, is on the list of endangered plants in China. Its pseudobulb is abundant in polysaccharide and has been used for centuries as a herbal remedy. However, a recent rise in demand has placed it at risk of extinction, and therefore, research on its propagation and genetic improvement is essential. Since polyploids tend to possess advantageous qualities, we incubated B. striata seeds with colchicine with the aim of creating tetraploid plantlets. Aseptic seeds treated with 0.1% colchicine for 7 days showed the highest tetraploid induction rate of 40.67 ± 0.89%. Compared with the wild-type, the tetraploids could be identified by their morphological characteristics including larger stomata at a lower density, larger leaf blades, and a thicker petiole. Contents of polysaccharide and phenolic compounds were also determined in the tetraploid pseudobulbs, revealing significantly higher values than in the wild-type. In vitro colchicine treatment can therefore be used to successfully produce B. striata tetraploids with superior pseudobulbs.

Cytokine or growth factor activated STAT3 undergoes multiple post-translational modifications, dimerization and translocation into nuclei, where it binds to serum-inducible element (SIE, ‘TTC(N3)GAA’)-bearing promoters to activate transcription. The STAT3 DNA binding domain (DBD, 320–494) mutation in hyper immunoglobulin E syndrome (HIES), called the HIES mutation (R382Q, R382W or V463Δ), which elevates IgE synthesis, inhibits SIE binding activity and sensitizes genes such as TNF-α for expression. However, the mechanism by which the HIES mutation sensitizes STAT3 in gene induction remains elusive. Here, we report that STAT3 binds directly to the AGG-element with the consensus sequence ‘AGG(N3)AGG’. Surprisingly, the helical N-terminal region (1–355), rather than the canonical STAT3 DBD, is responsible for AGG-element binding. The HIES mutation markedly enhances STAT3 AGG-element binding and AGG-promoter activation activity. Thus, STAT3 is a dual specificity transcription factor that promotes gene expression not only via SIE- but also AGG-promoter activity.