Effects of genetic and environmental factors on variations of seed heteromorphism in Suaeda aralocaspica.

Seed heteromorphism is an adaptive strategy towards adversity in many halophytes. However, the underlying mechanisms and ecological significance of seed heteromorphism have not been deeply explored. Using Suaeda aralocaspica, a typical C4 annual halophyte without Kranz anatomy, we studied seed morphology, differentiation of morphs and fruit-setting patterns, and correlated these traits with germination responses, seed characteristics and heteromorphic seed ratio. To elucidate the genetic basis of seed heteromorphism, we analysed correlated patterns of gene expression for seed development-related genes as well. We observed that S. aralocaspica produced three types of seed morph: brown, large black and small black with differences in colour, size, mass and germination behaviour; the latter two were further distinguished by their origin in female or bisexual flowers, respectively. Further analysis revealed that seed heteromorphism was associated with genetic aspects including seed positioning, seed coat differentiation and seed developmental gene expression, while variations in seed heteromorphism may be associated with environmental conditions, e.g. annual precipitation, temperature, daylight and their monthly distribution in different calendar years. Seed heteromorphism and its variations in S. aralocaspica show multilevel regulation of the bet-hedging strategy that influences phenotypic plasticity, which is a consequence of internal genetic and external environmental factor interaction. Our findings contribute to the understanding of seed heteromorphism as a potential adaptive trait of desert plant species.

MiR-20a-5p suppressed TGF-ß1-triggered apoptosis of human bronchial epithelial BEAS-2B cells by targeting STAT3.

Apoptosis of bronchial epithelial cells contributes to lung diseases, including asthma. Although miR-20a-5p is reportedly downregulated in the bronchial epithelia of asthmatic patients, its function and mechanism still need to be explored. Here, we explored how miR-20a-5p affects human bronchial epithelial cells stimulated with transforming growth factor (TGF)-ß1. Using qRT-PCR, we observed downregulated miR-20a-5p levels in these cells. After transfecting miR-20a-5p mimics or inhibitors into human bronchial epithelium BEAS-2B cells, a Cell Counting Kit-8 assay and flow cytometry analysis showed that the mimics mitigated suppression of cell viability and acceleration of apoptosis that was triggered by TGF-ß1, whereas the inhibitors exerted the opposite effects. TGF-ß1 induced a decrease in expression of Bcl-2 and an increase in expression of Bax, both of which were inhibited by miR-20a-5p mimics and further enhanced by miR-20a-5p inhibitors. Further study verified that miR-20a-5p targeted the signal transducer and activator of transcription 3 (STAT3) and the STAT3 level was inversely related to the miR-20a-5p level. Furthermore, STAT3 overexpression partly counteracted the miR-20a-5p-induced anti-apoptotic effect in TGF-ß1-treated BEAS-2B cells. In summary, this study suggested that miR-20a-5p restrained apoptosis in TGF-ß1-stimulated BEAS-2B cells by targeting STAT3. MiR-20a-5p thus may be a novel therapeutic target for asthma treatment.

MiR-153 inhibits the resistance of lung cancer to gefitinib via modulating expression of ABCE1.

BACKGROUND: Gefitinib-resistance in lung cancers has become an intractable clinical problem. However, the mechanisms underlying this resistance are not fully understood. OBJECTIVE: Present study aims to investigate the roles and underlying mechanism of miR-153 in modulating gefitinib resistance in lung cancers. METHODS: In the present study, genes expression of miR-153, MDR-1 and ABCE1 were detected by qRT-PCR and western blot. The cell viability was examined by MTT assays. The regulation of miR-153 on ABCE1 was examined by luciferase reporter gene assays. The interaction of miR-153 and ABCE1 was detected by gene over-expression and siRNA interference technology. RESULTS: The mRNA level of miR-153 was significantly down-regulated in gefitinib-resistance (GR) tissues and HCC827 cells, while the protein level of ABCE1 was up-regulated in GR tissues and HCC827 cells. Besides, miR-153 over-expression evidently increased miR-153 level and suppressed cell viability and multi drug resistance gene (MDR-1) expression in HCC827/Gef cells, while silence of miR-153 caused adverse alterations in HCC827 cells. Luciferase reporter assay results showed that miR-153 directly targeted ABCE1. Further studies showed that ABCE1 over-expression improved the expression of ABCE1 and MDR-1 and increased cell viability in HCC827/Gef cells, while ABCE1 silencing resulted in contrary trends in HCC827 cells. What's more, miR-153 over-expression inhibited tumorigenesis and ABCE1 expression, while increased miR-153 level in tumor tissues. CONCLUSIONS: MiR-153 regulates gefitinib resistance by modulating expression of ABCE1 in lung cancers. Our findings may provide a worthwhile therapeutic target to reverse gefitinib resistance in lung cancers in the future.