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Infertility is an area of increasing in life science research. Although follicular maturation disorders and anovulation are the primary causations of infertility, its molecular mechanism is not well understood. Recent research has shown that microRNAs (miRNAs) might play an important role in the regulation of ovarian follicle development and maturation. In this study, the expression of miRNAs in metaphase I (MI) oocytes treated with or without insulin-like growth factor 1 (IGF-1) was observed by microRNA microarray analysis. Results show that 145 miRNAs were up-regulated and 200 miRNAs were down-regulated in MI oocytes after IGF-1 treatment. MiR-133b, which was up-regulated more than 30-fold, was chosen for further research. As a potential target of miR133b, transgelin 2 (TAGLN2) gene was down-regulated, at both transcription and translation levels, in miR-133b- over-expressed 293T cells, but TAGLN2 was up-regulated when the expression of miR-133b was inhibited. Furthermore, the expression level of TAGLN2 in the ovaries of 8-week- old mice was higher than that observed in 4-week-old mice. Immunofluorescence experiments showed that TAGLN2 was located in the cytoplasm. In general, our results indicate that miR-133b may play important roles in the growth and maturation of oocytes by regulating its potential target, TAGLN2, at both transcription and translation levels. Therefore, our research provides a potential new target for infertility therapy.

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In addition to the known function in the glycolytic pathway, phosphoglycerate kinase 1 (PGK‐1) promotes reduction of plasmin disulfide bonds leading to angiostatin formation and inhibition of tumor angiogenesis. In this study, the effects of PGK‐1 on anti‐ tumor immunity against lung cancer were evaluated using the Tet‐Off control of PGK‐1 expression in the Lewis lung carcinoma (LLC‐1). There was no significant difference in cell proliferation between parental LLC‐1 and LLC‐1 transduced with PGK‐1 (PGK‐LLC‐1). However, expression of PGK‐1 was found to limit tumor growth in mice subcutaneously injected with the cell lines and tumor growth was restored after doxycycline treatment. In addition, the cell invasion ability of PGK‐LLC‐1 became weaker than that of LLC‐1. Expressions of COX‐2, TGF‐β1 and PGE2 were all found to be down‐regulated in PGK‐LLC‐1. PGK‐LLC‐1 cells treated with doxycycline recovered their COX‐2 protein expression. In the presence of conditioned medium from PGK‐LLC‐1, the endothelial cell migration was reduced. Moreover, PGK‐LLC‐1 also stimulated T lymphocytes to express higher levels of Th1 cytokine (IFN‐γ) and lower levels of IL‐10 in comparison with parental LLC‐1. PGK‐LLC‐1 cells restored the growth rate in immunodeficient mice when compared with the growth rate in normal mice. In the tissue sections, reduced COX‐2 expressions and marked infiltrated CD3 T lymphocytes were observed in the PGK‐LLC‐1 injected group. These findings indicate that overexpression of PGK‐1 in LLC‐1 reduces the COX‐2 expression, and, in turn, affect PGE2, cell invasion, angiogenesis, and the immune functions, and finally inhibit the tumor progression. © 2008 Wiley‐Liss, Inc.