miR-206 inhibits the proliferation and invasion of estrogen-induced ER-α36-positive gastric cancer BGC-823 cells by targeting CDK14 / 中国肿瘤生物治疗杂志

@#[摘 要] 目的：探讨miR-206对雌激素诱导的ER-α36阳性胃癌（gastric cancer, GC）细胞BGC-823增殖和侵袭的影响及其相关机制。方法: 用不同浓度（1、10和100 pmol/L）的雌二醇（estradiol，E2）刺激ER-α36阳性BGC-823细胞后，用qPCR法检测miR-206表达水平，MTT法和Transwell实验分别检测细胞的增殖和侵袭能力，WB法检测细胞中CDK14的表达。将miR-206 mimic、miR-NC、pcDNA-CDK14、pcDNA-vector等转染ER-α36阳性BGC-823细胞，并给予100 pmol/L的E2处理后，用MTT法和Transwell小室法分别检测细胞的增殖和侵袭能力，WB法检测细胞中CDK14的表达。用双荧光素酶报告基因实验验证miR-206与CDK14之间的靶向关系。结果: E2能显著降低ER-α36阳性BGC-823细胞中miR-206表达水平（P<0.05或P<0.01）、增强细胞的增殖和侵袭能力（P<0.05或P<0.01）、上调细胞中CDK14的表达水平（P<0.01）。过表达miR-206能显著降低E2诱导的ER-α36阳性BGC-823细胞的增殖和侵袭能力（均P<0.01）。miR-206通过直接结合CDK14 mRNA的3'-UTR发挥抑制作用，从而负向调节CDK14的表达，进而抑制ER-α阳性BGC-823细胞的增殖和侵袭能力（均P<0.01）。结论: miR-206通过靶向CDK14从而抑制雌激素诱导的ER-α36阳性GC细胞的增殖和侵袭。

Effects of combination of dihydroartemisinin and Huobahua on expression of p-p38 MAPK and ICAM-1 in mice with delayed-type hypersensitivity / 中国中药杂志

The aim of this paper was to investigate the immunosuppressive effects of dihydroartemisinin and Huobahua compatibility in mice with delayed hypersensitivity and explore its possible mechanism. The delayed-type hypersensitivity(DTH) model in mice was established to observe the immunosuppressive effects of dihydroartemisinin and Huobahua compatibility in DTH mice. ELISA assay was used to detect the contents of interferon(IFN-γ); histopathological changes and degree of mononuclear infiltration of right ear tissues were examined by HE staining; the expression level of intercellular cell adhesion molecule-1(ICAM-1) in the right ear of mice was detected by immunohistochemistry; the protein expression levels of p38 phospho mitogen activated protein kinase(p-p38 MAPK) was detected by Western blot analysis. As compared with the control group, the degree of ear swelling, thymus/spleen index, serum IFN-γ as well as the number and degree of infiltration of monocytes were significantly increased in the model group. As compared with the model group, the degree of ear swelling and thymus/spleen index of the mice in the combination group were significantly reduced; the number and degree of infiltration of monocytes were significantly relieved; the serum levels of IFN-γ and the expression levels of p-p38 MAPK and ICAM-1 proteins in the right ear were also significantly reduced. The combination of dihydroartemisinin and Huobahua can significantly inhibit the DTH response, and it may regulate the production and secretion of related inflammatory factor IFN-γ by inhibiting the phosphorylation activity of p38 MAPK, thereby further reducing the expression of ICAM-1 and thus exerting the immunosuppressive effect.

X-linked Severe Combined Immunodeficiency Syndrome: The First Korean Case with gamma c Chain Gene Mutation and Subsequent Genetic Counseling

X-linked severe combined immunodeficiency (X-SCID) is a rare, life-threatening immune disorder, caused by mutations in the gamma c chain gene, which encodes an essential component of the cytokine receptors for interleukin-2 (IL-2), IL-4, IL-7, IL-9, IL-15, and IL-21. A 13-month-old boy with recurrent infections who had reduced serum immunoglobulin levels and decreased numbers of CD3, CD16/56 cells was evaluated for gamma c chain gene mutation and protein expression. The patient had a C-to-T point mutation at nucleotide position 690, one of the hot spots, resulting in a single amino acid substitution of cysteine for arginine (R226C), as determined by direct sequencing and PCR-RFLP. The patient's mother was a heterozygous carrier. Percutaneous umbilical cord blood sampling was performed at the 6-month of gestation in a subsequent pregnancy. As the immunophenotype of the fetus showed an identical pattern, the pregnancy was terminated and genetic analysis of the abortus confirmed recurrence. This is the first report of the molecular diagnosis of X-SCID in Korea. Genetic analysis of the gamma c chain gene is useful for definite diagnosis and genetic counseling for X-SCID.