Publications by authors named "Xiao-Xin Cheng"

Medulloblastoma (MB) cells exhibit different responses to retinoid acid (RA) for reasons that are poorly understood. RA signaling can be transduced by two approaches that are mediated by cellular retinoic acid-binding protein 2 (CRABP-II) as a tumor-suppressive pathway, and by fatty acid-binding protein 5 (FABP5) as a tumor-promoting pathway. The biological effects of RA on cancer cells are largely determined by the patterns of CRABP-II and FABP5 expression.

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Anaplastic thyroid cancer (ATC) is a highly lethal undifferentiated malignancy without reliable therapies. Retinoic acid (RA) has been employed to promote redifferentiation of thyroid cancers by increasing their I uptake and radio-sensitivity, but its effect(s) on ATCs has not yet been ascertained. Likewise, resveratrol induces cancer redifferentiation but, also in this case, its effects on ATCs remain unknown.

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The importance of signal transducer and activator of transcription 3 (STAT3) signaling in the growth and survival of glioblastoma cells has been well documented, while the reasons leading to STAT3 activation remains to be elucidated. Suppressors of cytokine signaling (SOCS) 1 and SOCS3, SH2 domain‑containing phosphatase (SHP2) and protein inhibitors of activated STAT3 (PIAS3) are known to inhibit STAT3 signal transduction, while their expression statuses in the four grades of astrocytomas and relevance with STAT3 activation remain to be described. The present study aimed to address these issues by tissue microarray‑based immunohistochemical profiling the expression levels of phosphorylated (p)‑STAT3, SOCS1, SOCS3, PIAS3 and p‑SHP2.

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Objectives: Although it is well accepted that there is a close relationship between hypothyroidism and depression, previous studies provided inconsistent or even opposite results in whether subclinical hypothyroidism (SCH) increased the risk of depression. One possible reason is that the etiology of SCH in these studies was not clearly distinguished. We therefore investigated the relationship between SCH resulting from 131I treatment of Graves' disease and depression.

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Our previous study has showed that co-grafted Schwann cells (SCs) promote proliferation and migration of the grafted oligodendrocyte precursor cells (OPCs). However, how the co-grafted SCs affect OPCs has not been clarified. In the present study, we confirmed that SC-induced proliferation and migration of OPCs were mediated by SC-secreted factors using SC-conditioned medium (SCM).

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Hypothyroidism leads to somatic, neuropsychological, and psychiatric changes that are similar to depression. The mechanisms underlying the behavioral abnormalities in adult onset hypothyroidism remain ambiguous. Hypothyroidism was induced in adult male Wistar rats by the maintenance of 0.

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Background: Caspase-3 is a critical apoptosis-promoting element but its status during stepwise gastrocarcinogenesis needs to be further clarified.

Materials And Methods: By the use of frozen tissue microarrays constructed with the tissue spots cored from defined histological regions in tissue blocks, the pattern of caspase-3 expression in noncancerous, premalignant (atrophic gastritis and intestinal metaplasia) tissue and cancer spots were analyzed under the same experimental conditions by the methods of immunohistochemistry and mRNA-in situ hybridization.

Results: Caspase-3 was expressed in all 34 of the noncancerous mucosa (100%), in 16 of the 17 premalignant tissues (94.

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Interaction of nuclear beta-catenin and TCF4 is the end point of canonical Wnt signaling, which is believed to trigger the transcription of multiple cancer-associated genes, including CD44. So far, the combined status of beta-catenin and TCF4 and its relevance for lymph node metastasis and CD44 expression have not been well studied in gastric cancers (GCs). To address these issues, we examined 31 GCs, 17 premalignant tissues, 10 noncancerous gastric mucosae, 17 regional lymph node metastases, and 4 human GC cell lines (MGC803, MGC823, AGS, and HGC-27) using immunohistochemical and immunofluorescence staining, reverse transcriptase polymerase chain reaction, and Western blot analysis.

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The potential correlation of E-cadherin reduction and Wnt2 up-regulation in determining the intracellular distribution of beta-catenin in gastric cancers was investigated by the methods of frozen tissue array-based immunohistochemistry, Western blot and RT-PCR analysis. It was revealed that membranous E-cadherin was reduced frequently in the two major subtypes of gastric cancer (intestinal gastric cancer, i-GC and diffuse gastric cancer, d-GC) and closely correlated with the risk of lymphoid node metastasis (P < 0.05).

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Wnt/beta-catenin signalling pathway is integrally associated with human tumour development and progression. Aberrant beta-catenin intracellular distribution has been found in gastric cancer, but the pattern of Wnt expression in stepwise gastrocarcinogenesis and its potential influence in beta-catenin distribution are still lesser known. By the methods of frozen tissue array-based immunohistochemistry, Western blot analysis and RT-PCR, a paralleled study was conducted to check Wnt2 expression and beta-catenin intracellular distribution in two major subtypes of gastric cancers (intestinal gastric cancer, i-GC and diffuse gastric cancer, d-GC) and their premalignant (intestinal metaplasia, IM and chronic gastritis, CG) and noncancerous counterparts.

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Altered distribution of beta-catenin has been found in many human malignancies including gastric cancer, but its reason(s) and biological implications have not yet been fully clarified. By the methods of frozen tissue array-based immunohistochemistry, RT-PCR and PCR-SSCP followed by DNA sequencing, the patterns of beta-catenin distribution in the subtypes of gastric cancers and their premalignant and non-cancerous counterparts were examined and the potential correlation of beta-catenin alteration with invasion was elucidated. Membranous beta-catenin was detected constantly in non-cancerous mucosa but became reduced or absent in cancer tissues.

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Aim: To study whether the immunosuppressant tripchlorolide (T4) exerts neuroprotective effect on dopaminergic neurons.

Methods: A rat model of Parkinson's disease (PD) was set up by transection of the medial forebrain bundle (MFB) with a wire knife. The rotational behavior, HPLC-ECD, tyrosine hydroxylase (TH) immunocytochemistry, ELISA methods were used to evaluate the influence on the dopaminergic neurons following T4 treatment.

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It has been reported recently that the immunosuppressant FK506 produced neurotrophic and neuroprotective effects on dopaminergic neurons in vitro and in vivo. We investigated whether tripchlorolide, an immunosuppressive extract of Chinese herb Tripterygium wilfordii Hook F, could exert similar neurotrophic and neuroprotective effects similar to those of FK506. It was found that tripchlorolide promoted axonal elongation and protected dopaminergic neurons from a neurotoxic lesion induced by 1-methyl-4-phenylpyridinium ion (MPP+) at concentrations of as low as 10(-12) to 10(-8) M.

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