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Guangzhou, China

Liu Y.,Guangzhou University | Lu R.,Guangzhou University | Gu J.,Shandong University | Chen Y.,Guangzhou University | And 5 more authors.
Environmental Toxicology and Pharmacology | Year: 2016

Recently, Aldehyde dehydrogenase 1A1 (ALDH1A1) has been proposed to be a common marker of cancer stem cells and can be induced by benzo[a]pyrene (B[a]P) exposure. However, the underlying mechanism of how ALDH1A1 contributes to B[a]P-induced carcinogenesis in human bronchial epithelial cells remains unclear. Here, we found that B[a]P up-regulated expression levels of stem cell markers (ABCG2, SOX2, c-Myc and Klf4), epithelial-mesenchymal transition (EMT) associated genes (SNAIL1, ZEB1, TWIST and β-CATENIN) and cancer-related long non-coding RNAs (lncRNAs; HOTAIR and MALAT-1) in malignant B[a]P-transformed human bronchial epithelial cells (BEAS-2B-T cells), and these up-regulations were dependent on increased expression of ALDH1A1. The inhibition of endogenous ALDH1A1 expression down-regulated expression levels of stem cell markers and reversed the malignant phenotype as well as reduced the chemoresistance of BEAS-2B-T cells. In contrast, the overexpression of ALDH1A1 in BEAS-2B cells increased the expression of stem cell markers, facilitated cell transformation, promoted migratory ability and enhanced the drug resistance of BEAS-2B cells. Overall, our data indicates that ALDH1A1 promotes a stemness phenotype and plays a critical role in the BEAS-2B cell malignant transformation induced by B[a]P. © 2016 Elsevier B.V.

Li Z.,Biological Experiment Center | Zhang Z.,Biological Experiment Center | Li L.,Guangzhou University | Yao Y.,Biological Experiment Center | And 5 more authors.
Hemoglobin | Year: 2015

We report a novel β-globin gene promoter mutation in a Chinese family identified using fluorescence resolution melting curve analysis and gene sequencing. The proband, who showed the phenotype of β-thalassemia intermedia (β-TI), was found to be a compound heterozygote for the novel mutation -25 (G>T) (HBB: c.-75G>T) and a codon 17 (HBB: c.52A>T) mutation. Moreover, conservation analysis using phyloP and phastCons indicated that the mutated base in the proband was conserved. This novel point mutation on the β-globin gene is in close proximity to the conserved ATAA sequence located at position -25 relative to the mRNA Cap site. We performed a further comparative analysis of the clinical phenotypes and hematological parameters in this pedigree and found that the father was a carrier of the novel point mutation and showed low levels of hemoglobin (Hb), mean corpuscular volume (MCV) and mean corpuscular Hb (MCH). Thus, the available evidence suggests that this novel mutation, -25, results in β+-thalassemia (β+-thal). © 2015 Informa Healthcare USA, Inc.

Dai L.,Guilin Medical College | Tian X.,Guilin Medical College | Tan N.,Biological Experiment Center | Wen H.,Biological Experiment Center | Huang L.,Biological Experiment Center
Chinese-German Journal of Clinical Oncology | Year: 2011

Objective: Colon cancer metastasis is the key in fertility rate of colon cancer. Many recent results about metastasis research indicated that EMMPRIN played an important role in cancer metastasis. So, we designed this experiment to investigate whether EMMPRIN can enhance the metastatic ability of murine colon adenocarcinoma cell, CT26. Methods: EMMPRIN was over expressed in CT26 cells through transfecting pCMV-HA2-EMMPRIN into the CT26 cells. Invasion assay, wound migration assay and adhesion assay were utilized to analyze the metastasis of CT26 cells in vitro after EMMPRIN over expression. Results: After EMMPRIN over expression, invasion assay showed that invasive cells were 103.33 + 8.49 in EMMPRIN group and 48.67 + 5.3 in control group (P < 0.001). Migration assay showed that migrating cells were 40.67 + 2.49 in EMMPRIN group and 18.33 + 2.05 in control group (P < 0.001). CCK-8 absorbance value in adhesion assay were 3.33 + 0.17 in EMMPRIN group and 2.10 + 0.22 in control group (P < 0.001). Conclusion: Over expression of EMMPRIN could enhance the CT26 cell capacity of invasion and migration, and inhibit CT26 cell capacity of adhesion remarkably. The results suggest that EMMPRIN may be involved in cancer metastasis and play an important role in promotion of cancer metastasis. © 2011 Springer-Verlag Berlin Heidelberg.

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