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author:("Lei, xiaoming")
1.  QKI impairs self-renewal and tumorigenicity of oral cancer cells via repression of SOX2 
Cancer Biology & Therapy  2014;15(9):1174-1184.
Cancer stem cells (CSCs) may contribute to tumor initiation, distant metastasis and chemo-resistance. One of RNA-binding proteins, Quaking (QKI), was reported to be a tumor suppressor. Here we showed that reduced QKI levels were observed in many human oral cancer samples. Moreover further reduction of QKI expression in CSCs was detected compared with non-CSCs in oral cancer cell lines. Overexpressing QKI in oral cancer cells significantly reduced CSC sphere formation and stem cell-associated genes. In tumor implanting nude mice model, QKI significantly impeded tumor initiation rates, tumor sizes and lung metastasis rates. As a contrast, knocking down QKI enhanced the above effects. Among the putative CSC target genes, SOX2 expression was negatively affected by QKI, mechanism study revealed that QKI may directly regulate SOX2 expression via specific binding with its 3′UTR in a cis element-dependent way. Loss of SOX2 even completely reversed the sphere forming ability in QKI knockdown cell line. Taken together, these data demonstrated that SOX2 is an important CSC regulator in oral cancer. QKI is a novel CSC inhibitor and impaired multiple oral CSC properties via partial repression of SOX2. Therefore, reduced expression of QKI may provide a novel diagnostic marker for oral cancer.
doi:10.4161/cbt.29502
PMCID: PMC4128860  PMID: 24918581
QKI; SOX2; cancer stem cell; oral cancer; self-renewal
2.  Pulmonary sequestration in children: a clinical analysis of 48 cases 
Background: This study aimed to explore clinical features, diagnosis, treatment, and outcomes of children’s pulmonary sequestration (PS) to reduce misdiagnosis. Methods: Clinical records of 48 children with PS in Children’s Hospital of Chongqing Medical University between April 1994 and April 2013 were retrieved, and the literature was reviewed. Results: 48 cases were collected, 30 cases confirmed (Group A) and 18 suspicious cases (Group B). In Group A, 16 cases were confirmed before operation by 64-row enhanced CT (4 cases), enhanced CT combined with three-dimensional reconstruction (9 cases), and digital subtraction angiography (3 cases). Misdiagnosis rate was 36.7%, while missed diagnosis rate 10%. 26 cases received surgery and were confirmed finally. Aberrant arterial supply mainly originated from thoracic aorta (22 cases) and abdominal aorta (5 cases). Hypoplasia and chronic inflammation were shown by postoperative histopathological examinations in all children with surgery. There was no operative mortality. Encapsulated pleural effusion occurred in one patient as only post-operation complication. All were discharged after successful treatment. Conclusion: Chest X-ray and color Doppler ultrasound can be used for routine screening for PS. Technique of choice for confirmation is three-dimensional chest CT. Identifying anomalous systemic artery is key for confirmed diagnosis. Surgery is recommended as early as possible. X-ray plus ultrasound as routine screening combined with three-dimensional CT for definitive diagnosis and video-assisted thoracoscopic surgery might be best choice for PS in future.
PMCID: PMC4073756  PMID: 24995095
Children; pulmonary sequestration; diagnosis; treatment
3.  Hepatitis B viral core protein disrupts human host gene expression by binding to promoter regions 
BMC Genomics  2012;13:563.
Background
The core protein (HBc) of hepatitis B virus (HBV) has been implicated in the malignant transformation of chronically-infected hepatocytes and displays pleiotropic functions, including RNA- and DNA-binding activities. However, the mechanism by which HBc interacts with the human genome to exert effects on hepatocyte function remains unknown. This study investigated the distribution of HBc binding to promoters in the human genome and evaluated its effects on the related genes’ expression.
Results
Whole-genome chromatin immunoprecipitation microarray (ChIP-on-chip) analysis was used to identify HBc-bound human gene promoters. Gene Ontology and pathway analyses were performed on related genes. The quantitative polymerase chain reaction assay was used to verify ChIP-on-chip results. Five novel genes were selected for luciferase reporter assay evaluation to assess the influence of HBc promoter binding. The HBc antibody immunoprecipitated approximately 3100 human gene promoters. Among these, 1993 are associated with known biological processes, and 2208 regulate genes with defined molecular functions. In total, 1286 of the related genes mediate primary metabolic processes, and 1398 encode proteins with binding activity. Sixty-four of the promoters regulate genes related to the mitogen-activated protein kinase (MAPK) pathways, and 41 regulate Wnt/beta-catenin pathway genes. The reporter gene assay indicated that HBc binding up-regulates proto-oncogene tyrosine-protein kinase (SRC), type 1 insulin-like growth factor receptor (IGF1R), and neurotrophic tyrosine kinase receptor 2 (NTRK2), and down-regulates v-Ha-ras Harvey rat sarcoma viral oncogene (HRAS).
Conclusion
HBc has the ability to bind a large number of human gene promoters, and can disrupt normal host gene expression. Manipulation of the transcriptional profile in HBV-infected hepatocytes may represent a key pathogenic mechanism of HBV infection.
doi:10.1186/1471-2164-13-563
PMCID: PMC3484065  PMID: 23088787
Hepatitis B virus; Hepatitis B core protein; Chromatin immunoprecipitation microarray; ChIP-on-chip; Gene expression; DNA-protein interaction

Results 1-3 (3)