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Liu S.,Central South University | Tao Y.,Central South University | Tao Y.,Key Laboratory of Carcinogenesis and Cancer Invasion | Tao Y.,Key Laboratory of Carcinogenesis
Biological Reviews | Year: 2013

The dynamic interplay between chromatin modification (e.g. DNA methylation) and RNA polymerase II (Pol II) plays a critical role in gene transcription during stem cell development, establishment, and maintenance and in the cellular response to extracellular stimuli such as those that cause DNA damage. Pol II is recruited to the promoter-proximal regions of numerous inactive genes at high conentrations in a process called Pol II stalling. This is a key process prior to gene activation and it involves many interacting factors. Chromatin modification including nucleosome position is dependent on chromatin structure. Stalled genes create a particular structural conformation of chromatin, which acts as a target for chromatin modification. In this way, Pol II stalling may be regarded as a type of signal for chromatin modification in these regions during the dynamic transition between stalled and activated genes. © 2012 Cambridge Philosophical Society.


Jiang Y.,Central South University | Jiang Y.,Key Laboratory of Carcinogenesis and Cancer Invasion | Jiang Y.,Key Laboratory of Carcinogenesis | Liu S.,Central South University | And 7 more authors.
Biochimica et Biophysica Acta - Reviews on Cancer | Year: 2013

DNA methylation plays an important role in the regulation of gene expression, as it is the first epigenetic modification to take place on a given DNA strand. Several factors may directly or indirectly regulate the dynamic distribution of DNA methylation and demethylation between intergenic and intragenic gene regions, thereby controlling gene expression. CpG islands have direct implications for the understanding of DNA methylation patterns in normal conditions and in some common disease states, including cancer. Here, we summarize several recent studies on the genome-wide distribution of DNA methylation and demethylation and their related factors, and we discuss the potential of DNA methylation and demethylation patterns to contribute to gene transcription patterns in tumorigenesis. © 2012.


Guo F.,Central South University | Guo F.,Key Laboratory of Carcinogenesis and Cancer Invasion | Guo F.,Key Laboratory of Carcinogenesis | Guo F.,Tianjin Medical University | And 9 more authors.
PLoS ONE | Year: 2013

STC1 is a glycoprotein hormone involved in calcium/phosphate (Pi) homeostasis. There is mounting evidence that STC1 is tightly associated with the development of cancer. But the function of STC1 in cancer is not fully understood. Here, we found that STC1 is down-regulated in Clinical tissues of cervical cancer compared to the adjacent normal cervical tissues (15 cases). Subsequently, the expression of STC1 was knocked down by RNA interference in cervical cancer CaSki cells and the low expression promoted cell growth, migration and invasion. We also found that STC1 overexpression inhibited cell proliferation and invasion of cervical cancer cells. Moreover, STC1 overexpression sensitized CaSki cells to drugs. Further, we showed that NF-κB p65 protein directly bound to STC1 promoter and activated the expression of STC1 in cervical cancer cells. Thus, these results provided evidence that STC1 inhibited cell proliferation and invasion through NF-κB p65 activation in cervical cancer. © 2013 Guo et al.


Liu X.,Central South University | Liu X.,Key Laboratory of Carcinogenesis | Chen X.,Central South University | Chen X.,Key Laboratory of Carcinogenesis | And 8 more authors.
Journal of Experimental and Clinical Cancer Research | Year: 2013

Similar to protein-coding genes, miRNAs are also susceptible to epigenetic modulation. Although numerous miRNAs have been shown to be affected by DNA methylation, the regulatory mechanism of histone modification on miRNA is not adequately understood. EZH2 and HDACs were recently identified as critical histone modifiers of deregulated miRNAs in cancer and can be recruited to a miRNA promoter by transcription factors such as MYC. Because miRNAs can modulate epigenetic architecture and can be regulated by epigenetic alteration, they could reasonably play an important role in mediating the crosstalk between epigenetic regulators. The complicated network between miRNAs and epigenetic machineries underlies the epigenetic-miRNA regulatory pathway, which is important in monitoring gene expression profiles. Regulation of miRNAs by inducing epigenetic changes reveals promising avenues for the design of innovative strategies in the fight against human cancer. © 2013 Liu et al.; licensee BioMed Central Ltd.


Hu Z.-Y.,Central South University | Hu Z.-Y.,Key Laboratory of Carcinogenesis and Cancer Invasion | Hu Z.-Y.,Key Laboratory of Carcinogenesis | Hu Z.-Y.,First Hospital of Changsha City | And 8 more authors.
Journal of Molecular Medicine | Year: 2014

Nearly a hundred years of scientific research has revealed a notable preference of cancer cells to utilize aerobic glycolysis rather than mitochondrial oxidative phosphorylation for glucose-dependent ATP production, which is thought to be the root of tumor formation and growth. Glycolysis is a complex biochemical process that is mediated by multiple glycolytic genes. Besides regulating glucose metabolism, these genes are also suggested to possess various other functions related to cancer, including roles in cancer development and promotion, inhibition of apoptosis, cell cycle progression, and tumor metastasis. This article highlights the biological functions of glycolytic genes beyond their role in regulation of glycolysis and discusses their clinical implications, especially in regard to the use of glycolytic genes as biomarkers for early detection of cancer or as targets for novel anticancer treatments. © 2014 Springer-Verlag.


Shi Y.,Central South University | Shi Y.,Key Laboratory of Carcinogenesis and Cancer Invasion | Shi Y.,Key Laboratory of Carcinogenesis | Tao Y.,Central South University | And 18 more authors.
Carcinogenesis | Year: 2012

The epidermal growth factor receptor (EGFR), a ubiquitously expressed receptor tyrosine kinase, is an important factor in carcinogenesis. Transcriptional intermediary factor 2 (TIF2), a member of the p160 nuclear receptor co-activator gene family, is linked to the proliferation of cancer cells. However, the direct interplay between the EGFR and the nuclear receptors remains unclear. Our previous study demonstrated that nuclear EGFR could directly bind to the cyclin D1 promoter under the regulation of the oncoprotein latent membrane protein 1 (LMP1), but it also indicated that other factors are involved in the activation of target genes. In this study, we found that LMP1 upregulated the expression of TIF2 and promoted the interaction of EGFR with TIF2 in nasopharyngeal carcinoma. Furthermore, we demonstrated that the intact complex was linked with cyclin D1 promoter activity in an LMP1-dependent manner. The physiological functions of the intact complex were associated with cell proliferation and cell cycle progression. These findings suggest that TIF2 is a novel binding partner for nuclear EGFR and is involved in regulating its target gene expression. Abbreviations: ATRSAT-rich region sequence. ChIPchromatin immunoprecipitation. DNA-PKDNA protein kinase. EBVEpstein-Barr virus. EGFepidermal growth factor. EGFRepidermal growth factor receptor. LMPlatent membrane protein. MAPKmitogen-activated protein kinase. NPCnasopharyngeal carcinoma. PBSphosphate-buffered saline. PCRpolymerase chain reaction. RHARNA helicase A. SFKSrc family kinase. STAT signal transducer and activator of transcription. TIFtranscriptional intermediary factor. TNF-atumor necrosis factor-a. © The Author 2012. Published by Oxford University Press. All rights reserved.


Zhao L.,Central South University | Zhao L.,Key Laboratory of Carcinogenesis and Invasion | Zhao L.,Key Laboratory of Carcinogenesis | Bode A.M.,University of Minnesota | And 4 more authors.
Carcinogenesis | Year: 2012

MicroRNA (miRNA) influences carcinogenesis at multiple stages and it can effectively control tumor radiosensitivity by affecting DNA damage repair, cell cycle checkpoint, apoptosis, radio-related signal transduction pathways and tumor microenvironment. MiRNA also efficiently modulates tumor radiosensitivity at multiple levels by blocking the two essential non-homologous end-joining repair and homologous recombination repair pathways in the DNA damage response. It interferes with four radio-related pathways in ionizing radiation, including the PI3-K/Akt, NF-κB, MAPK and TGFβ signaling pathways. Moreover, the regulatory effect of miRNA in radiosensitivity can be enhanced when interacting with various key molecules, including H2AX, BRCA1, ATM, DNA-PK, RAD51, Chk1, Cdc25A, p53, PLK1, HIF-1 and VEGF, which are involved in these processes. Therefore, thoroughly understanding the mechanism of miRNA in tumor radiosensitivity could assist in finding novel targets to improve the radiotherapeutic effects and provide new clinical perspectives and insights for developing effective cancer treatments. © The Author 2012. Published by Oxford University Press.


Li N.,Central South University | Li N.,Hunan Key Laboratory of Nonresolving Inflammation and Cancer | Tang A.,Central South University | Tang A.,Hunan Key Laboratory of Nonresolving Inflammation and Cancer | And 14 more authors.
Molecular and Cellular Biochemistry | Year: 2013

Recent data strongly suggests the profound role of miRNAs in cancer progression. Here, we showed miR-126 expression was much lower in HCT116, SW620 and HT-29 colon cancer cells with highly metastatic potential and miR-126 downregulation was more frequent in colorectal cancers with metastasis. Restored miR-126 expression inhibited HT-29 cell growth, cell-cycle progression and invasion. Mechanically, microarray results combined with bioinformatic and experimental analysis demonstrated miR-126 exerted cancer suppressor role via inhibiting RhoA/ROCK signaling pathway. These results suggest miR-126 function as a potential tumor suppressor in colon cancer progression and miR-126/RhoA/ROCK may be a novel candidate for developing rational therapeutic strategies. © 2013 Springer Science+Business Media New York.


Zhao L.,Central South University | Zhao L.,Key Laboratory of Carcinogenesis and Invasion | Zhao L.,Key Laboratory of Carcinogenesis | Lu X.,University of Houston | And 3 more authors.
Cellular Signalling | Year: 2013

Tumor radiation response is an essential issue in radiotherapy and a core determining factor of tumor radioresistance or radiosensitivity. Multiple factors can influence tumor radiation response, and among them tumor genetic and epigenetic background, tumor microenvironment and tumor blood flow status may take a leading role. During the whole process of tumor radiation response, tumor radiosensitivity can be regulated in an orderly manner through some classical signal transduction pathways. Although these pathways have already owned multiple biological functions and involved in the process of carcinogenesis, their regulatory roles in tumor radiation response can not be ignored. MicroRNA (miRNA) is a class of non-coding RNA of about 22 nucleotides in length, which binds to the 3'-untranslated region (3'-UTR) of target gene and controls the expression of it at the post-transcriptional level. MiRNA participates in numerous physiology and pathology processes and acts as oncogene or tumor suppressor to affect cancer progression. Through interplaying with the key components in radiation related signal transduction pathways, miRNA could effectively activate the expression of DNA damage response genes and cell cycle related genes in the nucleus, and play a critical role in the modulation of radiation response and radiosensitivity in tumor cells. In this review, we mainly elucidate the regulatory mechanisms and functions of miRNA in these radiation related signal transduction pathways from three different aspects which include the upstream receptors, midstream transducer pathways, and downstream effector genes. © 2013 Elsevier Inc.


Zhao L.,Key Laboratory of Carcinogenesis and Invasion | Zhao L.,Key Laboratory of Carcinogenesis | Zhao L.,Central South University | Chen X.,Key Laboratory of Carcinogenesis and Invasion | And 5 more authors.
Acta Biochimica et Biophysica Sinica | Year: 2011

MicroRNA (miRNA) is a cluster of small non-encoding RNA molecules of 2123 nucleotides in length, which controls the expression of target gene at the post-transcriptional level. Recent researches have indicated that miRNA plays an essential role in carcinogenesis, such as affecting the cell growth, differentiation, apoptosis, and cell cycle. Nowadays, multiple promising roles of miRNA involved in carcinogenesis are emerging, and it is shown that miRNA closely relates to the process of epithelial-mesenchymal transition (EMT), the regulation of cancer stem cells (CSCs), the development of tumor invasion and migration. miRNA also acts as a biomarker stably expressed in serum and provides new target for molecular target therapy of various cancers. The aim of this review is to illustrate the new role of miRNA in carcinogenesis and highlight the new prospects of miRNA in cancer clinical application, such as in serological diagnosis and molecular-targeted therapeutics. © The Author 2011. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.

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