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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. Source

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 12 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. Source

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. Source

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. Source

Hu Z.-Y.,Central South University | Hu Z.-Y.,Key Laboratory of Carcinogenesis and Cancer Invasion | Hu Z.-Y.,Key Laboratory of Carcinogenesis | Xiao L.,Central South University | And 7 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. Source

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