20:I[654155,["/_next/static/chunks/bb923814e1f4d2e9.js","/_next/static/chunks/dd3ee9f5b7716ca6.js","/_next/static/chunks/4204a0ae82542ca8.js","/_next/static/chunks/1270dead247da766.js","/_next/static/chunks/6e1aa89a642f40be.js","/_next/static/chunks/2d7aa753e81324a8.js","/_next/static/chunks/8ffd0b71567920d8.js","/_next/static/chunks/67ea6dfd21f16c5f.js","/_next/static/chunks/24eb4379f68013fd.js","/_next/static/chunks/b8cd775ffdf935bd.js","/_next/static/chunks/983103cd9eb7b428.js","/_next/static/chunks/263f2cdcb9aa2341.js","/_next/static/chunks/294b9525248c8e5f.js"],"default"] 21:T545,Basic helix-loop-helix (bHLH) proteins are a large superfamily of transcription factors that play critical roles in many physiological processes including cellular differentiation, cell cycle arrest and apoptosis. Based on structural and phylogenetic analysis, mammalian bHLH-Orange (bHLH-O) proteins, which constitute the repressor family of bHLH factors, can be grouped into four subfamilies: Hes, Hey, Helt and Stra13/Dec. In addition to the bHLH domain that mediates DNA-binding and protein dimerization, all members of this family are characterized by a distinctive motif called the "Orange domain" which is present exclusively in these factors. Genetic studies using targeted mutagenesis in mice have revealed essential roles for many bHLH-O genes in embryonic development, cell fate decisions, differentiation of a number of cell types and in apoptosis. Furthermore, growing evidence of crosstalk between bHLH-O proteins with the tumor suppressors p53 and hypoxia-inducible factor, have started to shed light on their possible roles in oncogenesis. Consistently, deregulated expression of several bHLH-O factors is associated with various human cancers. Here, we review the structure and biological functions of bHLH-O factors, and discuss recent studies that suggest a potential role for these factors in tumorigenesis and tumor progression.22:T497,Oxidative stress is considered an important factor in the development of endometriosis, including its malignant transformation. Previous studies have found that AT-rich interactive domain 1A (ARID1A), a tumor suppressor gene, is frequently mutated and inactivated in endometriosis-associated ovarian cancer (EAOC), and such a change in this gene is considered an early event in malignant transformation. We observed oxidative stress status by measuring the activity of the antioxidant enzyme manganese superoxide dismutase (MnSOD), malondialdehyde (MDA), and ARID1A gene expression in tissue samples from patients with endometriosis, EAOC, or non-endometriosis-associated ovarian cancer (non-EAOC). We also induced oxidative stress in the cultured cells from patients with primary endometriosis by adding H₂O₂ and tested for any alteration of ARID1A gene expression based on different H₂O₂ concentrations. The results showed that MnSOD activity in endometriosis and EAOC was lower than in non-EAOC, but MDA levels were higher. This study also showed that oxidative stress reduced ARID1A gene expression.23:T47b,Prostate cancer is the second leading cause of cancer death among men in the United States of America. However, the molecular mechanisms underlying the disease remain largely unknown. Therefore, the identification of tumor specific molecules that serve as targets for the development of new cancer drugs is considered to be a major goal in cancer research. The mouse Engrailed-2 (En-2) gene, which is a homeobox-containing transcription factor was recently identified as a candidate oncogene in breast cancer. Here, we demonstrate that En-2 is over-expressed in human prostate cancer cells as compared to normal prostate epithelial cells. In addition, our data suggests that EN2 expression may be positively modulated by PAX2 transcription factor. Furthermore, down-regulation of EN2 expression by siRNA resulted in a decrease in PAX2 expression. We also provide evidence that down-regulation of EN2 expression causes a dramatic decrease in prostate cancer cell pr

#	Concept	H-Index	Publications	Citations
1	Medicine	6	6	166
2	Health Sciences	2	2	26
3	Natural Sciences	2	2	74
4	Engineering	1	1	32
5	Biochemistry	1	1	18

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