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Epigenetics breast

Kedarlal Sharma, JuhiSingh, Emma E Frost, Prakash P Pillai
MethylCpG binding protein-2 (MeCP2) is an epigenetic regulator and essential for brain development.MeCP2 mutations are associated with a spectrum of neuro-developmental disorders that vary depending on the patient gender, most notably Rett Syndrome. MeCP2 is essential for normal neuronal maturation, and glial cell function in the brain. Besides, its role in neurodevelopmental disorders, MeCP2 is involved in many cancers such as breast, colorectal, lung, liver, and prostate cancer. Glioma is the most lethal form of brain cancer...
March 11, 2018: Neuroscience Letters
Hsin-Chen Lin, Ching-Ching Yeh, Lo-Yun Chao, Mong-Hsun Tsai, Hung-Hsin Chen, Eric Y Chuang, Liang-Chuan Lai
Hypoxia can lead to solid tumor aggressiveness by driving multiple signaling pathways. Long non-coding RNAs respond to several extrinsic stimuli, causing changes in cancer cells by participating in multiple steps of gene expression. However, genomic profiling of long non-coding RNAs regulated by oxygen in breast cancer remained unclear. Therefore, the aims of this study were to identify oxygen-responsive long non-coding RNAs in breast cancer cells, and to delineate their regulatory mechanisms. The expression profiling of long non-coding RNAs in breast cancer cells growing under normoxic, hypoxic, and re-oxygenated conditions was examined using next-generation sequencing technology...
February 13, 2018: Oncotarget
Qiong Song, Qiu Chen, Qimin Wang, Longqiu Yang, Dongdong Lv, Guangli Jin, Jiaying Liu, Baolin Li, Xuejie Fei
BACKGROUND: Breast cancer is one of the leading causes of death in women worldwide. Fast growth is the important character of breast cancer, which makes sure the subsequent metastasize and invasion breast cancer. Golgi related genes GOLPH3 has been reported to regulate many kinds of cancers proliferation. However, its upregulator remains largely unknown. miRNA modulate gene expression by post-transcriptional repression to participate in many signaling pathway of breast cancer cell proliferation...
March 9, 2018: BMC Cancer
Sarada Achyutuni, Revathy Nadhan, Satheesh Kumar Sengodan, Priya Srinivas
Chromosome 17 (Chr17) harbors crucial genes that encode proteins implicated in a variety of cancers, including some that guard cancer cells from genomic instability and others that interfere with metastasis. Included amongst the genes on chr17 that regulate biological processes fundamental to the genesis of cancer are TP53, BRCA1, CCL5, NF-1, and GRB7. As many as 50% of all human tumors and at least 30% of breast carcinomas contain p53 mutations, while 30%-40% of breast cancers have defective BRCA1. A large number of proteins regulate the expression of these cancer genes on chr17 with miRNAs, the most widely studied class of regulatory RNAs, playing a major role in epigenetically controlling the gene expression programs, thereby managing various cellular functions...
August 2017: Seminars in Oncology
Ivana Maleva Kostovska, Milena Jakimovska, Katerina Popovska-Jankovic, Katerina Kubelka-Sabit, Mitko Karagjozov, Dijana Plaseska-Karanfilska
Tumours presenting BRCAness profile behave more aggressively and are more invasive as a consequence of their complex genetic and epigenetic alterations, caused by impaired fidelity of the DNA repair processes. Methylation of promoter CpG islands represents an alternative mechanism to inactivate DNA repair and tumour suppressor genes. In our study, we analyzed the frequency of methylation changes of 24 tumour suppressor genes and explored their association with BRCAness profile. BRCA1ness profile and aberrant methylation were studied in 233 fresh frozen breast tumour tissues by Multiplex Ligation-dependent Probe Amplification (MLPA) and Methylation Specific (MS)-MLPA methods, respectively...
March 9, 2018: Pathology Oncology Research: POR
Vittoria Poli, Luca Fagnocchi, Alessandra Fasciani, Alessandro Cherubini, Stefania Mazzoleni, Sara Ferrillo, Annarita Miluzio, Gabriella Gaudioso, Valentina Vaira, Alice Turdo, Miriam Giaggianesi, Aurora Chinnici, Elisa Lipari, Silvio Bicciato, Silvano Bosari, Matilde Todaro, Alessio Zippo
Breast cancer consists of highly heterogeneous tumors, whose cell of origin and driver oncogenes are difficult to be uniquely defined. Here we report that MYC acts as tumor reprogramming factor in mammary epithelial cells by inducing an alternative epigenetic program, which triggers loss of cell identity and activation of oncogenic pathways. Overexpression of MYC induces transcriptional repression of lineage-specifying transcription factors, causing decommissioning of luminal-specific enhancers. MYC-driven dedifferentiation supports the onset of a stem cell-like state by inducing the activation of de novo enhancers, which drive the transcriptional activation of oncogenic pathways...
March 9, 2018: Nature Communications
Lisiane Silveira Zavalhia, Aline Weber Medeiros, Andrew Oliveira Silva, Adriana Vial Roehe
The fragile histidine triad (FHIT) gene encloses an active common chromosomal fragile site, FRA3B. This gene is known to be associated with genomic instability, apoptosis and DNA damage. FHIT disturbances have been related to carcinogenesis in different types of human tumor. Despite this, there are some controversies about the exact role of the FHIT gene in relation to tumor biology. Several pieces of evidence support the hypothesis that FHIT acts as a tumor suppressor gene. A loss or decrease in the Fhit protein expression appears to be related to tumor progression, poor prognostic factors and lower survival rates...
March 8, 2018: Asia-Pacific Journal of Clinical Oncology
Yoshimasa Miyagawa, Yosuke Matsushita, Hiromu Suzuki, Masato Komatsu, Tetsuro Yoshimaru, Ryuichiro Kimura, Ayako Yanai, Junko Honda, Akira Tangoku, Mitsunori Sasa, Yasuo Miyoshi, Toyomasa Katagiri
Triple-negative breast cancer (TNBC), defined as breast cancer lacking estrogen- and progesterone‑receptor expression and human epidermal growth factor receptor 2 (HER2) amplification, is a heterogeneous disease. RNA-sequencing analysis of 15 TNBC specimens and The Cancer Genome Atlas-TNBC dataset analysis identified the frequent downregulation of leucine-rich repeat-containing 26 (LRRC26), which negatively regulates nuclear factor-κB (NF-κB) signaling, in TNBC tissues. Quantitative polymerase chain reaction and bisulfite pyrosequencing analyses revealed that LRRC26 was frequently silenced in TNBC tissues and cell lines as a result of promoter methylation...
March 5, 2018: International Journal of Oncology
Hong Ding, Wen Chao Lu, Jun Chi Hu, Yu-Chih Liu, Chen Hua Zhang, Fu Lin Lian, Nai Xia Zhang, Fan Wang Meng, Cheng Luo, Kai Xian Chen
SET7, serving as the only histone methyltransferase that monomethylates 'Lys-4' of histone H3, has been proved to function as a key regulator in diverse biological processes, such as cell proliferation, transcriptional network regulation in embryonic stem cell, cell cycle control, protein stability, heart morphogenesis and development. What's more, SET7 is involved inthe pathogenesis of alopecia aerate, breast cancer, tumor and cancer progression, atherosclerosis in human carotid plaques, chronic renal diseases, diabetes, obesity, ovarian cancer, prostate cancer, hepatocellular carcinoma, and pulmonary fibrosis...
March 2, 2018: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
Maria Sol Brassesco, Julia Alejandra Pezuk, Karina Bezerra Salomao, Gabriela Molinari Roberto, Carlos Alberto Scrideli, Luiz Gonzaga Tone
Over the last decade, the inhibition of PLK1 has proven potent antiproliferative activity in vitro. However, the effectiveness of most synthetic targeted drugs has not translated into clinics. Herein, we investigated the in vitro effects of two second-generation PLK1 inhibitors BI 6727 and GSK461364 in breast cancer cell lines as monotherapy or in combination with other drugs or ionizing radiation. MATERIAL AND METHODS: Cell survival was analyzed through XTT®, clonogenicity and caspase-3 activation assays were also studied, and drug interactions analyzed through a nonlinear regression of a sigmoid dose response model...
February 28, 2018: Anti-cancer Agents in Medicinal Chemistry
Abdullah Al Emran, Diego M Marzese, Dinoop Ravindran Menon, Mitchell S Stark, Joachim Torrano, Heinz Hammerlindl, Gao Zhang, Patricia Brafford, Matthew P Salomon, Nellie Nelson, Sabrina Hammerlindl, Deepesh Gupta, Gordon B Mills, Yiling Lu, Richard A Sturm, Keith Flaherty, Dave S B Hoon, Brian Gabrielli, Meenhard Herlyn, Helmut Schaider
Besides somatic mutations or drug efflux, epigenetic reprogramming can lead to acquired drug resistance. We recently have identified early stress-induced multi-drug tolerant cancer cells termed induced drug-tolerant cells (IDTCs). Here, IDTCs were generated using different types of cancer cell lines; melanoma, lung, breast and colon cancer. A common loss of the H3K4me3 and H3K27me3 and gain of H3K9me3 mark was observed as a significant response to drug exposure or nutrient starvation in IDTCs. These epigenetic changes were reversible upon drug holidays...
February 2, 2018: Oncotarget
Linda Xiaoyan Li, Julie Xia Zhou, James P Calvet, Andrew K Godwin, Roy A Jensen, Xiaogang Li
We identified SMYD2, a SMYD (SET and MYND domain) family protein with lysine methyltransferase activity, as a novel breast cancer oncogene. SMYD2 was expressed at significantly higher levels in breast cancer cell lines and in breast tumor tissues. Silencing of SMYD2 by RNAi in triple-negative breast cancer (TNBC) cell lines or inhibition of SMYD2 with its specific inhibitor, AZ505, significantly reduced tumor growth in vivo. SMYD2 executes this activity via methylation and activation of its novel non-histone substrates, including STAT3 and the p65 subunit of NF-κB, leading to increased TNBC cell proliferation and survival...
February 27, 2018: Cell Death & Disease
Guochao Li, Dong Wang, Wencui Ma, Ke An, Zongzhi Liu, Xinyu Wang, Caiyun Yang, Fengxia Du, Xiao Han, Shuang Chang, Hui Yu, Zilong Zhang, Zitong Zhao, Yan Zhang, Junyun Wang, Yingli Sun
AIM: Cancer stem cells (CSCs) drive triple-negative breast cancer recurrence via their properties of self-renewal, invasiveness and radio/chemotherapy resistance. This study examined how CSCs might sustain these properties. MATERIALS & METHODS: Transcriptomes, DNA methylomes and histone modifications were compared between CSCs and non-CSCs. RESULTS: Transcriptome analysis revealed several pathways that were activated in CSCs, whereas cell cycle regulation pathways were inhibited...
February 26, 2018: Epigenomics
Yiyue Xu, Chun So, Hon-Ming Lam, Ming-Chiu Fung, Suk-Ying Tsang
It has long been a puzzle in cancer treatment that despite the initial appearance of apoptosis, the process could be reversed in some cancer cells and often results in more aggressive tumors and metastasis. The mechanism for this recurrence is yet unknown. Here we report that human mammary carcinoma cells induced to undergo apoptosis could recover with increased tumorigenicity in vitro and in vivo, and induced lymph node metastasis. Specifically, the reversed cells underwent epithelial-to-mesenchymal transitions in the primary tumors in situ, and mesenchymal-to-epithelial transitions in the metastatic cells...
March 2018: Neoplasia: An International Journal for Oncology Research
Ye Zhang, Yin-Long Yang, Fang-Lin Zhang, Xiao-Hong Liao, Zhi-Min Shao, Da-Qiang Li
Emerging evidence shows that ring finger protein 144A (RNF144A), a poorly characterized member of the Ring-between-Ring (RBR) family of E3 ubiquitin ligases, is a potential tumor suppressor gene. However, its regulatory mechanism in breast cancer remains undefined. Here, we report that RNF144A promoter contains a putative CpG island and the methylation levels of RNF144A promoter are higher in primary breast tumors than those in normal breast tissues. Consistently, RNF144A promoter methylation levels are associated with its transcriptional silencing in breast cancer cells, and treatment with DNA methylation inhibitor 5-Aza-2-deoxycytidine (AZA) reactivates RNF144A expression in cells with RNF144A promoter hypermethylation...
February 23, 2018: Cancer Medicine
Sumadi Lukman Anwar, Ulrich Lehmann
The retinoblastoma protein (pRb) plays a central role in the regulation of cell cycle by interaction with members of the E2F transcription factor family. As a tumor suppressor protein, pRb is frequently dysregulated in several major cancers. In addition to mutations, inactivation of pRb is also caused by epigenetic mechanisms including alterations of DNA methylation. There are three CpG islands located within the RB1 gene that encodes pRb that are closely associated with the regulation of pRb expression. Aberrant DNA methylation at the RB1 gene has been reported in sporadic retinoblastoma as well as other cancers including glioblastoma, hepatocellular carcinoma, and breast cancer...
2018: Methods in Molecular Biology
Isai Pratha Karthik, Pavitra Desai, Sudarkodi Sukumar, Aleksandra Dimitrijevic, Krishnaraj Rajalingam, Sundarasamy Mahalingam
Ras proteins are major human oncogenes and most of the studies are focussed on enzymatic RAS effectors. Recently, non-enzymatic Ras effectors (RASSF-Ras association domain family) have garnered special attention because of their tumor suppressive properties in contrast to the oncogenic potential of the classical enzymatic Ras effectors. While most members of RASSF family are deregulated by promoter hypermethylation, RASSF8 promoter remains unmethylated in many cancers but the mechanism(s) of its downregulation remains unknown...
February 21, 2018: Journal of Biological Chemistry
Miguel H Bronchud, Francesc Tresserra, Bernat Serra Zantop
Microenvironmental properties are thought to be responsible for feto-maternal tolerance. Speculatively, ectopic expression of placental gene programs might also be related to cancer cells' ability to escape from immune vigilance mechanisms during carcinogenesis and cancer progression. Recently, we published the first human genomic evidence of similar immune related gene expression profiles in both placenta (placenta and decidual tissue) and cancer (both primary and metastatic) in the same patient with lymph-node positive breast carcinoma during pregnancy...
January 19, 2018: Oncotarget
Yuanxin Xi, Jiejun Shi, Wenqian Li, Kaori Tanaka, Kendra L Allton, Dana Richardson, Jing Li, Hector L Franco, Anusha Nagari, Venkat S Malladi, Luis Della Coletta, Melissa S Simper, Khandan Keyomarsi, Jianjun Shen, Mark T Bedford, Xiaobing Shi, Michelle C Barton, W Lee Kraus, Wei Li, Sharon Y R Dent
BACKGROUND: Epigenetic regulators are frequently mutated or aberrantly expressed in a variety of cancers, leading to altered transcription states that result in changes in cell identity, behavior, and response to therapy. RESULTS: To define alterations in epigenetic landscapes in breast cancers, we profiled the distributions of 8 key histone modifications by ChIP-Seq, as well as primary (GRO-seq) and steady state (RNA-Seq) transcriptomes, across 13 distinct cell lines that represent 5 molecular subtypes of breast cancer and immortalized human mammary epithelial cells...
February 20, 2018: BMC Genomics
Ramesh Butti, Sumit Das, Vinoth Prasanna Gunasekaran, Amit Singh Yadav, Dhiraj Kumar, Gopal C Kundu
Breast cancer is a multifactorial disease and driven by aberrant regulation of cell signaling pathways due to the acquisition of genetic and epigenetic changes. An array of growth factors and their receptors is involved in cancer development and metastasis. Receptor Tyrosine Kinases (RTKs) constitute a class of receptors that play important role in cancer progression. RTKs are cell surface receptors with specialized structural and biological features which respond to environmental cues by initiating appropriate signaling cascades in tumor cells...
February 19, 2018: Molecular Cancer
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