As a member of the sirtuins family, also called Class III histone deacetylases (HDACs), SIRT6 has many catalytic enzyme activities and plays a pivotal role in biological processes including anti-aging, chromatin regulation, transcriptional control, glucose and lipid metabolism, and DNA damage repair. Recently, increasing evidences indicated that SIRT6 was related to initiation and development of tumors, such as hepatic cancer, lung cancer, breast cancer and genital system tumors. However, SIRT6 might play a dual role in tumorigenesis and progression. SIRT6 often acted as a tumor suppressor, but might play an oncogenic role. Based on our current study, we depicted the essential roles of SIRT6 in the initiation and progression of various tumors, and summarized its mode of actions, which might provide clues for cancer therapy.
Carcinogenesis ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Humans ; Neoplasms ; genetics ; pathology ; Oncogenes ; Sirtuins ; genetics ; metabolism

Excess iron is tightly associated with tumorigenesis in multiple human cancer types through a variety of mechanisms including catalyzing the formation of mutagenic hydroxyl radicals, regulating DNA replication, repair and cell cycle progression, affecting signal transduction in cancer cells, and acting as an essential nutrient for proliferating tumor cells. Thus, multiple therapeutic strategies based on iron deprivation have been developed in cancer therapy. During the past few years, our understanding of genetic association and molecular mechanisms between iron and tumorigenesis has expanded enormously. In this review, we briefly summarize iron homeostasis in mammals, and discuss recent progresses in understanding the aberrant iron metabolism in numerous cancer types, with a focus on studies revealing altered signal transduction in cancer cells.
Carcinogenesis ; genetics ; metabolism ; Homeostasis ; Humans ; Iron ; metabolism ; Neoplasms ; genetics ; metabolism ; pathology ; Signal Transduction

Hepatocellular carcinoma (HCC) is one of the five most common malignant tumors. According to the latest statistics of the World Health Organization (WHO), the incident and mortality rates of HCC ranks the eighth and third in the world, respectively, which severely affect people's health. Exosomes are extracellular vesicles with a bilayer of phospholipids, which carry active substances such as proteins and nucleic acids derived from their mother cells. These exosomes greatly facilitate the exchange of substances and information between cells, and coordinate physiological and pathological processes in the body. In recent years, a large number of studies have shown that exosomal proteins play important roles in the tumorigenesis, development, diagnosis and treatment of HCC. Here we review the composition and functions of exosomes and the role of exosomal proteins in HCC.
Carcinogenesis/genetics* ; Carcinoma, Hepatocellular/therapy* ; Exosomes/metabolism* ; Humans ; Liver Neoplasms/therapy* ; MicroRNAs/genetics* ; Proteomics

OBJECTIVEAberrant expression of ten-eleven translocation 1 (TET1) plays a critical role in tumor development and progression. We systematically summarized the latest research progress on the role and mechanisms of TET1 in cancer biology.

DATA SOURCESRelevant articles published in English from 1980 to April 2016 were selected from the PubMed database. The terms "ten-eleven translocation 1," "5mC," "5hmC," "microRNA," "hypoxia," and "embryonic stem cell" were used for the search.

STUDY SELECTIONArticles focusing on the role and mechanism of TET1 in tumor were reviewed, including clinical and basic research articles.

RESULTSTET proteins, the key enzymes converting 5-methylcytosine to 5-hydroxymethylcytosine, play vital roles in DNA demethylation regulation. Recent studies have shown that loss of TET1 is associated with tumorigenesis and can be used as a potential biomarker for cancer therapy, which indicates that TET1 serves as tumor suppressor gene. Moreover, besides its dioxygenase activity, TET1 could induce epithelial-mesenchymal transition and act as a coactivator to regulate gene transcription, such as developmental regulator in embryonic stem cells (ESCs) and hypoxia-responsive gene in cancer. The regulation of TET1 is also correlated with microRNA in a posttranscriptional modification process. Hence, it is complex but critical to comprehend the mechanisms of TET1 in the biology of ESCs and cancer.

CONCLUSIONSTET1 not only serves as a demethylation enzyme but also plays multiple roles during tumorigenesis and progression. More studies should be carried out to elucidate the exact mechanisms of TET1 and its associations with cancer before considering it as a therapeutic tool.

Animals ; Biomarkers ; metabolism ; Carcinogenesis ; genetics ; metabolism ; pathology ; Humans ; MicroRNAs ; genetics ; Mixed Function Oxygenases ; genetics ; metabolism ; Proto-Oncogene Proteins ; genetics ; metabolism

No abstract available.
Animals ; Carcinogenesis/*genetics ; Female ; *Gene Expression Regulation, Neoplastic ; Humans ; RNA, Long Noncoding/*genetics ; Stomach Neoplasms/*genetics/*pathology

Lung cancer is one of the most important malignant tumors in the world. The morbidity and mortality rank the first in all kinds of cancer. Long non-coding RNA (lncRNA) is at least 200 nt long and has no protein coding capacity. It plays an important role in the epigenetic regulation, cell cycle regulation, the regulation of cell differentiation, and many other life activities. The studies indicate that dysregulation of lncRNAs in non-small cell lung cancer (NSCLC) tissue and blood circulation is associated with the occurrence and development of cancer. The lncRNAs play an significant role in proliferation, differentiation, migration and apoptosis of the tumor cells. Explore the potential mechanism between lncRNAs and NSCLC is beneficial for the early diagnosis, target therpy and improve prognosis. Therefore, the study aims to demonstrate the latest studies on the lncRNAs related to occurence, diagnosis, therpy and prognosis of NSCLC. It can help to deeply understanding of lncRNA, and provide new ideas for the prevention of NSCLC.
Carcinogenesis ; genetics ; Carcinoma, Non-Small-Cell Lung ; diagnosis ; drug therapy ; genetics ; pathology ; Humans ; Molecular Targeted Therapy ; RNA, Long Noncoding ; genetics

The LIM domain only 1 (LMO1) gene belongs to the LMO family of genes that encodes a group of transcriptional cofactors. This group of transcriptional cofactors regulates gene transcription by acting as a key "connector" or "scaffold" in transcription complexes. All LMOs, including LMO1, are important players in the process of tumorigenesis. Unique biological features of LMO1 distinct from other LMO members, such as its tissue-specific expression patterns, interacting proteins, and transcriptional targets, have been increasingly recognized. Studies indicated that LMO1 plays a critical oncogenic role in various types of cancers, including T-cell acute lymphoblastic leukemia, neuroblastoma, gastric cancer, lung cancer, and prostate cancer. The molecular mechanisms underlying such functions of LMO1 have also been investigated, but they are currently far from being fully elucidated. Here, we focus on reviewing the current findings on the role of LMO1 in tumorigenesis, the mechanisms of its oncogenic action, and the mechanisms that drive its aberrant activation in cancers. We also briefly review its roles in the development process and non-cancer diseases. Finally, we discuss the remaining questions and future investigations required for promoting the translation of laboratory findings to clinical applications, including cancer diagnosis and treatment.
Carcinogenesis/genetics* ; DNA-Binding Proteins/genetics* ; Gene Expression Regulation, Neoplastic ; Humans ; LIM Domain Proteins/genetics* ; Male ; Transcription Factors/metabolism*

Humans ; Carcinogenesis/genetics* ; Gene Expression Regulation, Neoplastic ; Genes, cdc ; Nasopharyngeal Carcinoma/genetics* ; Nasopharyngeal Neoplasms/genetics* ; RNA Helicases/metabolism*

Myeloid differentiation factor (MyD88) is an important adaptor protein mediating the signal transduction of most Toll-like receptors (TLR), interleukin-1 receptor (IL-1R) and interleukin-18 receptor (IL-18R) that play a key role to mediate innate immune response. Recently, activating of MYD88 L265 mutation has been reported in about of 90% lymphoplasmacytoid lymphoma/Waldenström's Macroglobulinemia, about of 29% activated type diffuse large B-cell lymphoma and other subtypes of B cell tumors demonstrating the MyD88 signaling plays an important role in B cell tumorigenesis, and inhibitors targeting MyD88 might become a new remedy for B cell tumors. In this review, the latest advances in the roles of MyD88 L265P mutation in B cell tumorigenesis were summarized.
Carcinogenesis ; Humans ; Lymphoma, Large B-Cell, Diffuse ; Mutation ; Myeloid Differentiation Factor 88 ; genetics ; Signal Transduction

Epigenetics concerns gene regulatory mechanisms beyond DNA sequence，such as DNA methylation，histone modification，chromatin remodeling，and non-coding RNA. Epigenetic mechanisms play a key role in development，cell fate decision and tumorigenesis. Chromatin modifications and its high order structure across our genome are major forms of epigenetic information，and its establishment and maintenance are closely related to cell metabolism. Metabolic changes in cancer cells include aerobic glycolysis，increased glucose uptake，abnormally active glutamine metabolism，and the use of non-conventional energy supply. These changes meet the vigorous energy and matter needs for the development and spread of cancer，and help tumor cells adapt to hypoxia microenvironment for their survival，proliferation，invasion and migration. There is a complex relationship between epigenetic modifications and cell metabolism in tumor. On the one hand，metabolites in tumor cells may act as cofactors，modification donors or antagonists of epigenetic enzymes，thus modulating the epigenetic landscape. On the other hand，epigenetic modifications can directly regulate the expression of metabolic enzymes，transporters，signaling pathway and transcription factors to affect cell metabolism. This article reviews the crosstalk between epigenetics and cancer metabolism，to explore their potential future applications in the treatment of tumors.
Carcinogenesis ; DNA Methylation ; Epigenesis, Genetic ; Gene Expression Regulation ; Humans ; Neoplasms/genetics* ; Tumor Microenvironment