Long non-coding RNAs are known as key regulators in the progression and metastasis of breast cancer. MIAT originally has been considered as an lncRNA to be associated with a susceptibility to myocardial infarction. Here, we have detected the expression of MIAT in different cancer cells and a series of breast tumor tissue. MIAT expression was much higher in high-grade tumors compared to low-grade ones. Unlike P53 positive tumors, MIAT expression was upregulated in ER, PR, Her2 positive tumor tissues. Knockdown MIAT suppressed breast cancer cell proliferation and caused G1 arrest in cell cycle. Furthermore, downregulation of MIAT promoted apoptosis and significantly decreased migration of breast cancer cells. An increase in the expression of mir-302, mir-150, and a decrease in the expression of mir-29c were detected following MIAT silencing. More importantly, knockdown MIAT significantly elevated the expression of p16 and Cox2, which commitment cellular senescence in breast cancer cells. Altogether, our results suggest that MIAT involved in breast cancer progression and could be candidate as a novel tumor marker for diagnosis and treatment of breast cancer.
The octamer-binding transcription factor 4 (OCT4) is involved in regulating pluripotency and self-renewal maintenance of embryonic stem cells. Recently, misexpression of OCT4 has been also reported in some adult stem as well as cancer cells; a finding which is still controversial. In addition to the previously described spliced variants of the gene (e.g., OCT4A and OCT4B), we have recently identified a novel variant of the gene, designated as OCT4-B1. In this study, we investigated a potential expression and function of OCT4B1 in a series of gastric cancer tissues and a gastric adenocarcinoma cell line, AGS. Using the Taqman real-time PCR approach, we have detected the expression of OCT4B1 in tumors with no or much lower expression in marginal samples of the same patients (p < 0.002). We have also analyzed the effects of OCT4B1 knock-down in AGS cell line treated with specific siRNA directed toward OCT4B1. Our data revealed that interfering with the expression of OCT4B1 caused profound changes in the morphology and cell cycle distribution of the cells. Furthermore, down-regulation of OCT4B1 significantly elevated the relative activity of caspase-3/caspase-7 and the rate of apoptosis in the cells (more than 30%). All together, our findings suggest that OCT4B1 has a potential role in tumorigenesis of gastric cancer and candidates the variant as a new tumor marker with potential value in diagnosis and treatment of gastric cancer.On the basis of the cancer stem cell (CSC) hypothesis, a subpopulation of cells within tumors is responsible for the sustained growth and propagation of tumors. CSCs are also believed to be the main reason for the tumor relapse and resistance to therapy. These cells share various characteristics with normal tissue-specific adult stem cells, including selfrenewal potential. Based on this hypothesis, CSCs are originating either from the dysregulated self-renewal control in normal adult stem cells or through reprogramming of the somatic progenitor or differentiated cells within the tissue. [1][2][3][4][5] The octamer-binding transcription factor 4 (OCT4, also known as OCT3 and POU5F1) belongs to a family of transcription factors containing the POU DNA-binding domain. The encoded protein acts as a master self-renewal regulator in embryonic stem cells and plays a critical role in maintaining the pluripotent state of stem cells. OCT4 expression is strongly repressed following stem cell differentiation. 6-10 Several recent studies have demonstrated the unexpected expression of the OCT4 gene in some human cancer cell lines and tissues, 11-18 including gastric cancer. 19 The human OCT4 gene can potentially encode three spliced variants, designated as OCT4A, OCT4B and the newly discovered OCTB1. 20,21 OCT4A is primarily localized within the nucleus of the embryonic stem cells, where it sustains the selfrenewal and pluripotency properties of the cells. In contrast, OCT4B is mainly located within the cytoplasm of somatic cancer cell lines and apparently lacks any self-renewal regulatory role. 21,22 In ...
ES1 is a long non‐coding RNA (lncRNA) that regulates pluripotency of human embryonic stem cells, which is known to be a downstream target of stemness factors Oct4 and Nanog, and serves as a modular scaffold for Sox2. However, the role of ES1 in cancer biology is not fully characterized. The results of our study show that ES1 transcript is upregulated in both high‐grade and P53‐mutated breast tumor tissues. Knockdown experiments show that ES1 suppression in breast cancer cells restricts cancer cell proliferation and cell cycle progression. Moreover, ES1 inhibition can also induce apoptosis and cellular senescence. Additionally, our data reveal that ES1 transcript promotes cell migration as well as the epithelial to mesenchymal transition of breast cancer cells. Furthermore, loss of ES1 expression downregulates the expression of Oct4/Sox2 and consequently leads to downregulation of their targets, miR‐302 and miR‐106b. Altogether, for the first time, our findings reveal that ES1 controls the proliferation and death of breast cancer cells by regulating the Oct4/Sox2/miR‐302/miR‐106b axis.
Background: Electrochemical sensors and biosensors for pharmaceutical, food, agricultural and environmental analyses have been growing rapidly due to electrochemical behavior of drugs and biomolecules and partly due to advances in electrochemical measuring systems. In the present work, we describe the preparation of a new electrode composed of graphen (G) modified with 2,7-bis(ferrocenyl ethyl) fluoren-9-one (2,7-BFGPE) and investigate its performance for the electrocatalytic determination of methyldopa in aqueous solutions. Methods: Experimental section was carried out using cyclic voltammetry, square wave voltammetry and chronoamperometry. Results: Under the optimized conditions (pH 7.0), the square wave voltammetric peak current of methyldopa increased linearly with methyldopa concentration in the ranges of 9.0 × 10 −8 to 5.0 × 10 −4 M. The detection limit was 5.0 × 10 −8 M methyldopa. The diffusion coefficient (D= 9.35 × 10 −6 cm2/s) and electron transfer coefficient (α=0.52) for methyldopa oxidation were also determined.
The small nucleolar RNA host genes (SNHGs) belong to the long non-coding RNAs and are reported to be able to influence all three levels of cellular information-bearing molecules, that is, DNA, RNA, and proteins, resulting in the generation of complex phenomena. As the host genes of the small nucleolar RNAs (snoRNAs), they are commonly localized in the nucleolus, where they exert multiple regulatory functions orchestrating cellular homeostasis and differentiation as well as metastasis and chemoresistance. Indeed, worldwide literature has reported their involvement in the epithelial-mesenchymal transition (EMT) of different histotypes of cancer, being able to exploit peculiar features, for example, the possibility to act both in the nucleus and the cytoplasm. Moreover, SNHGs regulation is a fundamental topic to better understand their role in tumor progression albeit such mechanism is still debated. Here, we reviewed the biological functions of SNHGs in particular in the EMT process and discussed the perspectives for new cancer therapies.
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