Готові списки джерел за темами / MiR-194

Добірка наукової літератури з теми "MiR-194"

Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

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Статті в журналах з теми "MiR-194"

Tang, Hao, Ping Gong, Ling Tao, and Yurong Hua. "miR-194 Inhibits Ovarian Cancer Cell Proliferation and Reduces Cisplatin Resistance by Targeting Yes-Associated Protein." Journal of Biomaterials and Tissue Engineering 10, no. 8 (August 1, 2020): 1170–75. http://dx.doi.org/10.1166/jbt.2020.2379.

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Elevated expression of Yes-associated protein (YAP1) is associated with ovarian cancer. Bioinformatics analysis showed a relationship between miR-194 and YAP1. Our study intends to assess whether miR-194 regulates YAP1 expression and affects the proliferation of ovarian cancer cells and CDDP resistance. CDDP-resistant cell line A2780/CDDP was established and the expression of miR-194 and YAP1 in parental A2780 cells and normal ovarian epithelial IOSE80 cells were compared. A2780/CDDP cells were separated into miR-NC group and miR-194 mimic group followed by analysis of miR-194 and YAP1 expression, and cell apoptosis and proliferation by flow cytometry. There was a targeted relationship between miR-194 and YAP1 mRNA. A2780/CDDP cells had the lowest miR-194 expression followed by A2780 cells and IOSE80 cells. In addition, YAP1 level was highest in A2780/CDDP cells followed by A2780 cells and IOSE80 cells. Compared with miR-NC group, miR-194 expression was significantly increased in miR-194 mimic transfection group and YAP1 protein expression was significantly decreased, with increased cell apoptosis and reduced cell proliferation ability. Decreased miR-194 expression and increased YAP1 expression are related to ovarian cancer CDDP resistance. Increased miR-194 can down-regulate YAP1, inhibit ovarian cancer cell proliferation, promote cell apoptosis, and reduce CDDP resistance.

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Wu, Lei, Si Cheng, Yong Meng, and Yahui Huang. "miR-194 Regulates Cisplatin Resistance in Colorectal Cancer Cells Through Targeting Yes-Associated Protein." Journal of Biomaterials and Tissue Engineering 10, no. 2 (February 1, 2020): 157–62. http://dx.doi.org/10.1166/jbt.2020.2239.

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Elevated Yes-associated protein (YAP1) expression is associated with colorectal cancer. Bioinfor-matics analysis showed a targeting relationship between miR-194 and YAP13′-UTR. Our study assessed miR-194’s role in proliferation, apoptosis, and CDDP resistance of colorectal cancer cells. The CDDP-resistant cell line SW480/CDDP was established and miR-194 and YAP1 level in parental SW480 cells and normal intestinal epithelial HCoEpiC cells was measured. SW480/CDDP cells were separated into control group, miR-NC group and miR-194 mimic group followed by analysis of miR-194 and YAP1 level, cell apoptosis and proliferation by flow cytometry. There was a targeted regulatory relationship between miR-194 and YAP1 mRNA. miR-194 was significantly upregulated in SW480/CDDP cells compared to SW480 cells and downregulated in SW480 cells compared to HCoEpiC cells. Whereas, opposite YAP1 expression profiles were found in SW480/CDDP, SW480 and HCoEpiC cells. miR-194 mimic significantly upregulated miR-194 in the SW480/CDDP cells, with decreased YAP1 expression, increased cell apoptosis, decreased cell proliferation and reduced IC50. Decreased miR-194 and increased YAP1 expression involve in CDDP resistance of colorectal cancer. Increase of miR-194 expression can inhibit colorectal cancer cell proliferation, promote apoptosis and reduce CDDP resistance by down-regulating YAP1 expression.

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Lin, Dao-Hong, Peng Yue, Chengbiao Zhang, and Wen-Hui Wang. "MicroRNA-194 (miR-194) regulates ROMK channel activity by targeting intersectin 1." American Journal of Physiology-Renal Physiology 306, no. 1 (January 1, 2014): F53—F60. http://dx.doi.org/10.1152/ajprenal.00349.2013.

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The aim of the study is to explore the role of miR-194 in mediating the effect of high-K (HK) intake on ROMK channel. Northern blot analysis showed that miR-194 was expressed in kidney and that HK intake increased while low-K intake decreased the expression of miR-194. Real-time PCR analysis further demonstrated that HK intake increased the miR-194 expression in the cortical collecting duct. HK intake decreased the expression of intersectin 1 (ITSN1) which enhanced With-No-Lysine Kinase (WNK)-induced endocytosis of ROMK. Expression of miR-194 mimic decreased luciferase reporter gene activity in HEK293 T cells transfected with ITSN-1–3′UTR containing the complementary seed sequence for miR-194. In contrast, transfection of miR-194 inhibitor increased the luciferase activity. This effect was absent in the cells transfected with mutated 3′UTR of ITSN1 in which the complimentary seed sequence was deleted. Moreover, the inhibition of miR-194 expression increased the protein level of endogenous ITSN1 in HEK293T cells. Expression of miR-194 mimic also decreased the translation of exogenous ITSN1 in the cells transfected with the ITSN1 containing 3′UTR but not with 3′UTR-free ITSN1. Expression of pre-miR-194 increased K currents and ROMK expression in the plasma membrane in ROMK-transfected cells. Coexpression of ITSN1 reversed the stimulatory effect of miR-194 on ROMK channels. This effect was reversed by coexpression of ITSN1. We conclude that miR-194 regulates ROMK channel activity by modulating ITSN1 expression thereby enhancing ITSN1/WNK-dependent endocytosis. It is possible that miR-194 is involved in mediating the effect of a HK intake on ROMK channel activity.

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Miao, Jinglei, Weiguo Wang, Song Wu, Xiaofang Zang, Yuezhan Li, Jianlong Wang, Ruisen Zhan, et al. "miR-194 Suppresses Proliferation and Migration and Promotes Apoptosis of Osteosarcoma Cells by Targeting CDH2." Cellular Physiology and Biochemistry 45, no. 5 (2018): 1966–74. http://dx.doi.org/10.1159/000487973.

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Background/Aims: Studies have shown that miR-194 functions as a tumour suppressor and is associated with tumour growth and metastasis. This study intends to uncover the mechanism of tumour suppression by miR-194. The expression of miR-194 in osteosarcoma cell lines and tissues were monitored by real-time PCR. Methods: The proliferation ability was examined by MTT assay. Migration and apoptosis of cells were monitored by migration assay and flow cytometry, respectively. The regulation of miR-194 on CDH2 was determined by luciferase assays and western blot assays. Results: The results showed that miR-194 was significantly reduced in osteosarcoma compared with that in normal bone tissue. Overexpression of miR-194 significantly attenuated the proliferation and migration and induced the apoptosis of osteosarcoma cells. Furthermore, we demonstrated that miR-194 has inhibited the malignant behaviour of osteosarcoma by downregulating CDH2 expression. Conclusions: These findings suggested that miR-194 may act as a tumour suppressor in osteosarcoma. miR-194/CDH2 may be a novel therapeutic target in the treatment of osteosarcoma.

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Cui, Guanghui, Donglei Liu, Weihao Li, Yuhang Li, Youguang Liang, Wensong Shi, and Song Zhao. "Original Research: miR-194 inhibits proliferation and invasion and promotes apoptosis by targeting KDM5B in esophageal squamous cell carcinoma cells." Experimental Biology and Medicine 242, no. 1 (August 10, 2016): 45–52. http://dx.doi.org/10.1177/1535370216662712.

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Increasing evidence suggests that miR-194 is down-regulated in esophageal squamous cell carcinoma tumor tissue. However, the role and underlying mechanism of miR-194 in esophageal squamous cell carcinoma have not been well defined. We used DIANA, TargetScan and miRanda to perform target prediction analysis and found KDM5B is a potential target of miR-194. Based on these findings, we speculated that miR-194 might play a role in esophageal squamous cell carcinoma development and progression by regulation the expression of KDM5B. We detected the expression of miR-194 and KDM5B by quantitative real-time reverse transcription PCR (qRT-PCR) and Western blot assays, respectively, and found down-regulation of miR-194 and up-regulation of KDM5B existed in esophageal squamous cell carcinoma cell lines. By detecting proliferation, invasion and apoptosis of TE6 and TE14 cells transfected with miR-194 mimics or mimic control, miR-194 was found to inhibit proliferation and invasion and promote apoptosis of esophageal squamous cell carcinoma cells. miR-194 was further verified to regulate proliferation, apoptosis and invasion of esophageal squamous cell carcinoma cells by directly targeting KDM5B. Furthermore, animal studies were performed and showed that overexpression of miR-194 inhibited the growth of esophageal squamous cell carcinoma tumors in vivo. These results confirmed our speculation that miR-194 targets KDM5B to inhibit esophageal squamous cell carcinoma development and progression. These findings offer new clues for esophageal squamous cell carcinoma development and progression and novel potential therapeutic targets for esophageal squamous cell carcinoma.

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Jenkins, Robert H., John Martin, Aled O. Phillips, Timothy Bowen та Donald J. Fraser. "Transforming growth factor β1 represses proximal tubular cell microRNA-192 expression through decreased hepatocyte nuclear factor DNA binding". Biochemical Journal 443, № 2 (27 березня 2012): 407–16. http://dx.doi.org/10.1042/bj20111861.

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miR (microRNA)-192 plays key roles in renal pathological and physiological responses, by repressing targets including Zeb1, Zeb2 and Wnk1. In the present study, we have assessed the regulation of miR-192 expression. We found that TGF-β1 (transforming growth factor β1) down-regulates miR-192 and miR-194, co-transcribed in the shared precursor pri-miR (primary miR transcript)-192/194. Luciferase reporter analysis showed constitutive promoter activity within nucleotides +21 to −223. We identified HNF (hepatocyte nuclear factor) and p53 binding sites within this region that were required for constitutive promoter activity, which was decreased by TGF-β1 through an Alk5-dependent mechanism. TGF-β1 treatment decreased HNF binding to the miR-194-2/192 promoter, whereas knockdown of HNF-1 inhibited mature miR-192 and miR-194 expression. miR-192, miR-194 and HNF expression were restricted to a defined subset of human tissues including kidney, small intestine, colon and liver. Our results from the present study identify co-ordinated regulation of miR-192 and miR-194, with binding of HNF and p53 transcription factors necessary for activation of transcription, and TGF-β1-mediated repression through decreased HNF binding to its cognate promoter element.

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Xu, Zhishan, Bingyu Guo, Peng Chang, Qiang Hui, Wei Li, and Kai Tao. "The Differential Expression of miRNAs and a Preliminary Study on the Mechanism of miR-194-3p in Keloids." BioMed Research International 2019 (March 7, 2019): 1–10. http://dx.doi.org/10.1155/2019/8214923.

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The aim of this study was to detect abnormally expressed microRNA (miRNA) in keloids and to study their functions. The differential expression of miRNAs in keloids and normal tissue was detected by gene microarray. MiRNA expression was verified by real-time PCR. A luciferase reporter gene assay, western blot, and real-time PCR were used to detect the effect of miR-194-3p on RUNX2. An MTT assay and a transwell assay were used to detect the effect of miR-194-3p in both primary cultured fibroblasts and HKF cells. Related proteins were analysed by western blot and real-time PCR. The expression of miR-194-3p was lower in keloids, and MiR-194-3p was shown to target RUNX2 directly. MiR-194-3p inhibited the proliferation and migration of fibroblasts through the inhibition of CDK4 and MMP2. MiR-194-3p and RUNX2 may become new targets for the prevention and treatment of keloids.

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Yen, Yu-Ting, Jou-Chun Yang, Jiun-Bo Chang, and Shih-Chang Tsai. "Down-Regulation of miR-194-5p for Predicting Metastasis in Breast Cancer Cells." International Journal of Molecular Sciences 23, no. 1 (December 28, 2021): 325. http://dx.doi.org/10.3390/ijms23010325.

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MicroRNAs (miRNAs), as key negative regulators of gene expression, are closely related to tumor occurrence and progression. miR-194-5p (miR-194-1) has been shown to play a regulatory role in various cancers however, its biological function and mechanism of action in breast cancer have not yet been well explored. In this study, we use the UALCAN and LinkedOmics databases to analyze transcription expression in The Cancer Genome Atlas Breast Invasive Carcinoma (TCGA-BRCA). The epithelial-mesenchymal transition status of breast cancer cells was evaluated by wound-healing assay, trans-well assays, and gelatin zymography, while protein expression was assessed by Western blotting. miR-194-5p expression was found to be up-regulated in breast cancer clinical specimens but down-regulated in the triple-negative breast cancer (TNBC) cell line MDA-MB-231 and breast cancer clinical specimens in The Cancer Genome Atlas (TCGA). miR-194-5p significantly inhibited the expression of the epithelial marker ZO-1 and increased the expression of mesenchymal markers, including ZEB-1 and vimentin, in MDA-MB-231 cells. miR-194-5p significantly reduced the gelatin-degrading activity of matrix metalloproteinase-2 (MMP-2) and MMP-9 in zymography assays. In MDA-MB-231 cells and TCGA patient samples, ZEB-1 expression was significantly inversely correlated with miR-194-5p expression. High levels of miR-194-5p were associated with good overall survival. miR-194-5p regulates epithelial–mesenchymal transition (EMT) in TNBC. Our findings suggest that miR-194-5p functions as a tumor biomarker in breast cancer, providing new insights for the study of breast cancer development and metastasis.

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Niu, Tong, Liuzhong Jin, Shizhen Niu, Cunqi Gong, and Hui Wang. "Lycium Barbarum Polysaccharides Alleviates Oxidative Damage Induced by H2O2 Through Down-Regulating MicroRNA-194 in PC-12 and SH-SY5Y Cells." Cellular Physiology and Biochemistry 50, no. 2 (2018): 460–72. http://dx.doi.org/10.1159/000494159.

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Background/Aims: Currently, scientists attempt to improve outcome of spinal cord injury (SCI) via reducing secondary injury during SCI. Oxidative stress is critical for pathophysiology of secondary damage, thus we mainly focused on the anti-oxidant effects of Lycium barbarum polysaccharides (LBPs) on PC-12 and SH-SY5Y cells as well as the underlying mechanisms. Methods: Oxidative stress was induced by H2O2 stimulation. Effects of LBPs on cell viability, apoptosis, and expression of proteins associated with apoptosis and autophagy in H2O2-induced cells were assessed by CCK-8 assay, flow cytometry assay and Western blot analysis, respectively. Then, expression of miR-194 was determined by qRT-PCR. Expression of miR-194 was dysregulated, and whether LBPs affected H2O2-treated cells through modulating miR-194 was verified. The expression of key kinases in the PI3K/AKT pathway and the intracellular levels of ROS and NO were testified by Western blot analysis and flow cytometry with fluorescent probes. Results: H2O2-induced decrease of cell viability and increases of apoptosis and autophagy in PC-12 cells were mitigated by LBPs treatment. Next, we found that miR-194 expression was both down-regulated by LBPs treatment in PC-12 and SH-SY5Y cells. More experiments consolidated that influence of LBPs on H2O2-treated cells was reversed by miR-194 overexpression while was augmented by miR-194 inhibition. LBPs elevated the phosphorylated levels of PI3K and AKT and reduced levels of ROS and NO through miR-194. Conclusion: LBPs alleviated H2O2-induced decrease of cell viability, and increase of apoptosis and autophagy through down-regulating miR-194. Moreover, LBPs activated the PI3K/AKT pathway and reduced oxidative stress through miR-194.

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Li, Chang-feng, Yong-chao Li, Yun Wang, and Li-bo Sun. "The Effect of LncRNA H19/miR-194-5p Axis on the Epithelial-Mesenchymal Transition of Colorectal Adenocarcinoma." Cellular Physiology and Biochemistry 50, no. 1 (2018): 196–213. http://dx.doi.org/10.1159/000493968.

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Background/Aims: Since the combined actions of lncRNAs and miRNAs have been considered to be involved in the occurrence and development of various neoplasms, the main purpose of this study was to discover whether and how lncRNA H19 and miR-194 influenced the epithelial-mesenchymal transition (EMT) process of colorectal adenocarcinoma (CRA). Methods: Totally 214 pairs of CRA and adjacent normal tissues were collected, and 5 human CRA cell lines (i.e. HCT116, HT-29, RKO SW280 and Lovo) were purchased. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was adopted to quantify the H19 and miR-194-5p expressions in cells and tissues. The expressions of FoxM1, E-cadherin, vimentin, N-cadherin were determined using western blot. On the side, si-H19, si-NC, miR-194-5p mimic, miR-194-5p inhibitor and negative control (NC) were transfected into CRA cell lines. Meanwhile, the invasive, migratory and proliferative conditions of the cells were assessed through transwell, wound healing and colony-forming experiments, with final verification of the relationship between H19 and miR-194-5p employing dual-luciferase reporter gene assay. Results: Highly-expressed H19, lowly-expressed miR-194-5p, low-grade differentiation and lymph node metastasis appeared as the independent predictors of unfavorable prognosis in CRA patients’ (all P< 0.05). It indicated that FoxM1 expression displayed positive correlations with H19 expression, yet negative associations with miR-194-5p expression within CRA tissues (P< 0.05). In addition, transfection of H19-siRNA and miR-145-5p mimic triggered a conspicuous increase in E-cadherin expression, as well as an evidently down-regulation in vimentin and N-cadherin expressions within HT29 and RKO cells (P< 0.05). On the other hand, the invasive and migratory capacities of CRA cells were significantly hindered (P< 0.05). Moreover, the luciferase reporter gene assay confirmed that H19 modified miR-194-5p expression through directly targeting at it (P< 0.05). Ultimately, FoxM1 could reverse the role of miR-194-5p in inhibiting invasion, migration and EMT of CRA cells (P< 0.05). Conclusion: LncRNA H19/miR-194/FoxM1 axis could serve as a profound target for the diagnosis and treatment of CRA.

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Більше джерел

Дисертації з теми "MiR-194"

Fernandes, Rayzel Candida. "The role of microRNA-194 in prostate cancer progression." Thesis, 2019. http://hdl.handle.net/2440/124148.

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Prostate cancer is a major cause of cancer-related mortality in Australia men. Mortality is primarily due to metastasis and the development of resistance to therapy. While prostate cancer is primarily driven by the androgen receptor signalling, a number of other factors play important roles in its growth and progression. In particular, small non-coding RNA molecules called microRNAs (miRNAs) are known to be key regulators of progression in prostate cancer. Our group previously identified one specific miRNA, miR-194-5p (miR-194), as an important driver of prostate cancer metastasis; however, the molecular mechanisms by miR-194 mediates these effects is not fully understood. My PhD project aimed to identify target genes and pathways that miR-194 regulates in order to better understand its role in prostate cancer. I used cutting-edge genomic techniques and bioinformatics to identify 163 miR-194 target genes in prostate cancer. In Chapter 3, I used this data to identify a new role for miR-194 in prostate cancer. More specifically, I found that miR-194 activity was inversely correlated with androgen receptor (AR) activity in clinical samples, an observation explained mechanistically by AR-mediated repression of miR-194 expression. In concordance with these findings, miR-194 activity was significantly elevated in treatment-induced neuroendocrine prostate cancer (NEPC), an aggressive AR-independent subtype of prostate cancer. Furthermore, miR-194 can enhance transdifferentiation of epithelial LNCaP cells to neuroendocrine-like cells, a function mediated at least in part by its ability to target the FOXA1 transcription factor. Importantly, targeting miR-194 effectively inhibited the growth of aggressive models of NEPC, including patient-derived organoids. By integrating the miR-194 “targetome” with transcriptomic data, my work has provided important insights into miRNA function in cancer cells (Chapter 4). Specifically, I have found that miR-194 functions potently through canonical interactions and can mediate co-operative repression through targeting multiple sites in the same mRNA transcript. Further, I have demonstrated that miR-194 is associated with widespread non-canonical interactions that can regulate gene expression, albeit to a lesser extent than canonical sites. Finally, in Chapter 5 I have demonstrated that miR-194 has dichotomous effects on proliferation and invasion in breast and prostate cancer despite both cancers having several underlying biological similarities. Furthermore, in breast cancer I have found that miR-194 inhibits estrogen receptor expression, potentially by targeting FOXA1. Overall, my work has provided unique insights into the pathobiology of miR-194, demonstrated its role as a potential therapeutic target in aggressive AR-independent prostate cancer subtypes, and identified novel functions for miR-194 in breast cancer.
Thesis (Ph.D.) -- University of Adelaide, School of Medicine, 2020

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Частини книг з теми "MiR-194"

Okwudiri Ihegboro, Godwin, and Chimaobi James Ononamadu. "Drug-Induced Hepatotoxicity." In Hepatotoxicity [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.103766.

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This chapter aims at discussing the consequential effects of drug-induced hepatotoxicity on man. The liver carries out drug detoxification among other roles, but sometimes, drug toxicity can occur caused by either medication overdose or imbalance drug metabolic reactions (Phase 1 & 2), resulting in the formation of reactive (toxic) metabolites (electrophilic compounds or free radicals) that binds covalently to hepatocytes, leading to liver injury/diseases like acute and chronic hepatitis, cholestasis, steatosis among others. Mitochondrial dysfunction, oxidative stress and lipid peroxidation are some of the mechanisms of liver injury. Furthermore, drug hepatotoxicity results in hepatocellular, gastroenterological, cholestatic as well as immunological disorders. The clinical manifestations of drug toxicity arise from the abnormalities observed in liver’s biochemical and molecular indicators. Our findings, revealed that in the event of liver injury, liver function indices like aspartate and alanine aminotransferases, ALP (alkaline phosphatase) and gamma glutamyl transferase (GGT) activities, intracellular calcium (Ca2+) and lipid peroxidation increases whereas indices of oxidative stress such as glutathione and its allies, catalase and superoxide dismutase activity deplete. At molecular level, the gene expression levels of Bcl-2 mRNA and microRNA genes (miR-122, 192 and 194) reduces while mitochondrial genes (MMP-2 and MMP-9) overexpresses. Since drug abuse is deleterious to human health, therefore, adherence to doctors’ prescription guidelines should be followed.

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Тези доповідей конференцій з теми "MiR-194"

Zhai, Haiyan, Mihriban Karaayvaz, Peixin Dong, Noriaki Sakuragi, and Jingfang Ju. "Abstract 5293: Prognostic significance of miR-194 in endometrial cancer." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5293.

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Prema, Sundaram, Stacy Hultine, Lauren Smith, Dauren Biyashev, Janell Schelter, Michele Cleary, Olga Volpert, Andrei Thomas-Tikhonenko, and Andrei Thomas-Tikhonenko. "Abstract 3275: miR-194 counterbalances transcriptional activation of the anti-angiogenic factor thrombospondin-1 by p53." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3275.

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Le, Xiao-Feng, Riccardo Spizzo, Maggie Mao, Yun Wu, George A. Calin, and Robert C. Bast. "Abstract 2051: DNA (cytosine-5-)-methyltransferases 3A (DNMT3A) is a direct target of miR-194 in breast cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2051.

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Nakamura, Koji, Kenjiro Sawada, Akihiko Yoshimura, Erica Nakatsuka, Yasuto Kinose, Seiji Mabuchi, and Tadashi Kimura. "Abstract 3436: MiR-194 modulates paclitaxel resistance in ovarian cancer cells through the regulation of MDM-2 expression." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3436.

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Singh, Rajbir, Kamalakannan Palanichamy, John R. Jacob, and Arnab Chakravarti. "Abstract 1113: Mir-194-3p suppresses tumorigenic potential of glioblastoma stem cells by targeting the canonical NF-kB pathway." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1113.

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Valastyan, Scott, Amelia Chang, Nathan Benaich, Ferenc Reinhardt, and Robert A. Weinberg. "Abstract LB-194: Restoration of miR-31 function in already-established metastases elicits an anti-metastatic therapeutic responsein vivo." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-194.

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Wang, Anxun, Luodan Zhao, Qianting He, Tingting Zhao, Wei Wang, and Xiaofeng Zhou. "Abstract 194: Deregulation of miR-222-ABCG2 regulatory module in tongue squamous cell carcinoma contributes to chemoresistance and enhanced metastatic potential." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-194.

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Nakamura, Koji, Kenjiro Sawada, Yasuto Kinose, Kae Hashimoto, Seiji Mabuchi, and Tadashi Kimura. "Abstract 4386: Identification of microRNA which regulates paclitaxel resistance of ovarian cancer cells - a potential of miR-194 by attenuating paclitaxel resistance through the down-regulation of oncogene BMI-1." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4386.

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