Initial study of microRNA expression profiles of colonic cancer without lymph node metastasis

Wang, Ying Xin; Zhang, Xiao Yan; Zhang, Bao Feng; Yang, Chang; Chen, Xi Mei; Gao, Heng

doi:10.1111/j.1751-2980.2009.00413.x

Cited by 195 publications

(142 citation statements)

References 36 publications

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“…We identified 19 new miRNAs deregulated in CRC ( Table 1) that, to our knowledge, have never before been reported in cancer. We found deregulation of miR-1, miR-195, miR-143, miR-215, miR-31, miR-194, miR-30c, miR-133b, miR-192, miR-30b, miR-378*, miR-137, miR-133a, and miR-378 in CRC, which is consistent with earlier reports of miRNA expression in CRC (Michael et al, 2003;Bandres et al, 2006;Cummins et al, 2006;Volinia et al, 2006;Monzo et al, 2008;Arndt et al, 2009;Earle et al, 2010;Wang et al, 2010). Down-regulation of miR-378 in CRC compared with normal, observed in both our microarray and RT-PCR analysis, was also seen in a study by Wang et al (2010), who compared para-cancerous tissues and colorectal cancer samples.…”

Section: Mirna Profiling In Crc Versus Normal Colon Tissuesupporting

confidence: 82%

MicroRNA profiling differentiates colorectal cancer according to KRAS status

Mosakhani

Sarhadi

Borze

et al. 2011

Genes Chromosomes & Cancer

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Recent studies have shown the important role of microRNAs (miRNAs) in a variety of biological processes, and in its ability to distinguish tumors according to their prognostic and predictive properties. To identify miRNA signatures associated with colorectal carcinoma (CRC) and with KRAS status, we studied, using Agilent's miRNA microarrays, miRNA expression in primary tumors from 55 metastatic CRC patients, including 15 with mutant and 40 with wild-type KRAS. Comparing these with normal colon tissue, we identified 49 miRNAs-including 19 novel miRNAs-significantly deregulated in tumor tissue. The presence of the KRAS mutation was associated with up-regulation of miR-127-3p, miR-92a, and miR-486-3p and down-regulation of miR-378. Increased expression of miR-127-3p and miR-92a in KRAS mutant tumors was significantly confirmed by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) (P < 0.05). We identified some predicted target genes of differentially expressed miRNAs between mutated and wild-type KRAS, such as RSG3 and TOB1, which are involved in apoptosis and proliferation. Target prediction and pathway analysis suggest a possible role for deregulated miRNAs in nicotinamide adenine dinucleotide phosphate (NADPH) regeneration and G protein-coupled receptor signaling pathways.

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Section: Mirna Profiling In Crc Versus Normal Colon Tissuesupporting

confidence: 82%

MicroRNA profiling differentiates colorectal cancer according to KRAS status

Mosakhani

Sarhadi

Borze

et al. 2011

Genes Chromosomes & Cancer

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“…36 Particularly, the roles of miR-196a in cancer are elusive. Some reports suggest that miR-196a plays an oncogenic role in tumor development, 37,38 while others indicate that miR-196a may be a tumor suppressor. For instance, it was reported that the expression of miR-196a was dramatically decreased in melanoma cells when compared with healthy control melanocytes, and the low miR-196a expression in melanoma cells enhanced migratory potential of these melanoma cells.…”

Section: Discussionmentioning

confidence: 99%

IKKα-mediated biogenesis of miR-196a through interaction with Drosha regulates the sensitivity of cancer cells to radiotherapy

et al. 2016

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Radioresistance is a major obstacle in successful clinical cancer radiotherapy, and the underlying mechanisms are not clear. Here we show that IKKα-mediated miR-196a biogenesis via interaction with Drosha regulates the sensitivity of nasopharyngeal carcinoma (NPC) cells to radiotherapy. Phosphorylation of IKKα at T23 site (p-IKKαT23) promotes the binding of IKKα to Drosha that accelerates the processing of miR-196a primary transcripts, leading to increased expressions of both precursor and mature miR-196a. Dephosphorylation of p-IKKαT23 downregulates miR-196a expression and promotes the resistance of NPC cells to radiation treatment. The miR-196a mimic suppresses while its inhibitor promotes the resistance of NPC to radiation treatment. Importantly, the expression of p-IKKαT23 is positively related to the expression of miR-196a in human NPC tissues, and expression of p-IKKαT23 and miR-196a is inversely correlated with NPC clinical radioresistance. Thus, our studies establish a novel mechanistic link between the inactivation of IKKαT23-Drosha-miR-196a pathway and NPC radioresistance, and de-inactivation of IKKαT23-Drosha-miR-196a pathway would be an efficient way to restore the sensitivity of radioresistant NPC to radiotherapy.

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“…The underlined genes miR-34a, miR-191 and miR-378 were reported to be up-regulated in some studies [71][72][73] and down-regulated in others [74][75][76] . healthy controls.…”

Section: Mirna Biomarkers In Bloodmentioning

confidence: 99%

Advances in epigenetic biomarker research in colorectal cancer

Kuang

2014

WJG

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Colorectal cancer (CRC) causes approximately 600000 deaths annually and is the third leading cause of cancer mortality worldwide. Despite significant advancements in treatment options, CRC patient survival is still poor owing to a lack of effective tools for early diagnosis and a limited capacity for optimal therapeutic decision making. Since there exists a need to find new biomarkers to improve diagnosis of CRC, the research on epigenetic biomarkers for molecular diagnostics encourages the translation of this field from the bench to clinical practice. Epigenetic alterations are thought to hold great promise as tumor biomarkers. In this review, we will primarily focus on recent advances in the study of epigenetic biomarkers for colorectal cancer and discuss epigenetic biomarkers, including DNA methylation, microRNA expression and histone modification, in cancer tissue, stool, plasma, serum, cell lines and xenografts. These studies have improved the chances that epigenetic biomarkers will find a place in the clinical practices of screening, early diagnosis, prognosis, therapy choice and recurrence surveillance for CRC patients. However, these studies have typically been small in size, and evaluation at a larger scale of well-controlled randomized clinical trials is the next step that is necessary to increase the quality of epigenetic biomarkers and ensure their widespread clinical use.

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Initial study of microRNA expression profiles of colonic cancer without lymph node metastasis

Cited by 195 publications

References 36 publications

MicroRNA profiling differentiates colorectal cancer according to KRAS status

MicroRNA profiling differentiates colorectal cancer according to KRAS status

IKKα-mediated biogenesis of miR-196a through interaction with Drosha regulates the sensitivity of cancer cells to radiotherapy

Advances in epigenetic biomarker research in colorectal cancer

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