ArticleGenes & cancer2018
MicroRNA-messenger RNA interactions involving JAK-STAT signaling genes in colorectal cancer.
Article in Genes & cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Exploring the molecular pathways of miRNAs in testicular cancer: from diagnosis to therapeutic innovations.Functional & integrative genomics · 2025Review
- Inhibitory effect of miR-377 on the proliferative and invasive behaviors of prostate cancer cells through the modulation of MYC mRNA via its interaction with BCL-2/Bax, PTEN, and CDK4.Genes & cancer · 2024Article
- Important players in carcinogenesis as potential targets in cancer therapy: an update.Oncotarget · 2020Review
- Identification of Cerebrospinal Fluid MicroRNAs Associated With Leptomeningeal Metastasis From Lung Adenocarcinoma.Frontiers in oncology · 2020Article
- TYK2: An Upstream Kinase of STATs in Cancer.Cancers · 2019Review
- The functional role of miRNAs in colorectal cancer: insights from a large population-based study.Cancer biology & medicine · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
JAK-STAT signaling influences many downstream processes that, unchecked, contribute to carcinogenesis and metastasis. MicroRNAs (miRNAs) are hypothesized as a mechanism to prevent uncontrolled growth from continuous JAK-STAT activation. We investigated differential expression between paired carcinoma and normal colorectal mucosa of messenger RNAs (mRNAs) and miRNAs using RNA-Seq and Agilent Human miRNA Microarray V19.0 data, respectively, using a negative binomial mixed effects model to test 122 JAK-STAT-signaling genes in 217 colorectal cancer (CRC) cases. Overall, 42 mRNAs were differentially expressed with a fold change of >1.50 or <0.67, remaining significant with a false discovery rate of < 0.05; four were dysregulated in microsatellite stable (MSS) tumors, eight were for microsatellite unstable (MSI)-specific tumors. Of these 54 mRNAs, 17 were associated with differential expression of 46 miRNAs, comprising 116 interactions: 16 were significant overall, one for MSS tumors only. Twenty of the 29 interactions with negative beta coefficients involved miRNA seed sequence matches with mRNAs, supporting miRNA-mediated mRNA repression; 17 of these mRNAs encode for receptor molecules. Receptor molecule degradation is an established JAK-STAT signaling control mechanism; our results suggest that miRNAs facilitate this process. Interactions involving positive beta coefficients may illustrate downstream effects of disrupted STAT activity, and subsequent miRNA upregulation.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.