ArticleAmerican journal of translational research2016
MicroRNA-130a regulates cell malignancy by targeting RECK in chronic myeloid leukemia.
Article in American journal of translational research, 2016. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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, 14 citations in OpenAlex.
- RECK as a Potential Crucial Molecule for the Targeted Treatment of Sepsis.Journal of inflammation research · 2025Review
- Stem Cell Responsiveness to Imatinib in Chronic Myeloid Leukemia.International journal of molecular sciences · 2023Article
- Overexpression of microRNA-130a represses uveal melanoma cell migration and invasion through inactivation of the Wnt/β-catenin signaling pathway by downregulating USP6.Cancer gene therapy · 2022Article
- MiR-125a-3p and MiR-320b Differentially Expressed in Patients with Chronic Myeloid Leukemia Treated with Allogeneic Hematopoietic Stem Cell Transplantation and Imatinib Mesylate.International journal of molecular sciences · 2021Article
- MicroRNA-130a inhibits proliferation of vascular smooth muscle cells by suppressing autophagy via ATG2B.Journal of cellular and molecular medicine · 2021Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence has indicated that microRNAs are involved in tumor development and progression, acting as either tumor suppressors or oncogenes. In this study, we aimed to investigate the role of miR-130a in the pathogenesis of chronic myeloid leukemia (CML). Functional studies indicate that over-expression of miR-130a in A562 CML cells dramatically suppresses cell proliferation and induces cell apoptosis both in vitro and in vivo. Furthermore, we demonstrate that the transcriptional regulator RECK is a target of miR-130a. In conclusion, our study suggests that miR-130a may function as a novel tumor suppressor in CML, and its anti-oncogenic activity may involve the direct targeting and inhibition of RECK.
Indexed as
Identifiers
27158382PMC4846939W2366198723What 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.