ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
Direct targeting of HGF by miR-16 regulates proliferation and migration in gastric cancer.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Serum miR-16 as a potential biomarker for human cancer diagnosis: results from a large-scale population.Journal of cancer research and clinical oncology · 2019Pooled it
- Hepatocyte growth factor/c-Met signaling axis in human diseases: Mechanistic insights and therapeutic potential.Journal of cell communication and signaling · 2026Review
- Research progress on the development of hepatocyte growth factor/c-Met signaling pathway in gastric cancer: A review.World journal of gastrointestinal oncology · 2024Review
- Ferroptosis regulating lipid peroxidation metabolism in the occurrence and development of gastric cancer.World journal of gastrointestinal oncology · 2024Article
- Identification of tumor biomarkers for pathological complete response to neoadjuvant treatment in locally advanced breast cancer.Breast cancer research and treatment · 2022Article
- The therapeutic potential of stem cell-derived exosomes in the ulcerative colitis and colorectal cancer.Stem cell research & therapy · 2022Review
- MicroRNAs and Long Non-coding RNAs in c-Met-Regulated Cancers.Frontiers in cell and developmental biology · 2020Review
- Crosstalk Mechanisms Between HGF/c-Met Axis and ncRNAs in Malignancy.Frontiers in cell and developmental biology · 2020Review
- Oncogenic role of long non-coding RNA SNHG12 in gastric cancer cells by targeting miR-16.Experimental and therapeutic medicine · 2019Article
- Identify gene expression pattern change at transcriptional and post-transcriptional levels.Transcription · 2019Article
- HGF/c-MET: A Promising Therapeutic Target in the Digestive System Cancers.International journal of molecular sciences · 2018Review
- Clinical utility of circulating non-coding RNAs - an update.Nature reviews. Clinical oncology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) have been reported to be involved in each stage of tumor development in various types of cancers. We have previously showed that miR-16 is downregulated in cancer and acts as a tumor suppressor. Other studies indicated that hepatocyte growth factor (HGF)/c-Met is implicated in proliferation, migration, and other pathophysiological processes. However, little is known about the relationship between miR-16 and HGF/c-Met in gastric cancer (GC). In the present study, we used bioinformatics tools and related experiments to search for miRNAs targeting HGF. Here, we found that miR-16 suppressed HGF protein expression by directly targeting 3'-untranslated region (UTR) of HGF mRNA. Subsequently, it was illustrated the downregulation of miR-16 promotes, while overexpressed of miR-16 significantly inhibits cell proliferation and migration by negatively regulating HGF/c-Met pathway. Moreover, the biological role of HGF in GC cells was determined by using HGF siRNA and HGF-overexpressing plasmid, respectively. To conclude, our results provide a potential target by using miR-16 for the future clinical treatment of GC.
Indexed as
Identifiers
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.