ArticleEuropean journal of medical research2025
Inhibition of esophageal squamous cell carcinoma progression by MIR210HG and activation of the P53 signaling pathway to promote apoptosis and autophagy.
Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Long non-coding RNAs and autophagy: dual drivers of Hepatocellular carcinoma progression.Cell death discovery · 2025Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEsophageal squamous cell carcinoma (ESCC) stands among the frequently occurring malignancies. The lack of efficient early detection methods and therapeutic approaches leads to a high mortality rate for ESCC. The long noncoding RNA MIR210HG is strongly related to various malignant tumors. However, its involvement in ESCC remains unexplored. Thus, this investigation aimed to assess the involvement of MIR210HG in ESCC development.
methodsThe MIR210HG expression was analyzed in numerous tumor types through pan-cancer analysis of The Cancer Genome Atlas(TCGA) database. This research investigated the MIR210HG role in the survival and prognosis of individuals with ESCC. The biological functions of MIR210HG were examined by enrichment analyses, including GO, GSEA, and KEGG. Moreover, immune cell infiltration, tumor microenvironment (TME) characteristics, and immune checkpoint expression levels associated with MIR210HG were explored. To get more insight into the connection between MIR210HG and ESCC, we assessed related gene and protein expression using Western blotting and qRT-PCR. To evaluate the proliferation, invasion, migration, apoptosis, and autophagy of ESCC cells, various techniques were employed, including EdU proliferation tests, monodansylcadaverine (MDC) staining, wound healing assays, cell colony formation, transwell assays, flow cytometry, and an established xenograft mouse model.
resultsMIR210HG exhibited low expression levels in ESCC. High expression of MIR210HG correlated with a higher survival rate among patients. The elevated expression of MIR210HG hindered the ESCC cell's ability to proliferate, invade, and migrate, both in vivo and in vitro settings. Furthermore, a positive correlation between MIR210HG and the P53 signaling pathway was observed, which could affect autophagy and apoptosis in ESCC cells.
conclusionsMIR210HG emerges as a pivotal gene in ESCC, influencing both the immunity and prognosis of patients. Moreover, it may affect autophagy and apoptosis via the P53 signaling pathway. Overall, these outcomes present novel ideas for ESCC treatment.
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.