ArticleDiscover oncology2024
miR-328-3p suppresses hepatocellular carcinoma progression by regulating HMOX1 expression.
Article in Discover oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- A reliable prognostic model for hepatocellular carcinoma using neutrophil extracellular traps and immune related genes.Scientific reports · 2025Article
- Tumor Suppressive Role of Hsa-miR-328-3p in Colon Cancer by RegulatingCancer genomics & proteomicsArticle
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
introductionMost oncogenic genes contribute to cancer progression, but their role and regulatory mechanisms are not yet fully understood in hepatocellular carcinoma (HCC). This study aimed to explore the role of miR-328-3p and the regulatory relationship between miR-328-3p and HMOX1 in HCC.
methodsWe utilized Cox and LASSO regression to identify a panel of oncogenic genes associated with hepatocellular carcinoma (HCC) progression within the TCGA-LIHC cohort and the GSE104580 dataset. The expression levels of the hub gene, HMOX1, were assessed in HCC cell lines using qPCR. The functional roles of miR-328-3p and HMOX1 were evaluated through a series of in vitro assays, including CCK-8 for proliferation, colony formation, wound healing, and Transwell assays for migration and invasion. The direct interaction between miR-328-3p and HMOX1 was explored using a luciferase reporter assay, Western blot (WB) for protein expression analysis, and functional assays to determine the impact on cell proliferation and migration.
resultsEight candidate genes (BIRC5, TNSF4, SPP1, HMOX1, ADM, RBP2, IGF1, and LECT2) were screen out. The hub gene HMOX1 among had high expression level in HCC cell lines. High HMOX1 expressing cell line had significantly increased proliferation and migration capacities. Moreover, HMOX1 was identified as a target of miR-328-3p, which regulated the HMOX1 expression in qPCR and WB assays. High miR-328-3p expressing HCC cell had diminished capacities for proliferation and migration. However, concurrent upregulation of HMOX1 expression resulted in enhanced proliferative and migratory abilities in these cells.
conclusionOur study has advanced our understanding of the roles of miR-328-3p and HMOX1 in HCC, demonstrating the inhibitory effect of miR-328-3p on the oncogenic activity of HMOX1. Hence, these results revealed the function of miR-328-3p and a novel mechanistic pathway for HCC and suggested the potential therapeutic targeting of miR-328-3p and HMOX1 for HCC intervention strategies.
Indexed as
Identifiers
What Socratic 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 Socratic graph.