ArticleCancer management and research2021
HCP5 Promotes Proliferation and Contributes to Cisplatin Resistance in Gastric Cancer Through miR-519d/HMGA1 Axis.
Article in Cancer management and research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- The expression and clinical significance of miR-635 and miR-519d in gastric cancer patients.Frontiers in genetics · 2026Article
- Complicated crosstalk between HMGA and non-coding RNAs modulates hallmarks of cancer.Cancer cell international · 2025Review
- Long Non-Coding RNAs in Drug Resistance of Gastric Cancer: Complex Mechanisms and Potential Clinical Applications.Biomolecules · 2024Review
- HCP5 prevents ubiquitination-mediated UTP3 degradation to inhibit apoptosis by activating c-Myc transcriptional activity.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Construction of miRNA-lncRNA-mRNA co-expression network affecting EMT-mediated cisplatin resistance in ovarian cancer.Journal of cellular and molecular medicine · 2022Article
- HMGA1 Has Predictive Value in Response to Chemotherapy in Gastric Cancer.Current oncology (Toronto, Ont.) · 2021Article
- LncRNA HCP5 as a potential therapeutic target and prognostic biomarker for various cancers: a meta‑analysis and bioinformatics analysis.Cancer cell international · 2021Review
- Long Non-coding RNA ASNR Targeting miR-519e-5p Promotes Gastric Cancer Development by Regulating FGFR2.Frontiers in cell and developmental biology · 2021Article
- IGF2BP3 is upregulated in endometrial cancer and tightly regulates the growth of drug-resistant endometrial cancer cells via HMGA1.Science progressArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe long-non-coding RNA HCP5 (HLA complex P5) has been extensively linked to the ability of cancer cells to resist chemotherapeutic interventions. Here, we investigated the role of HCP5 in gastric cancer (GC) which to-date has been poorly characterized. Our results indicated that HCP5 expression was up-regulated in GC cells.
methodsHCP5, miR-519d, and high mobility group A1 (HMGA1) expression levels in GC cells were measured using quantitative real-time PCR (qRT-PCR) and Western blot analysis. Drug sensitivity and apoptosis of tumor cells were assessed using cell counting kit-8, flow cytometry, and caspase activity assay. Bioinformatics and luciferase reporter assays were employed for analyzing the interactions between HCP5, miR-519d, and HMGA1.
resultsHCP5 knockdown suppressed proliferation and weakened the resistance to cisplatin (DDP) of GC cells. miR-519d was down-regulated in GC cells and sponged by HCP5. HMGA1 was directly inhibited by miR-519d and its expression was up-regulated in GC cells. HCP5 exacerbated the resistance to cisplatin of GC cells in vitro by enhancing HMGA1 expression via sponging miR-519d.
conclusionIn summary, HCP5 promoted proliferation and contributed to DDP resistance in GC cells through miR-519d/HMGA1 axis.
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