ArticleMolecular medicine reports2022
Long non‑coding RNA HCG18 facilitates the progression of laryngeal and hypopharyngeal squamous cell carcinoma by upregulating FGFR1 via miR‑133b.
Article in Molecular medicine reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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Who cites it
3 citing papers in PubMed, 10 citations in OpenAlex.
- Review
- Review
- Diagnostic and Prognostic Value of microRNAs in Patients with Laryngeal Cancer: A Systematic Review.Non-coding RNA · 2023Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been reported that long non‑coding RNA HLA complex group 18 (HCG18) is involved in the progression of cancer, acting as an oncogenic gene. The aim of the present study was to investigate the mechanism underlying the action of HCG18 in laryngeal and hypopharyngeal squamous cell carcinoma (LHSCC). The expression levels of HCG18, microRNA (miR)‑133b and fibroblast growth factor receptor 1 (FGFR1) in LHSCC tissues and transfected LHSCC cells were evaluated by reverse transcription‑quantitative PCR or immunohistochemistry. The viability, migration and invasion of transfected LHSCC cells were detected by Cell Counting Kit‑8, wound healing and Transwell assays, respectively. The targeting relationships of HCG18, miR‑133b and FGFR1 were predicted by bioinformatics analysis and confirmed using a dual‑luciferase reporter assay. Moreover, the expression levels of FGFR1, phosphorylated (p)‑PI3K, PI3K, p‑AKT, AKT, p53, Bax and Bcl‑2 in transfected LHSCC cells were measured by western blotting. It was found that the expression levels of HCG18 and FGFR1 were upregulated, but those of miR‑133b were downregulated in LHSCC tissues. Short hairpin RNA (sh) HCG18 and miR‑133b mimic inhibited LHSCC cell viability, while enhancing miR‑133b expression. HCG18 could competitively bind with miR‑133b. Moreover, the miR‑133b inhibitor promoted cell viability, migration, invasion and the expression levels of Bcl‑2, p‑PI3K and p‑AKT, but inhibited the expression levels of p53 and Bax, which were abrogated by shHCG18. miR‑133b could competitively bind with FGFR1, and the miR‑133b mimic decreased the expression level of FGFR1 in transfected LHSCC cells. shFGFR1 promoted the expression levels of p53 and Bax, while inhibiting viability, migration, invasion and Bcl‑2, p‑PI3K and p‑AKT expression in LHSCC cells. In conclusion, the current results indicated that HCG18 facilitated the progression of LHSCC by upregulating FGFR1 via miR‑133b. The present study evaluated the mechanism with regards to the action of HCG18 in LHSCC, and these experimental results may provide novel evidence for targeted therapy of LHSCC.
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