Observational studyOncology reports2020
RP11‑156L14.1 regulates SSR1 expression by competitively binding to miR‑548ao‑3p in hypopharyngeal squamous cell carcinoma.
Observational study in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- The TRAP complex (SSR1-SSR4): mechanistic roles and therapeutic opportunities.Annals of medicine · 2026Review
- Current Advances of Treatments, Therapeutic Targets, Biomarkers, Novel Drugs, and Machine Learning for Hypopharyngeal Squamous Cell Carcinoma.World journal of otorhinolaryngology - head and neck surgery · 2026Review
- Exploring SSR1 as a novel diagnostic and prognostic biomarker in hepatocellular carcinoma, and its relationship with immune infiltration.Translational cancer research · 2024Article
- SSR1 and CKAP4 as potential biomarkers for intervertebral disc degeneration based on integrated bioinformatics analysis.JOR spine · 2024Article
- Article
- Downregulation of RBM17 enhances cisplatin sensitivity and inhibits cell invasion in human hypopharyngeal cancer cells.Open medicine (Warsaw, Poland) · 2023Article
- PBX2-Mediated circTLK1 Activates JAK/STAT Signaling to Promote Gliomagenesis via miR-452-5p/SSR1 Axis.Frontiers in genetics · 2021Article
- Clinical Value for Diagnosis and Prognosis of Signal Sequence Receptor 1 (SSR1) and Its Potential Mechanism in Hepatocellular Carcinoma: A Comprehensive Study Based on High-Throughput Data Analysis.International journal of general medicine · 2021Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging studies have demonstrated that long non‑coding RNAs (lncRNAs) play essential roles in tumorigenesis. However, the role and function of lncRNAs in hypopharyngeal squamous cell carcinoma (HSCC) have not been completely elucidated. The present study explored the function of a novel lncRNA, RP11‑156L14.1, in HSCC. RP11‑156L14.1 was revealed to be highly expressed in HSCC tissues and cell lines. Knockdown of RP11‑156L14.1 inhibited proliferation, migration, and invasion in HSCC cells. Furthermore, RP11‑156L14.1 regulated epithelial‑mesenchymal transition (EMT) by controlling EMT‑related protein expression. Mechanistically, RP11‑156L14.1 exerted its function as a competing endogenous RNA (ceRNA) and directly interacted with miR‑548ao‑3p. The present study also demonstrated that miR‑548ao‑3p regulated signal sequence receptor subunit 1 (SSR1) expression by targeting SSR1 3'‑UTR. Moreover, the xenograft HSCC tumor model revealed that knockdown of RP11‑156L14.1 markedly suppressed HSCC tumor growth in vivo. In summary, these findings indicated that the lncRNA RP11‑156L14.1 functions as an oncogene in HSCC by competing with miR‑548ao‑3p in regulating SSR1 expression. The RP11‑156L14.1/miR‑548ao‑3p/SSR1 axis could be utilized as a potential novel biomarker and therapeutic target for HSCC.
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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.