ArticleInternational journal of molecular medicine2021
Upregulated long non‑coding RNA LincIN promotes tumor progression via the regulation of nuclear factor 90/microRNA‑7/HOXB13 in esophageal squamous cell carcinoma.
Article in International journal of molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- MicroRNA-7: a versatile player and core target in brain disorders.Journal of translational medicine · 2026Pooled it
- Epigenetically-Upregulated CD98 Shed Light on the Precancerous Diagnosis and Prognosis Prediction of Esophageal Cancer.Cancer science · 2025Article
- Roles of long non‑coding RNAs in esophageal cell squamous carcinoma (Review).International journal of molecular medicine · 2024Review
- Biomarkers of lymph node metastasis in esophageal cancer.Frontiers in immunology · 2024Review
- A Pleiotropic Role of Long Non-Coding RNAs in the Modulation of Wnt/β-Catenin and PI3K/Akt/mTOR Signaling Pathways in Esophageal Squamous Cell Carcinoma: Implication in Chemotherapeutic Drug Response.Current oncology (Toronto, Ont.) · 2022Review
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non‑coding RNA LincIN has been reported to be overexpressed and to be involved in the metastasis of breast cancer. However, the expression and role of LincIN in esophageal squamous cell carcinoma (ESCC) remain unsolved. In the present study, LincIN expression was examined in ESCC by RT‑qPCR, and the roles of LincIN in ESCC were determined using cell growth, migration and invasion assays. In addition, the effects of LincIN on nuclear factor 90 (NF90) and microRNA/miR (miR)‑7 were examined by RNA immunoprecipitation assay, RT‑qPCR, dual‑luciferase reporter assay and western blot analysis. The results revealed that LincIN expression was significantly increased in ESCC tissues and cell lines. The increased expression of LincIN was positively associated with invasion depth, lymph node metastasis, TNM stage and a poor prognosis. Functional assays revealed that the overexpression of LincIN promoted ESCC cell growth, migration and invasion. Mechanistic analysis revealed that LincIN physically bound to NF90, enhanced the binding between NF90 and primary miR‑7 (pri‑miR‑7), and further enhanced the inhibitory effects of NF90 on miR‑7 biogenesis. Therefore, LincIN downregulated miR‑7 expression in ESCC. The expression of miR‑7 inversely correlated with that of LincIN in ESCC tissues. By downregulating miR‑7, LincIN increased the expression of HOXB13, a target of miR‑7. The overexpression of miR‑7 or the depletion of HOXB13 both attenuated the tumor‑promoting roles of LincIN in ESCC cell growth, migration and invasion. On the whole, the findings of the present study suggest that LincIN is overexpressed and plays an oncogenic role in ESCC via the regulation of the NF90/miR‑7/HOXB13 axis. Thus, LincIN may prove to be a promising prognostic biomarker and therapeutic target for ESCC.
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