ArticleFrontiers in oncology2021
HOTTIP Enhances Gemcitabine and Cisplatin Resistance Through Sponging miR-637 in Cholangiocarcinoma.
Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 32 citations in OpenAlex.
- The long antisense non-coding RNA HOXA transcript at the distal tip (LncRNA HOTTIP) in health and disease: a comprehensive review and in silico analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Molecular mechanisms and therapeutic strategies in overcoming chemotherapy resistance in cancer.Molecular biomedicine · 2025Review
- The Diagnostic and Prognostic Potentials of Non-Coding RNA in Cholangiocarcinoma.International journal of molecular sciences · 2024Review
- Non-coding RNA and Drug resistance in cholangiocarcinoma.Non-coding RNA research · 2024Review
- Loss of miR-637 promotes cancer cell stemness via WASH/IL-8 pathway and serves as a novel prognostic marker in esophageal squamous cell carcinoma.Biomarker research · 2022Article
- Dysfunction and ceRNA network of the tumor suppressor miR-637 in cancer development and prognosis.Biomarker research · 2022Review
- Long Non-Coding RNAs as Molecular Biomarkers in Cholangiocarcinoma.Frontiers in cell and developmental biology · 2022Review
- Lnc-PKD2-2-3/miR-328/GPAM ceRNA Network Induces Cholangiocarcinoma Proliferation, Invasion and 5-FU Chemoresistance.Frontiers in oncology · 2022Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemo-resistance prominently hampers the effects of systemic chemotherapy to cholangiocarcinoma (CCA). Long non-coding RNAs (lncRNAs) have been shown to have great importance not only in tumorigenesis but also in therapeutic prognosis. The aim of this study is to investigate the role of lncRNA HOTTIP in the chemo-resistance to cisplatin and gemcitabine (CG) in CCA. The upregulated expression of HOTTIP was observed in CCA patients and the upregulation was associated with therapeutic responsiveness and prognosis. HOTTIP silencing powerfully increased the chemotherapy sensitivity through weakening proliferation and colony formation and increasing apoptosis. Subsequently, miR-637 was identified as the functional target of HOTTIP, since mechanically it could be targeted by HOTTIP and functionally its overexpression dismissed the changes by HOTTIP silencing
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