ArticleCancer cell international2021
LncRNA CTD-3252C9.4 modulates pancreatic cancer cell survival and apoptosis through regulating IFI6 transcription.
Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- Targeting lncRNA-regulated macrophage polarization: a novel therapeutic strategy for pancreatic ductal adenocarcinoma.Journal of physiology and biochemistry · 2026Review
- The Multi-Target lncRNA-miRNA-mRNA TRIAD in Pancreatic Cancer Diagnosis and Therapy.International journal of molecular sciences · 2026Review
- Non-Coding RNAs as key regulators of interferon signaling in cancer immunotherapy: mechanistic insights and clinical prospects.Clinical and experimental medicine · 2026Review
- Nanotechnology for the Treatment of Radiation Dermatitis: Advances and Translational Perspectives.International journal of nanomedicine · 2026Review
- Multi-Omics Analysis Reveals the IFI6 Gene as a Prognostic Indicator and Therapeutic Target in Esophageal Cancer.International journal of molecular sciences · 2024Article
- BM-MSCs display altered gene expression profiles in B-cell acute lymphoblastic leukemia niches and exert pro-proliferative effects via overexpression of IFI6.Journal of translational medicine · 2023Article
- LncRNA-MALAT1: A Key Participant in the Occurrence and Development of Cancer.Molecules (Basel, Switzerland) · 2023Review
- Long noncoding RNAs in pancreas cancer: from biomarkers to therapeutic targets.Turkish journal of medical sciences · 2023Review
- Tumor mutation burden-related long non-coding RNAs is predictor for prognosis and immune response in pancreatic cancer.BMC gastroenterology · 2022Article
- An IFI6-based hydrogel promotes the healing of radiation-induced skin injury through regulation of the HSF1 activity.Journal of nanobiotechnology · 2022Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundPancreatic cancer (PC) is one of the most lethal cancer types with high degree of malignancy and poor prognosis. Recent studies have shown that long non-coding RNAs (lncRNAs) were associated with the initiation and progression of pancreatic cancer. In the current study, we have investigated the expression, biological function and mechanism of a lncRNA CTD-3252C9.4 in pancreatic cancer.
methodsThe expression of CTD-3252C9.4 in pancreatic cancer cells and tissues was measured by qRT-PCR. In vitro and in vivo functional experiments assays were implemented for identifying CTD-3252C9.4 function in pancreatic cancer. Molecular relationships among CTD-3252C9.4, IRF1 and IFI6 were investigated via luciferase reporter assay, pulldown assay and ChIP assays.
resultsCTD-3252C9.4 was found remarkably decreased in pancreatic cancer cells and tissues. Overexpression of CTD-3252C9.4 suppressed migration, invasion and proliferation, yet facilitated apoptosis of pancreatic cancer cells both in vitro and in vivo. Then, IFI6 was identified as a downstream target that could be down-regulated by CTD-3252C9.4 and IFI6 overexpression could counteract the effects of CTD-3252C9.4 upregulation on the survival and apoptosis of pancreatic cancer cells. Furthermore, mechanism experiments revealed that IRF1 was a transcriptional factor of IFI6 that can be blocked by CTD-3252C9.4 to inhibit IFI6 transcription.
conclusionOur data indicated that CTD-3252C9.4 could promote pancreatic cancer cell apoptosis and restrain cell growth via binding IRF1 and preventing the transcription of IFI6, which may become a potential therapeutic target for pancreatic cancer.
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