ArticleMolecular cancer2020
Hypoxia induced LUCAT1/PTBP1 axis modulates cancer cell viability and chemotherapy response.
Article in Molecular cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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Who cites it
98 citing papers in PubMed, 192 citations in OpenAlex.
- Loss of the RAGE function in hypoxic conditions exacerbates the malignant progression of lung adenocarcinoma via damage-associated molecular pattern signaling.Translational oncology · 2026Article
- The mechanisms of lncBMP4 mediating BMP4 promoter activity to regulate the proliferation of dermal papilla cells in Hu sheep.Animal bioscience · 2026Article
- Deconvoluting the multi-faceted roles of alternative splicing events in cancer: From underlying mechanisms to innovative therapeutics.Acta pharmaceutica Sinica. B · 2026Review
- Screening, Prognostic, and Predictive Molecular Tools for Colorectal Cancer: Recent Advances in the Classical Background.International journal of molecular sciences · 2026Review
- Alternative splicing in cancer drug resistance: Mechanisms and therapeutic prospects (Review).Oncology reports · 2026Review
- LUCAT1 promotes stemness in head and neck squamous cell carcinoma by sponging miR-128.Frontiers in oncology · 2026Article
- Therapeutic potential of the LUCAT1/miR- 2278/STAT5A axis in pulmonary fibrosis.BMC pulmonary medicine · 2025Article
- Hypoxia-induced exosomal LUCAT1 promotes osimertinib resistance in lung adenocarcinoma by stabilizing c-MET.Cell death & disease · 2025Article
- Living photosynthetic micro/nano-platforms: Engineering unicellular algae for biomedical applications.Bioactive materials · 2025Review
- LncRNA EP300-AS1 interacts with PTBP1 to destabilize PRMT5 mRNA and suppresses NSCLC growth and metastasis.Cell death & disease · 2025Article
- PTBP1 and Cancer: From RNA Regulation to Therapeutic Potential.Journal of cellular and molecular medicine · 2025Review
- Exosome-transmitted LUCAT1 promotes stemness transformation and chemoresistance in bladder cancer by binding to IGF2BP2.Journal of experimental & clinical cancer research : CR · 2025Article
- HIF-1α-induced long noncoding RNA LINC02776 promotes drug resistance of ovarian cancer by increasing polyADP-ribosylation.Clinical and translational medicine · 2025Article
- The long noncoding RNA LUCAT1 regulates endometrial receptivity via the miR-495-3p/S100P axis.Communications biology · 2025Article
- Long noncoding RNA GDIL acts as a scaffold for CHAC1 and XRN2 to promote platinum resistance of colorectal cancer through inhibition of glutathione degradation.Cell death & disease · 2025Article
- Review
- Role of Hypoxia-Associated Long Noncoding RNAs in Cancer Chemo-Therapy Resistance.International journal of molecular sciences · 2025Review
- The regulatory role of lncRNA in tumor drug resistance: refracting light through a narrow aperture.Oncology research · 2025Review
- Engineered exosomes: a promising design platform for overcoming cancer therapy resistance.Frontiers in cell and developmental biology · 2025Review
- Noncoding RNAs as regulators of FOSL1 in cancer.Frontiers in immunology · 2025Review
38 more citing papers are in PubMed but not listed here.
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
backgroundHypoxic tumors are refractory to DNA damage drugs. However, the underlying mechanism has yet to be elucidated. We aimed to identify lncRNAs that upregulated under hypoxia and their effects on colorectal cancer (CRC).
methodsCRC cells were treated with 1% O
resultsWe identified a hypoxia-induced lncRNA LUCAT1 that facilitated the growth of CRC cells and contributed to drug resistance of CRC cells both in vitro and in vivo. Mechanically, LUCAT1 interacts with polypyrimidine tract binding protein 1 (PTBP1) in CRC cells, facilitates the association of a set of DNA damage related genes with PTBP1, thus resulting in altered alternative splicing of these genes. Moreover, ectopic expression of PTBP1 in CRC cells with knockdown of LUCAT1 abrogated the effects induced by LUCAT1 knockdown. Chemotherapeutics drug combined with LUCAT1 knockdown via antisense oligonucleotides (ASO) would get a better outcome in vivo, compared with group treated with chemotherapeutic drug only. Notably, LUCAT1 is upregulated in CRC tissues, compared to adjacent normal tissues; and CRC patients with higher LUCAT1 have a worse prognosis and poorly responded to chemotherapy in the clinic.
conclusionsOur data suggested CRC cells utilizes LUCAT1 to develop resistance to DNA damage drugs, and disrupting the LUCAT1/PTBP1 axis might be a promising therapeutic strategy for refractory hypoxic tumors.
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