ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2023
Estrogen-Induced LncRNA, LINC02568, Promotes Estrogen Receptor-Positive Breast Cancer Development and Drug Resistance Through Both In Trans and In Cis Mechanisms.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- A systematic review of progress toward unlocking the power of epigenetics in breast cancer: latest updates and perspectives.Frontiers in pharmacology · 2025Pooled it
- Repurposed ethoxzolamide reprograms antitumor immunity through β-TrCP-dependent PD-L1 ubiquitination.Cell reports. Medicine · 2026Article
- In vivo inhibition of TDO2 in fibroids results in widespread alteration in the tumor transcriptome.Clinical science (London, England : 1979) · 2026Article
- The Intricate Interplay of Noncoding RNAs and the Gut Microbiome in Gastrointestinal and Endocrine-Related Cancers.Sub-cellular biochemistry · 2026Review
- The role of UPR-related long noncoding RNAs in development of endocrine resistance in breast cancer.International journal of cancer · 2025Review
- In Silico Analysis of the Role of Estrogen Signaling in the Expression of Metabolic Genes in Breast Cancer.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- [Targeting chimera technology: A new tool for undruggable in breast cancer].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Review
- Review
- LncRNA HIF1A-AS2 promotes triple-negative breast cancer progression and paclitaxel resistance via MRPS23 protein.Heliyon · 2024Article
- Relationship between lncRNA MALAT1 and Chemo-radiotherapy Resistance of Cancer Cells: Uncovered Truths.Cell biochemistry and biophysics · 2024Review
- Potential Intersections between lncRNA, Vascular Cognitive Impairment, and Immunization Strategies: Insights and Future Directions.Vaccines · 2024Review
- Endocrine nuclear receptors and long non‑coding RNAs reciprocal regulation in cancer (Review).International journal of oncology · 2024Review
- LncRNA-MUF: A Novel Oncogenic Star with Potential as a Biological Marker and Therapeutic Target for Gastrointestinal Malignancies.Journal of Cancer · 2024Review
- Enhancing breast cancer treatment: mesoporous dopamine nanoparticles in synergy with chrysin for photothermal therapy.Frontiers in oncology · 2024Article
- Potential therapies for non-coding RNAs in breast cancer.Frontiers in oncology · 2024Review
- Mechanisms of tamoxifen resistance: insight from long non-coding RNAs.Frontiers in oncology · 2024Review
- Estrogen-Induced LncRNA, LINC02568, Promotes Estrogen Receptor-Positive Breast Cancer Development and Drug Resistance Through Both In Trans and In Cis Mechanisms.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
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Abstract
Endocrine therapy is the frontline treatment for estrogen receptor (ER) positive breast cancer patients. However, the primary and acquired resistance to endocrine therapy drugs remain as a major challenge in the clinic. Here, this work identifies an estrogen-induced lncRNA, LINC02568, which is highly expressed in ER-positive breast cancer and functional important in cell growth in vitro and tumorigenesis in vivo as well as endocrine therapy drug resistance. Mechanically, this work demonstrates that LINC02568 regulates estrogen/ERα-induced gene transcriptional activation in trans by stabilizing ESR1 mRNA through sponging miR-1233-5p in the cytoplasm. Meanwhile, LINC02568 contributes to tumor-specific pH homeostasis by regulating carbonic anhydrase CA12 in cis in the nucleus. The dual functions of LINC02568 together contribute to breast cancer cell growth and tumorigenesis as well as endocrine therapy drug resistance. Antisense oligonucleotides (ASO) targeting LINC02568 significantly inhibits ER-positive breast cancer cell growth in vitro and tumorigenesis in vivo. Furthermore, combination treatment with ASO targeting LINC02568 and endocrine therapy drugs or CA12 inhibitor U-104 exhibits synergistic effects on tumor growth. Taken together, the findings reveal the dual mechanisms of LINC02568 in regulating ERα signaling and pH homeostasis in ER-positive breast cancer, and indicated that targeting LINC02568 might represent a potential therapeutic avenue in the clinic.
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Registered trials
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