ArticleOncogene2015
A long non-coding RNA links calreticulin-mediated immunogenic cell removal to RB1 transcription.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- A Comprehensive Review of Long Non-Coding RNAs in the Cancer-Immunity Cycle: Mechanisms and Therapeutic Implications.International journal of molecular sciences · 2025Review
- Long Non-Coding RNAs in Ovarian Cancer: Mechanistic Insights and Clinical Applications.Cancers · 2025Review
- Article
- Construction of immune-related LncRNAs classifier to predict prognosis and immunotherapy response in thymic epithelial tumors.Bioscience reports · 2022Article
- Construction and validation of immune-related LncRNAs classifier to predict prognosis and immunotherapy response in laryngeal squamous cell carcinoma.World journal of surgical oncology · 2022Article
- A four immune-related long noncoding RNAs signature as predictors for cervical cancer.Human cell · 2022Article
- MicroRNAs and Long Noncoding RNAs as Novel Therapeutic Targets in Estrogen Receptor-Positive Breast and Ovarian Cancers.International journal of molecular sciences · 2021Review
- Tumor-intrinsic determinants of immunogenic cell death modalities.Oncoimmunology · 2021Review
- Noncoding RNAs: the shot callers in tumor immune escape.Signal transduction and targeted therapy · 2020Review
- Review
- Consensus guidelines for the definition, detection and interpretation of immunogenic cell death.Journal for immunotherapy of cancer · 2020Review
- Long Noncoding RNAs, New Critical Regulators in Cancer Immunity.Frontiers in oncology · 2020Review
- Non-Coding RNAs in Retinoblastoma.Frontiers in genetics · 2019Review
- CRlncRC: a machine learning-based method for cancer-related long noncoding RNA identification using integrated features.BMC medical genomics · 2018Article
- H3K4me2 and WDR5 enriched chromatin interacting long non-coding RNAs maintain transcriptionally competent chromatin at divergent transcriptional units.Nucleic acids research · 2018Article
- Long noncoding RNAs in cancer-immunity cycle.Journal of cellular physiology · 2018Review
- Article
- The transcriptional profiles and functional implications of long non-coding RNAs in the unfolded protein response.Scientific reports · 2018Article
- ZEB1-AS1: A crucial cancer-related long non-coding RNA.Cell proliferation · 2018Review
- Dying to Be Noticed: Epigenetic Regulation of Immunogenic Cell Death for Cancer Immunotherapy.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A subset of promoters bidirectionally expresses long non-coding RNAs (ncRNAs) of unknown function and protein-coding genes (PCGs) in parallel. Here, we define a set of 1107 highly conserved human bidirectional promoters that mediate the linked expression of long ncRNAs and PCGs. Depletion of the long ncRNA expressed from the RB1 promoter, ncRNA-RB1, reveals regulatory effects different from the RB1-controlled transcriptional program. ncRNA-RB1 positively regulates the expression of calreticulin (CALR) that in response to certain therapeutic interventions can translocate from the endoplasmic reticulum to the cell surface, hence activating anticancer immune responses. Knockdown of ncRNA-RB1 in tumor cells reduced expression of CALR, impaired the translocation of the protein to the cell surface upon treatment with anthracylines and consequently inhibited the cellular uptake by macrophages. In conclusion, co-transcription of ncRNA-RB1 and RB1 provides a positive link between the expression of the two tumor suppressors RB1 and the immune-relevant CALR protein. This regulatory interplay exemplifies disease-relevant co-regulation of two distinct gene products, in which loss of expression of one oncosuppressor protein entails the abolition of additional tumor-inhibitory mechanisms.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.