Long non-coding RNAs in hematological malignancies: translating basic techniques into diagnostic and therapeutic strategies

Wong, Nonthaphat Kent; Huang, Chien‐Ling; Islam, Rabiul; Yip, Shea Ping

doi:10.1186/s13045-018-0673-6

Cited by 37 publications

(20 citation statements)

References 189 publications

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“…This is of particular importance, because miRNAs lack an exclusive link to one target gene or disease and thus lack the high specificity, which is a requested feature of biomarkers [72,84]. Future studies should also include further investigations on the role of long noncoding RNAs in imatinib resistance as studies indicate that imatinib resistance can be modulated by long-non coding RNAs which target miRNAs thereby changing the expression of target associated with drug resistance like ABCB1 or ABCC2 [85][86][87].…”

Section: Discussionmentioning

confidence: 99%

Expression differences of miR-142-5p between treatment-naïve chronic myeloid leukemia patients responding and non-responding to imatinib therapy suggest a link to oncogenic ABL2, SRI, cKIT and MCL1 signaling pathways critical for development of therapy resistance

et al. 2020

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Background Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm characterized by constitutive activity of the tyrosine kinase BCR-ABL1. Although the introduction of tyrosine kinase inhibitors (TKIs) has substantially improved patients’ prognosis, drug resistance remains one of the major challenges in CML therapy. MicroRNAs (miRNAs), a class of short non-coding RNAs acting as post-transcriptional regulators, are implicated in CML progression and drug resistance. The aim of the present study was to analyze the miRNA expression profiles of 45 treatment-naïve CML patients in chronic phase (28 peripheral blood and 17 bone marrow samples) with respect to future response to imatinib therapy. Methods TaqMan low density arrays were used to analyze the miRNA expression pattern of the patient samples. For selected microRNAs, reporter gene assays were performed to study their ability to regulate CML associated target genes. Results Significant lower expression levels of miR-142-5p were identified in both, peripheral blood and bone marrow samples of future non-responders suggesting a potential tumor suppressor role of this miRNA. This was supported by reporter gene assays that identified the survival, proliferation and invasion promoting CML related genes ABL2, cKIT, MCL1 and SRI as targets of miR-142-5p and miR-365a-3p, the latter identified as potential biomarker in peripheral blood samples. Conclusion MiR-142-5p and to a certain extend also miR-365a-3p were able to discriminate treatment-naïve CML patients not responding to imatinib in the course of their treatment from patients, who responded to therapy. However, further large-scale studies should clarify if the identified miRNAs have the potential as predictive biomarkers for TKI resistance.

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Section: Discussionmentioning

confidence: 99%

Expression differences of miR-142-5p between treatment-naïve chronic myeloid leukemia patients responding and non-responding to imatinib therapy suggest a link to oncogenic ABL2, SRI, cKIT and MCL1 signaling pathways critical for development of therapy resistance

et al. 2020

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“…57 In acute myeloid leukemia (AML), UCA1 promotes the proliferation of malignant cells by suppressing p27 kip1 . 14 Sedlarikova et al found that UCA1 was downregulated in MM patients, when compared to healthy donors. 58 Their results also revealed that higher levels of UCA1 were correlated to advanced ISS stage and 1q21 gain.…”

Section: Uca1mentioning

confidence: 99%

“…Metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1), an 8.5‐Kb lncRNA (7 kb in mice) located on chromosome 11 (11q13.1), consists of two exons and is one of the few biologically well‐studied lncRNAs, and it has been reported to involve the regulation of gene expressions and the regulation of alternative splicing and cell cycle . MALAT1 misregulation has been shown to play a role in the development of several solid tumors, including lung, colorectal, bladder, and laryngeal cancers …”

Section: Mechanisms Of Lncrnas In MMmentioning

confidence: 99%

“…Upregulated UCA1 can increase bladder cancer cell proliferation, migration, and invasion, and inhibit apoptosis by regulating CREB expression, which encodes a transcriptional factor that affects oncogenesis . In acute myeloid leukemia (AML), UCA1 promotes the proliferation of malignant cells by suppressing p27 kip1 . Sedlarikova et al found that UCA1 was downregulated in MM patients, when compared to healthy donors .…”

Section: Mechanisms Of Lncrnas In MMmentioning

confidence: 99%

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The role of long non‐coding RNAs in multiple myeloma

Cui

Song

Fang

2019

European J of Haematology

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Multiple myeloma (MM) is still an incurable disease, and its pathogenesis involves cytogenetics and epigenetics. In recent years, the roles of long non‐coding RNAs (lncRNAs) in MM have been deeply studied by scholars. LncRNAs are defined as a class of non‐protein‐coding transcripts greater than 200 nucleotides in length, which are involved in a large spectrum of biological processes, including proliferation, differentiation, apoptosis, invasion, and chromatin remodeling. However, little is known about the specific mechanisms of these lncRNAs. They can act as oncogenic and/or tumor‐suppressive factors in the development and progression of MM. But that how do they work remains unclear. In this review, the recent progress in the study of functional lncRNAs associated with MM was summarized and the present knowledge about their expression and roles was discussed, to provide guidance for the in‐depth functional study of lncRNAs.

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“…However, the mechanism of drug resistance to chemotherapeutic agents is not fully elucidated. Currently, more and more evidences have been proved that non-coding RNAs play critical roles in drug resistance [3][4][5][6]. ncRNAs including long non-coding RNAs (lncRNAs), microRNAs (miRNAs), circular RNAs (circRNAs), and PIWI-interacting RNAs (piRNAs) are suggested to be the potential promising therapeutic targets for overcoming drug resistance in the treatment of human cancers [7][8][9][10].…”

Section: To the Editormentioning

confidence: 99%

NoncoRNA: a database of experimentally supported non-coding RNAs and drug targets in cancer

Wang

et al. 2020

J Hematol Oncol

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NoncoRNA (http://www.ncdtcdb.cn:8080/NoncoRNA/) is a manually curated database of experimentally supported noncoding RNAs (ncRNAs) and drug target associations that aim to potentially provide a high-quality data resource for exploring drug sensitivity/resistance-related ncRNAs in various human cancers. ncRNA are RNA molecular that do not encode proteins, but are involved in gene regulation and cellular functions in variety of human diseases, including neurodegenerative diseases and cancers. Here, we developed NoncoRNA which contained 8233 entries between 5568 ncRNAs and 154 drugs in 134 cancers. Each entry in the NoncoRNA contains detailed information on the ncRNAs, drugs, and cancers, the ncRNA expression pattern and experimental detection techniques, drug response and other targets, literature references, and other information. NoncoRNA offers a user-friendly, open access web interface to easily browse, search, and download data. NoncoRNA also provides a submission page for researchers to submit newly validated ncRNA-drug-cancer associations. NoncoRNA might serve as an immeasurable resource for understanding the roles of ncRNAs in cancer therapy.

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Long non-coding RNAs in hematological malignancies: translating basic techniques into diagnostic and therapeutic strategies

Cited by 37 publications

References 189 publications

Expression differences of miR-142-5p between treatment-naïve chronic myeloid leukemia patients responding and non-responding to imatinib therapy suggest a link to oncogenic ABL2, SRI, cKIT and MCL1 signaling pathways critical for development of therapy resistance

Expression differences of miR-142-5p between treatment-naïve chronic myeloid leukemia patients responding and non-responding to imatinib therapy suggest a link to oncogenic ABL2, SRI, cKIT and MCL1 signaling pathways critical for development of therapy resistance

The role of long non‐coding RNAs in multiple myeloma

NoncoRNA: a database of experimentally supported non-coding RNAs and drug targets in cancer

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