LncRNA H19 overexpression induces bortezomib resistance in multiple myeloma by targeting MCL-1 via miR-29b-3p

Pan, Yafang; Zhang, Yu; Liu, Wenwen; Huang, Yan; Shen, Xianjuan; Jing, Rongrong; Pu, Jun; Wang, Xudong; Ju, Shaoqing; Cong, Hui; Chen, Hongmei

doi:10.1038/s41419-018-1219-0

Cited by 80 publications

(65 citation statements)

References 41 publications

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“…Increasing studies indicate that lncRNAs are involved in resistance of tumour cells to chemotherapy via multiple mechanisms, such as regulation of tumour cell apoptosis, epithelial–mesenchymal transition, and DNA methylation . LncRNA ANRIL has been shown to contribute to drug resistance in many tumours, such as osteosarcoma, gastric cancer, and colorectal cancer .…”

Section: Discussionmentioning

confidence: 99%

Hypoxia‐induced lncRNA ANRIL promotes cisplatin resistance in retinoblastoma cells through regulating ABCG2 expression

Yin

Liao

Xiong

et al. 2020

Clin Exp Pharma Physio

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Cisplatin (DDP) resistance limits its efficacy for retinoblastoma (Rb). Hypoxia‐inducible factor‐1α (HIF‐1α) has been shown to contribute to chemotherapy resistance in tumours under hypoxic conditions. This study was designed to explore the role and mechanism of long non‐coding RNA (lncRNA) antisense non‐coding RNA in the INK4 locus (ANRIL) in regulating DDP resistance in Rb cells under hypoxia and to validate whether HIF‐1α was involved in this process. The interaction between HIF‐1α and the promoter of ANRIL was analyzed using ChIP assay. Cell proliferation and apoptosis, as well as protein levels of drug resistance‐related proteins (ABCG2 and MDR1) were examined to evaluate DDP resistance in Rb cells. The interactions between miR‐328 and ANRIL as well as miR‐328 and ABCG2 were analyzed using dual‐luciferase reporter assays. Upon hypoxia, HIF‐1α directly bound to the ANRIL promoter region to transcriptionally activate ANRIL. The hypoxia‐induced ANRIL promoted Rb cell resistance to DDP, as evidenced by facilitation of cell proliferation, inhibition of cell apoptosis and upregulation of ABCG2 and MDR1. Mechanistically, ANRIL promoted Rb cell resistance to DDP by acting as a sponge of miR‐328 to upregulate expression of ABCG2, which was confirmed as a direct target of miR‐328. Collectively, hypoxia‐induced ANRIL promotes DDP resistance in Rb cells by sponging miR‐328 to upregulate ABCG2 expression.

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Section: Discussionmentioning

confidence: 99%

Hypoxia‐induced lncRNA ANRIL promotes cisplatin resistance in retinoblastoma cells through regulating ABCG2 expression

Yin

Liao

Xiong

et al. 2020

Clin Exp Pharma Physio

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“…MiR‐29b‐3p, a member of miR‐29 family, has important roles in clinical practice. Pan et al () have found low expression level of miR‐29b‐3p in serum of multiple myeloma patients. Circulating basal level of miR‐29b‐3p can predict the outcome of patients with metastatic colorectal cancer treated with bevacizumab (Ulivi et al, ).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐29b‐3p reduces intestinal ischaemia/reperfusion injury via targeting of TNF receptor‐associated factor 3

Dai

Zhang

Han

et al. 2019

British J Pharmacology

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Background and Purpose The microRNA miR‐29b‐3p shows important roles in regulating apoptosis and inflammation. However, its effects on intestinal ischaemia/reperfusion (II/R) injury have not been reported. Here we have investigated the functions of miR‐29b‐3p on II/R injury on order to find drug targets to treat the injury. Experimental Approach Two models ‐ in vitro hypoxia/reoxygenation (H/R) of IEC‐6 cells; in vivo, II/R injury in C57BL/6 mice were used. Western blotting and dual‐luciferase reporter assays were used and mimic and siRNA transfection tests were applied to assess the effects of miR‐29b‐3p on II/R injury via targeting TNF receptor‐associated factor 3 (TRAF3). Key Results The H/R procedure decreased cell viability and promoted inflammation and apoptosis in IEC‐6 cells, and the II/R procedure also promoted intestinal inflammation and apoptosis in mice. Expression levels of miR‐29b‐3p were decreased in H/R‐induced cells and II/R‐induced intestinal tissues of mice compared with control group or sham group, which directly targeted TRAF3. Decreased miR‐29b‐3p level markedly increased TRAF3 expression via activating TGF‐α‐activated kinase 1 phosphorylation, increasing NF‐κB (p65) levels to promote inflammation, up‐regulating Bcl2‐associated X expression, and down‐regulating Bcl‐2 expression to trigger apoptosis. In addition, the miR‐29b‐3p mimetic and TRAF3 siRNA in IEC‐6 cells markedly suppressed apoptosis and inflammation to alleviate II/R injury via inhibiting TRAF3 signallimg. Conclusions and Implications The miR‐29b‐3p played a critical role in II/R injury, via targeting TRAF3, which should be considered as a significant drug target to treat the disease.

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“…Drug resistance of cancer cells is one of the major causes of chemotherapy failure [22]. LncRNAs are reported to induce the drug resistance by regulating drug metabolism, autophagy, apoptosis and epithelial-mesenchymal transition [23][24][25][26]. We previously elucidated that lncRNA UCA1 promotes tumor development and metastasis in GC [18,27].…”

Section: Discussionmentioning

confidence: 99%

LncRNA UCA1 promotes cisplatin resistance in gastric cancer via recruiting EZH2 and activating PI3K/AKT pathway

et al. 2020

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Background: Drug resistance of cancer cells is one of the major causes of chemotherapy failure. Recently research demonstrated that long non-coding RNA Urothelial cancer associated 1 (UCA1) could promote tumor cisplatin resistance. In this study, we aim to investigate the role of UCA1 in the cisplatin treatment of gastric cancer and its underlying mechanism. Methods: Cell counting kit-8 (CCK-8) assay and apoptosis assay were used to detect the effects of different doses of cisplatin on the proliferation and apoptosis of gastric cancer. We examined the expression relationship between the Enhancer of Zeste Homologue 2 (EZH2) and UCA1 by quantitative Real-time polymerase chain reaction (qRT-PCR) and western blot analysis. Western blot analysis was also performed to detect the expression levels of apoptosis-related proteins, EZH2 and key genes in PI3K/AKT signaling pathway, RIP and RNA pull down assays were performed to explore the interaction between UCA1 and EZH2. Results: We demonstrated that higher the UCA1 expression levels in GC tissues correlated with the poorer the prognosis of patients according to the TCGA database, the GEO database. Moreover, overexpression of UCA1 promotes GC cell proliferation and inhibits cisplatin-induced apoptosis. Knockdown of UCA1 showed the opposite results. Besides, UCA1 exerted its function through interacting with EZH2 and regulates EZH2 expression, knockdown of EZH2 decreased cisplatin resistance of GC cells. Hence, UCA1 promotes cisplatin resistance of GC via recruiting EZH2 and activating PI3K/AKT pathway. Conclusion: Our research revealed the lncRNA UCA1 promoted the cisplatin resistance of GC by recruiting EZH2 and activating PI3K/AKT pathway to modulate cell apoptosis, indicating treatments targeting UCA1 or EZH2 might provide meaningful therapeutic strategies for cisplatin-resistance GC patients.

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LncRNA H19 overexpression induces bortezomib resistance in multiple myeloma by targeting MCL-1 via miR-29b-3p

Cited by 80 publications

References 41 publications

Hypoxia‐induced lncRNA ANRIL promotes cisplatin resistance in retinoblastoma cells through regulating ABCG2 expression

Hypoxia‐induced lncRNA ANRIL promotes cisplatin resistance in retinoblastoma cells through regulating ABCG2 expression

MicroRNA‐29b‐3p reduces intestinal ischaemia/reperfusion injury via targeting of TNF receptor‐associated factor 3

LncRNA UCA1 promotes cisplatin resistance in gastric cancer via recruiting EZH2 and activating PI3K/AKT pathway

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