Knockdown of long non-coding RNA Taurine Up-Regulated 1 inhibited doxorubicin resistance of bladder urothelial carcinoma via Wnt/β-catenin pathway

Xie, Dalong; Zhang, Hui; Hu, Xuanhao; Shang, Chao

doi:10.18632/oncotarget.20927

Cited by 38 publications

(26 citation statements)

References 35 publications

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“…Moreover, knockdown of these lncRNAs promoted UBC carcinogenesis and drug resistance. 5 – 7 , 24 , 25 Our results indicated that NEAT1 knockdown inhibited the sensitivity of J82 and T24 cells to DOX, which might provide a promising therapeutic target for UBC with DOX resistance.…”

Section: Discussionmentioning

confidence: 68%

Non-coding RNA NEAT1/miR-214-3p contribute to doxorubicin resistance of urothelial bladder cancer preliminary through the Wnt/β-catenin pathway

Guo

Zhang

Xie

et al. 2018

CMAR

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BackgroundUrothelial bladder cancer (UBC) is one of the most lethal urological malignancies in the world. Patients with UBC are routinely given chemotherapy which results in a median survival of 12-15 months. Nuclear-enriched abundant transcript 1 (NEAT1) functions as an oncogene and could be used as a therapeutic target for human UBC. However, the involvement of NEAT1 in doxorubicin (DOX) resistance of UBC has been poorly demonstrated.MethodsQuantitative Real-time PCR (qRT-PCR) was used to detect the expression levels of NEAT1 and miR-214-3p in UBC tissues and cells. Bioinformatics prediction, RNA pull-down and qRT-PCR were used to assay the regulation manner of NEAT1 and miR-214-3p. Loss/gain function of NEAT1 and miR-214-3p together with western blot, drug resistance assay and flow cytometry were used to explore the influence of NEAT1 in DOX resistance was correlative with miR-214-3p. Finally, luciferase assay system was applied to determine the Wnt/β-catenin signal activity.ResultsNEAT1 was upregulated and miR-214-3p was downregulated in DOX-resistant UBC tissues and cells. NEAT1 knockdown inhibited J82 and T24 cells to DOX chemosensitivity by negatively regulating miR-214-3p expression. NEAT1/miR-214-3p contributed to DOX resistance of UBC preliminary through the Wnt/β-catenin pathway.ConclusionNEAT1 contributed to DOX resistance of UBC through the Wnt/β-catenin pathway partly by negatively regulating miR-214-3p expression. Our findings will provide a promising ncRNA targeted therapeutic strategy for UBC with DOX resistance.

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Section: Discussionmentioning

confidence: 68%

Non-coding RNA NEAT1/miR-214-3p contribute to doxorubicin resistance of urothelial bladder cancer preliminary through the Wnt/β-catenin pathway

Guo

Zhang

Xie

et al. 2018

CMAR

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“…Previous studies have suggested that lncRNA dysregulation in NSCLC is associated with lymph node metastasis, advanced stage, metastasis development, and poor patient prognosis. Anti‐tumor drug resistance in various carcinomas, including colon, bladder, ovarian, and gastric cancers, and NSCLC, is associated with lncRNAs. Although advances have been achieved in diagnosis and treatment, NSCLC is still one of the most common malignancies, with five‐year survival rates < 15% .…”

Section: Resultsmentioning

confidence: 99%

Role of long non‐coding RNA in drug resistance in non‐small cell lung cancer

Wang

et al. 2018

Thoracic Cancer

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Lung cancer is the leading cause of cancer‐associated death, and non‐small cell lung cancer (NSCLC) accounts for 85% of all lung cancer cases. Many drugs have been used to treat NSCLC in order to improve patient prognosis. Platinum‐based chemotherapy is the first‐line treatment for locally advanced or metastatic patients. For patients with activating EGFR mutations, tyrosine kinase inhibitors are the best treatment choice. NSCLC initially exhibits an excellent response to treatment; however, acquired resistance has been observed in many patients, leading to ineffective treatment. Clinical resistance is an impediment in the treatment of patients with advanced NSCLC. Many sequencing technologies have shown that long non‐coding RNA (lncRNA) is expressed differently between drug‐resistant and drug‐sensitive lung cancer cells. We review the literature on lncRNA in drug resistance of NSCLC. The aim of this review is to gain insight into the molecular mechanisms of drug resistance, mainly focusing on the role of lncRNA in NSCLC.

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“…Numerous studies have suggested the importance of Wnt-b-catenin signaling in several cancers (44). Furthermore, Wnt-b-catenin has been shown to play important roles during epithelial-mesenchymal transition (45), cell proliferation and metastasis (24), and drag resistance (46) in bladder cancer. In the present study, RBM5 knockdown activated the Wnt-b-catenin pathway by promoting the expression of b-catenin and cyclin D1 while decreasing the apoptosis marker caspase-3 at the protein level.…”

Section: Discussionmentioning

confidence: 99%

Down‐regulated RBM5 inhibits bladder cancer cell apoptosis by initiating an miR‐432‐5p/β‐catenin feedback loop

et al. 2019

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RNA‐binding motif protein 5 (RBM5) acts as a tumor suppressor in various human cancers and presents with several important characteristics, such as the potentiation of apoptosis, inhibition of the cell cycle, and alternative splicing of Fas and caspase‐2 precursor mRNA. However, its role in bladder urothelial carcinoma (BUC) remains unknown. In this study, we found that RBM5 expression was significantly down‐regulated in BUC tissues when compared with the adjacent nontumor tissues. The down‐regulation of RBM5 activates ²‐catenin, which binds to the T‐cell factor/lymphocyte enhancer factor element of the miR‐432‐5p promoter and elevates the expression of miR‐432‐5p in bladder cancer cells. The up‐regulated miR‐432‐5p directly targets 3′‐UTR and depresses RBM5 expression. Thus, RBM5–miR‐432‐5p–²‐catenin forms a feedback loop in regulating bladder cancer cell apoptosis. Our findings provide evidence that the regulatory feedback loop among RBM5, miR‐432‐5p, and Wnt–²‐catenin is responsible for the progress of bladder cancer cells.—Zhang, Y.‐P., Liu, K.‐L., Wang, Y.‐X., Yang, Z., Han, Z.‐W., Lu, B.‐S., Qi, J.‐C, Yin, Y.‐W., Teng, Z.‐H., Chang, X.‐L., Li, J.‐D., Xin, H., Li, W. Down‐regulated RBM5 inhibits bladder cancer cell apoptosis by initiating an miR‐432‐5p/²‐catenin feedback loop. FASEB J. 33, 10973–10985 (2019). http://www.fasebj.org

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Knockdown of long non-coding RNA Taurine Up-Regulated 1 inhibited doxorubicin resistance of bladder urothelial carcinoma via Wnt/β-catenin pathway

Cited by 38 publications

References 35 publications

Non-coding RNA NEAT1/miR-214-3p contribute to doxorubicin resistance of urothelial bladder cancer preliminary through the Wnt/β-catenin pathway

Non-coding RNA NEAT1/miR-214-3p contribute to doxorubicin resistance of urothelial bladder cancer preliminary through the Wnt/β-catenin pathway

Role of long non‐coding RNA in drug resistance in non‐small cell lung cancer

Down‐regulated RBM5 inhibits bladder cancer cell apoptosis by initiating an miR‐432‐5p/β‐catenin feedback loop

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Knockdown of long non-coding RNA Taurine Up-Regulated 1 inhibited doxorubicin resistance of bladder urothelial carcinoma via Wnt/β-catenin pathway

Cited by 38 publications

References 35 publications

Non-coding RNA NEAT1/miR-214-3p contribute to doxorubicin resistance of urothelial bladder cancer preliminary through the Wnt/&beta;-catenin pathway

Non-coding RNA NEAT1/miR-214-3p contribute to doxorubicin resistance of urothelial bladder cancer preliminary through the Wnt/&beta;-catenin pathway

Role of long non‐coding RNA in drug resistance in non‐small cell lung cancer

Down‐regulated RBM5 inhibits bladder cancer cell apoptosis by initiating an miR‐432‐5p/β‐catenin feedback loop

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Non-coding RNA NEAT1/miR-214-3p contribute to doxorubicin resistance of urothelial bladder cancer preliminary through the Wnt/β-catenin pathway

Non-coding RNA NEAT1/miR-214-3p contribute to doxorubicin resistance of urothelial bladder cancer preliminary through the Wnt/β-catenin pathway