Abstract

The pivotal role of the long non-coding RNA (lncRNA) urothelial carcinoma associated 1 (UCA1) in anti-cancer drug resistance has been confirmed in many cancers. Overexpression of lncRNA UCA1 correlates with resistance to chemotherapeutics such as cisplatin, gemcitabine, 5-FU, tamoxifen, imatinib and EGFR-TKIs, whereas lncRNA UCA1 knockdown restores drug sensitivity. These studies highlight the potential of lncRNA UCA1 as a diagnostic and prognostic biomarker, and a therapeutic target in malignant tumors. In this review, we address the role of lncRNA UCA1 in anti-cancer drug resistance and discuss its potential in future clinical applications.

Highlights

  • A recent comprehensive analysis of RNA sequencing data from human tissues identified nearly 60,000 long non-coding RNAs, 3 times the number of protein-coding mRNAs [1]

  • Knockdown of SRPK1 overcomes cisplatin resistance in SKOV3-pcDNA-urothelial carcinoma associated 1 (UCA1) cells and increased Bcl-2 and decreased Bax, Caspase-3 and Caspase-9 expression is observed. These results revealed that SRPK1 and apoptosis related proteins played an important role in the long non-coding RNA (lncRNA) UCA1 induced cisplatin resistance [24]

  • Forced expression of lncRNA UCA1 in tamoxifen-sensitive MCF-7 cells substantially reduced www.impactjournals.com/oncotarget tamoxifen induced apoptosis, which could be abrogated by the mTOR specific inhibitor rapamycin [76]. These results revealed that lncRNA UCA1 induced tamoxifen resistance in breast cancer cells partly through activation of the mTOR signal pathway [76]

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Summary

Introduction

A recent comprehensive analysis of RNA sequencing data from human tissues identified nearly 60,000 long non-coding RNAs (lncRNAs), 3 times the number of protein-coding mRNAs [1]. Liu et al showed that lncRNA UCA1 expression was upregulated in the tamoxifen resistant breast cancer cells compared to their parental MCF-7 and T47D cells [77].

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