TUG1 mediates methotrexate resistance in colorectal cancer via miR-186/CPEB2 axis

Li, Changfeng; Gao, Yongjian; Li, Yongchao; Ding, Dayong

doi:10.1016/j.bbrc.2017.03.042

Cited by 86 publications

(54 citation statements)

References 26 publications

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“…They are involved in several pathways that regulate cell growth, autophagy, apoptosis and cell proliferation (393–401) or miR-34a (105), lnc-SCD and lnc-PTMS (402) modulates the effects of celecoxib. Both doxorubicin and etoposide block DNA replication by topoisomerase II inhibition: thus causing errors in DNA synthesis and promoting apoptosis in cancer cells.…”

Section: Drugs/non-coding Rnas Subnetworkmentioning

confidence: 99%

The Network of Non-coding RNAs in Cancer Drug Resistance

et al. 2018

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Non-coding RNAs (ncRNAs) have been implicated in most cellular functions. The disruption of their function through somatic mutations, genomic imprinting, transcriptional and post-transcriptional regulation, plays an ever-increasing role in cancer development. ncRNAs, including notorious microRNAs, have been thus proposed to function as tumor suppressors or oncogenes, often in a context-dependent fashion. In parallel, ncRNAs with altered expression in cancer have been reported to exert a key role in determining drug sensitivity or restoring drug responsiveness in resistant cells. Acquisition of resistance to anti-cancer drugs is a major hindrance to effective chemotherapy and is one of the most important causes of relapse and mortality in cancer patients. For these reasons, non-coding RNAs have become recent focuses as prognostic agents and modifiers of chemo-sensitivity. This review starts with a brief outline of the role of most studied non-coding RNAs in cancer and then highlights the modulation of cancer drug resistance via known ncRNAs based mechanisms. We identified from literature 388 ncRNA-drugs interactions and analyzed them using an unsupervised approach. Essentially, we performed a network analysis of the non-coding RNAs with direct relations with cancer drugs. Within such a machine-learning framework we detected the most representative ncRNAs-drug associations and groups. We finally discussed the higher integration of the drug-ncRNA clusters with the goal of disentangling effectors from downstream effects and further clarify the involvement of ncRNAs in the cellular mechanisms underlying resistance to cancer treatments.

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Section: Drugs/non-coding Rnas Subnetworkmentioning

confidence: 99%

The Network of Non-coding RNAs in Cancer Drug Resistance

et al. 2018

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“…In a ceRNA model, lncRNA release or upregulate target mRNA of miRNAs by competitively binding with the same miRNAs Zhang et al [27][28][29][30][31]. TUG1 participates in the progression and development of multiple tumors by acting as a ceRNA Zhang et al [22,24,26,[32][33][34][35][36]. To determine whether TUG1 acts as a ceRNA in HCC, we applied bioinformatics analysis (http://starbase.sysu.edu.…”

Section: Tug1 Regulates Zeb1 By Competitively Binding With Mir-142-3pmentioning

confidence: 99%

“…The lncRNA taurine upregulated gene 1 (TUG1) plays a role in the progression of several human cancers by interacting with miRNAs Wang et al [22][23][24]. For example, TUG1 accelerates the malignancy of pancreatic cancer through sponging miR-382 Zhao et al [25], mediates methotrexate resistance in colorectal cancer (CRC) by interacting with miR-186 Li et al [26], acts as an oncogene in osteosarcoma by binding with miR-335 Wang et al [22], and improves gastric cancer progression through sponging miR-145-5p Ren et al [24]. Thus, this study aimed to clarify the interaction between TUG1 and miR-142-3p in HCC.…”

Section: Introductionmentioning

confidence: 99%

lncRNA TUG1-Mediated Mir-142-3p Downregulation Contributes to Metastasis and the Epithelial-to-Mesenchymal Transition of Hepatocellular Carcinoma by Targeting ZEB1

Liu

Jin

et al. 2018

Cell Physiol Biochem

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Background/Aims: MicroRNA-142-3p (miR-142-3p) is dysregulated in many malignancies and may function as a tumor suppressor or oncogene in tumorigenesis and tumor development. However, few studies have investigated the clinical significance and biological function of miR-142-3p in hepatocellular carcinoma (HCC). Methods: The expression levels of taurine upregulated gene 1 (TUG1), miR-142-3p, and zinc finger E-box-binding homeobox 1 (ZEB1) were evaluated in HCC tissues and cell lines by quantitative real-time PCR. MTT and colony formation assays were used to detect cell proliferation ability, transwell assays were used to assess cell migration and invasion, and luciferase reporter assays were used to examine the interaction between the long noncoding RNA TUG1 and miR-142-3p. Tumor formation was evaluated through in vivo experiments. Results: miR-142-3p was significantly downregulated in HCC tissues, but TUG1 was upregulated in HCC tissues. Knockdown of TUG1 and upregulation of miR-142-3p inhibited cell proliferation, cell migration, cell invasion, and the epithelial-mesenchymal transition (EMT). miR-142-3p was found to be a prognostic factor of HCC, and the mechanism by which TUG1 upregulated ZEB1 was via direct binding to miR-142-3p. In vivo assays showed that TUG1 knockdown suppressed cell proliferation and the EMT in nude mice. Conclusion: The results of this study suggest that the TUG1/miR-142-3p/ ZEB1 axis contributes to the formation of malignant behaviors in HCC.

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“…LncRNA H19 mediates resistance to MTX in CRC on condition that the Wnt/β-catenin pathway is activated (109). Through the miR-186/CPEB2 axis, lncRNA taurine upregulated 1 (TUG1) affects resistance to MTX in CRC (110). Some studies indicated that lncRNAs are the key factors in the development of resistance to radiation in CRC.…”

Section: Drug Resistancementioning

confidence: 99%

Emerging Roles of lncRNAs in the Formation and Progression of Colorectal Cancer

Long

Yin

et al. 2020

Front. Oncol.

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Colorectal cancer (CRC) is the primary cause of cancer-related death worldwide; however, specific and sensitive tools for the early diagnosis and targeted therapy of CRC are currently lacking. High-throughput sequencing technology revealed that gene expression of long-chain non-coding RNAs (lncRNAs) in a number of cancers directly or indirectly interferes with various biological processes. Emerging evidence suggests that lncRNAs regulate target genes and play an important role in the biological processes of malignancies, including CRC. Many carcinostatic/oncogenic lncRNAs have been identified as biomarkers for metastasis and prognosis in CRC; hence, they serve as therapeutic tools. In this article, we systematically review the literature on the disordered lncRNAs in CRC from four aspects: DNA transcription, RNA level regulation, post-translational level, and the translation of lncRNAs into polypeptides. Subsequently, we analyze the mechanism through which lncRNAs participate in the biological process of CRC. Finally, we discuss the application and prospects of these lncRNAs in CRC.

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TUG1 mediates methotrexate resistance in colorectal cancer via miR-186/CPEB2 axis

Cited by 86 publications

References 26 publications

The Network of Non-coding RNAs in Cancer Drug Resistance

The Network of Non-coding RNAs in Cancer Drug Resistance

lncRNA TUG1-Mediated Mir-142-3p Downregulation Contributes to Metastasis and the Epithelial-to-Mesenchymal Transition of Hepatocellular Carcinoma by Targeting ZEB1

Emerging Roles of lncRNAs in the Formation and Progression of Colorectal Cancer

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