Overexpression of MEG3 sensitizes colorectal cancer cells to oxaliplatin through regulation of miR-141/PDCD4 axis

Wang, Hongjian; Li, Hui; Zhang, Lei; Yang, Dongyuan

doi:10.1016/j.biopha.2018.07.131

Cited by 63 publications

(45 citation statements)

References 29 publications

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“…Its administration induced upregulation of many lncRNAs, including MEG3, TUG1, H19, and DICER1-AS1. Previous reports have indicated that enhanced expression of MEG3 renders colorectal cells more sensitive to oxaliplatin therapy by regulating the mir-141/PDCD4 axis (33). In human pituitary tumor-derived cells, enforced MEG3 expression was shown to significantly inhibit tumor growth (34).…”

Section: Discussionmentioning

confidence: 99%

Long Non-coding RNAs Contribute to the Inhibition of Proliferation and EMT by Pterostilbene in Human Breast Cancer

Huang

et al. 2018

Front. Oncol.

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Background: There is increasing evidence that long non-coding RNAs (lncRNAs) are involved in the process of carcinogenesis and treatment using chemotherapy. Pterostilbene, a phytochemical agent with natural antioxidant and anti-inflammatory properties, has been shown to modulate oncogenic processes in many cancers. However, there has been limited research on the association between pterostilbene and the expression of lncRNAs.Methods: MCF7 breast cancer cells were treated with various concentrations of pterostilbene and their gene expression profile was analyzed by quantitative real-time PCR, Western blotting and immunofluorescence.Results: Treatment with pterostilbene inhibited cell proliferation and epithelial-to-mesenchymal transition (EMT), and increased cell apoptosis, autophagy and ER stress. The Akt/mTOR pathway was downregulated, but p38 MAPK/Erk signaling was activated in cells following treatment with pterostilbene. Pterostilbene increased the expression of the lncRNAs MEG3, TUG1, H19, and DICER1-AS1 whereas the expression of LINC01121, PTTG3P, and HOTAIR declined. Knockdown of lncRNA H19 resulted in a reduction of the cell invasion, with the cells becoming more sensitive to pterostilbene therapy.Conclusions: These results suggest that efficient optimum disruption of lncRNA expression might possibly improve the anti-tumor effects of phytochemical agents, thus serving as a potential therapy for breast cancer.

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Section: Discussionmentioning

confidence: 99%

Long Non-coding RNAs Contribute to the Inhibition of Proliferation and EMT by Pterostilbene in Human Breast Cancer

Huang

et al. 2018

Front. Oncol.

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“…These data demonstrated that TUG1 epigenetically silencing PDCD4 via recruiting EZH2 in ECA109/DDP cells. PDCD4 has been identified as a tumor suppressor in multiple cancers [ 31 , 32 ]. Moreover, PDCD4 could improve the sensitivity of cancer cells to chemotherapy drugs such as docetaxel and cisplatin [ 33 , 34 ].…”

Section: Discussionmentioning

confidence: 99%

TUG1 confers cisplatin resistance in esophageal squamous cell carcinoma by epigenetically suppressing PDCD4 expression via EZH2

Guo

Liu

et al. 2018

Cell Biosci

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BackgroundIncreasing evidence has suggested the involvement of long non-coding RNA taurine upregulated gene 1 (TUG1) in chemoresistance of cancer treatment. However, its function and molecular mechanisms in esophageal squamous cell carcinoma (ESCC) chemoresistance are still not well elucidated. In the present study, we investigate the functional role of TUG1 in cisplatin (DDP) resistance of ESCC and discover the underlying molecular mechanism.ResultsOur study revealed that TUG1 was up-regulated in DDP-resistant ESCC tissues and cells. High TUG1 expression was correlated with poor prognosis of ESCC patients. TUG1 knockdown improved the sensitivity of ECA109/DDP and EC9706/DDP cells to DDP. Moreover, TUG1 could epigenetically suppress PDCD4 expression via recruiting enhancer of zeste homolog 2. PDCD4 overexpression could mimic the functional role of down-regulated TUG1 in DDP resistance. PDCD4 knockdown counteracted the inductive effect of TUG1 inhibition on DDP sensitivity of ECA109/DDP and EC9706/DDP cells. Furthermore, TUG1 knockdown facilitated DDP sensitivity of DDP-resistant ESCC cells in vivo.ConclusionTUG1 knockdown overcame DDP resistance of ESCC by epigenetically silencing PDCD4, providing a novel therapeutic target for ESCC.Electronic supplementary materialThe online version of this article (10.1186/s13578-018-0260-0) contains supplementary material, which is available to authorized users.

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“…In the case of oxaliplatin CRC treatment, several lncRNAs such as GIHCG (172), LIN00152 (192), MALAT1 (197), H19 (20), and MEG3 (203, 204) promote apoptosis by inducing cytotoxicity by different mechanisms, mainly by axis with miRNAs targeting important genes in cell death behavior. Nevertheless, cisplatin CRC resistance is mainly mediated by HOTAIR and PVT1 through inhibition of apoptotic pathways, modulation of expression levels of miR-203a-3p and the activity of Wnt/β-catenin signaling pathway, respectively (116, 202).…”

Section: Lncrna As Regulator Of Drug Resistance In Crcmentioning

confidence: 99%

LncRNAs as Regulators of Autophagy and Drug Resistance in Colorectal Cancer

et al. 2019

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Colorectal cancer (CRC) is a common malignancy with 1. 8 million cases in 2018. Autophagy helps to maintain an adequate cancer microenvironment in order to provide nutritional supplement under adverse conditions such as starvation and hypoxia. Additionally, most of the cases of CRC are unresponsive to chemotherapy, representing a significant challenge for cancer therapy. Recently, autophagy induced by therapy has been shown as a unique mechanism of resistance to anticancer drugs. In this regard, long non-coding RNAs (lncRNAs) analysis are important for cancer detection, progression, diagnosis, therapy response, and prognostic values. With increasing development of quantitative detection techniques, lncRNAs derived from patients' non-invasive samples (i.e., blood, stools, and urine) has become into a novel approach in precision oncology. Tumorspecific GAS5, HOTAIR, H19, and MALAT are novels CRC related lncRNAs detected in patients. Nonetheless, the effect and mechanism of lncRNAs in cancer autophagy and chemoresistance have not been extensively characterized. Chemoresistance and autophagy are relevant for cancer treatment and lncRNAs play a pivotal role in resistance acquisition for several drugs. LncRNAs such as HAGLROS, KCNQ1OT1, and H19 are examples of lncRNAs related to chemoresistance leaded by autophagy. Finally, clinical implications of lncRNAs in CRC are relevant, since they have been associated with tumor differentiation, tumor size, histological grade, histological types, Dukes staging, degree of differentiation, lymph node metastasis, distant metastasis, recurrent free survival, and overall survival (OS).

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Overexpression of MEG3 sensitizes colorectal cancer cells to oxaliplatin through regulation of miR-141/PDCD4 axis

Cited by 63 publications

References 29 publications

Long Non-coding RNAs Contribute to the Inhibition of Proliferation and EMT by Pterostilbene in Human Breast Cancer

Long Non-coding RNAs Contribute to the Inhibition of Proliferation and EMT by Pterostilbene in Human Breast Cancer

TUG1 confers cisplatin resistance in esophageal squamous cell carcinoma by epigenetically suppressing PDCD4 expression via EZH2

LncRNAs as Regulators of Autophagy and Drug Resistance in Colorectal Cancer

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