MicroRNA-98 and microRNA-214 post-transcriptionally regulate enhancer of zeste homolog 2 and inhibit migration and invasion in human esophageal squamous cell carcinoma

Huang, Shengdong; Yuan, Yuan; Zhuang, Chong-Wen; Li, Bailing; Gong, Daozhi; Wang, Shugang; Zeng, Zhiyong; Cheng, He-Zhong

doi:10.1186/1476-4598-11-51

Cited by 100 publications

(79 citation statements)

References 37 publications

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“…Bioinformatic analysis revealed that HMGA1P6 and HMGA1P7 contain sequences that can be targeted by miRNAs that target High Mobility Group A2 (HMGA2) , Vascular Endothelial Growth Factor (VEGF) and Enhancer of Zeste Homolog 2 (EZH2) , all of which are known to be involved in carcinogenesis [34-36]. Accordingly, we found that HMGA1P6 or HMGA1P7 overexpression increased the level of the proteins coded for by these genes (Figure 5D).…”

Section: Resultsmentioning

confidence: 87%

HMGA1pseudogenes as candidate proto-oncogenic competitive endogenous RNAs

et al. 2014

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The High Mobility Group A (HMGA) are nuclear proteins that participate in the organization of nucleoprotein complexes involved in chromatin structure, replication and gene transcription. HMGA overexpression is a feature of human cancer and plays a causal role in cell transformation. Since non-coding RNAs and pseudogenes are now recognized to be important in physiology and disease, we investigated HMGA1 pseudogenes in cancer settings using bioinformatics analysis. Here we report the identification and characterization of two HMGA1 non-coding pseudogenes, HMGA1P6 and HMGA1P7. We show that their overexpression increases the levels of HMGA1 and other cancer-related proteins by inhibiting the suppression of their synthesis mediated by microRNAs. Consistently, embryonic fibroblasts from HMGA1P7-overexpressing transgenic mice displayed a higher growth rate and reduced susceptibility to senescence. Moreover, HMGA1P6 and HMGA1P7 were overexpressed in human anaplastic thyroid carcinomas, which are highly aggressive, but not in differentiated papillary carcinomas, which are less aggressive. Lastly, the expression of the HMGA1 pseudogenes was significantly correlated with HMGA1 protein levels thereby implicating HMGA1P overexpression in cancer progression. In conclusion, HMGA1P6 and HMGA1P7 are potential proto-oncogenic competitive endogenous RNAs.

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Section: Resultsmentioning

confidence: 87%

HMGA1pseudogenes as candidate proto-oncogenic competitive endogenous RNAs

et al. 2014

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“…miRNAs, including miR-21, miR-31, miR-577, etc, act as oncogenes, [19][20][21] while others such as Let-7, miR-98, miR-100, miR-138, miR-143, miR-150, etc, function as tumor suppressors. [22][23][24][25][26][27] However, the role of miR-186 in ESCC progression remains uninvestigated.…”

Section: Discussionmentioning

confidence: 99%

microRNA-186 inhibits cell proliferation and induces apoptosis in human esophageal squamous cell carcinoma by targeting SKP2

Jiao

Zhang

et al. 2016

Laboratory Investigation

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miR-186 has been demonstrated to have a significant role as a tumor suppressor in many types of cancers. Nevertheless, its biological function in esophageal squamous cell carcinoma (ESCC) remains unknown. In the present study, we found that the expression level of miR-186 was downregulated in ESCC in comparison with the adjacent normal tissues and was significantly associated with differentiation level, TNM stage, and lymph node metastasis of ESCC. Functional experiments revealed that enforced overexpression of miR-186 in ESCC cells suppressed the proliferation, invasion, and induced the apoptosis of cells. Luciferase reporter assay and western blotting analysis were performed to verify the target gene regulated by miR-186, SKP2. Our findings established that the miR-186 has a suppressive role in ESCC progression via SKP2-mediated pathway, and this implies that miR-186 could be a potential therapeutic target for ESCC.

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“…Hsa-mir-98-5p belongs to the let-7 family of microRNAs (miRNAs) [15–17] and is dysregulated in cancers of the lung [18], breast [19] and colon [20], and in esophageal squamous tumors [21]. Hsa-mir-98- 5p inhibits tumor cell growth and metastasis in oral squamous cell carcinoma by targeting IGFIR [22], and its overexpression prevents glioma cell line invasion by downregulating IKKε [23].…”

Section: Introductionmentioning

confidence: 99%

NEAT1 upregulates EGCG-induced CTR1 to enhance cisplatin sensitivity in lung cancer cells

et al. 2016

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Platinum-based drugs are the firstline of treatment for non-small cell lung cancer (NSCLC), but resistance to these drugs is a major obstacle to effective chemotherapy. Our previous study revealed that the green tea polyphenol, EGCG, induced cisplatin transporter CTR1 (copper transporter 1) and enhanced cisplatin sensitivity in ovarian cancer. In this study, we found that EGCG upregulated CTR1 and increased platinum accumulation in NSCLC (A549, H460 and H1299) cells, cDDP-resistant A549 cells and a nude mouse xenograft model. Cisplatin-induced inhibition of cell growth was enhanced by EGCG treatment in vitro and in vivo. MicroRNA hsa-mir-98-5p appears to suppress CTR1 gene expression, while long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) appears to enhance it. Bioinformatics analysis showed that hsa-mir-98-5p has specific complementary binding sites for NEAT1. In addition, hsa-mir-98-5p was predicted to be a putative CTR1 target. NEAT1 may act as a competing endogenous lncRNA to upregulate EGCG-induced CTR1 by sponging hsa-mir-98-5p in NSCLC. Our findings reveal a novel mechanism how NEAT1 upregulates EGCG-induced CTR1 and enhances cisplatin sensitivity in vitro and in vivo, and suggest EGCG could serve as an effective adjuvant chemotherapeutic in lung cancer treatment.

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MicroRNA-98 and microRNA-214 post-transcriptionally regulate enhancer of zeste homolog 2 and inhibit migration and invasion in human esophageal squamous cell carcinoma

Cited by 100 publications

References 37 publications

HMGA1pseudogenes as candidate proto-oncogenic competitive endogenous RNAs

HMGA1pseudogenes as candidate proto-oncogenic competitive endogenous RNAs

microRNA-186 inhibits cell proliferation and induces apoptosis in human esophageal squamous cell carcinoma by targeting SKP2

NEAT1 upregulates EGCG-induced CTR1 to enhance cisplatin sensitivity in lung cancer cells

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