miR-340 impedes the progression of laryngeal squamous cell carcinoma by targeting EZH2

Yu, Wenfa; Zhang, Guozheng; Lu, Baocai; Li, Jing; Wu, Zhiyan; Ma, Huimin; Wang, Huimin; Lian, Rong

doi:10.1016/j.gene.2015.11.045

Cited by 32 publications

(22 citation statements)

References 29 publications

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“…This previous result indicated that the roles of miR-340 may not be consistent with the pattern of its expression in melanoma cells; consequently, when assessing the function of a miRNA, the level of its expression may not be the sole consideration. miR-340 is involved in oncogenesis in various ways; miR-340 inhibits proliferation, migration and invasion, and induces apoptosis, in ovarian cancer, prostate cancer, laryngeal squamous cell carcinoma and glioblastoma (12,22,(24)(25)(26). The results of the present study demonstrated the same function of miR-340 in HCC compared with these previous studies.…”

Section: Discussionsupporting

confidence: 81%

MicroRNA-340 inhibits tumor cell proliferation, migration and invasion, and induces apoptosis in hepatocellular carcinoma

Wang

Song

Huang

2017

Molecular Medicine Reports

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MicroRNAs (miRs) are short RNAs that serve a role in the origination and progression of hepatocellular carcinoma (HCC). miR‑340 has been identified to be a novel tumor suppressor. The present study investigated the antitumor function of miR‑340 in HCC. In the present study, it was detected that miR‑340 was significantly decreased in HCC cancer tissues and human HCC cell lines using reverse transcription‑quantitative polymerase chain reaction analysis. Cell Counting kit‑8 and apoptosis assays demonstrated that miR‑340 reduced cell proliferation and induced cellular apoptosis in HCC cell lines. A Transwell invasion assay demonstrated that miR‑340 suppressed the migration and invasion of HCC cell lines. In addition, S‑phase kinase‑associated protein 2 (SKP2), which may be repressed by miR‑340 in HCC cell lines, was identified to be a potential target of miR‑340. The results of the present study revealed that miR‑340 serves a tumor suppressor role by influencing the proliferation, apoptosis, migration and invasion of HCC cell lines, which may be explained by the downregulation of SKP2 by miR‑340.

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Section: Discussionsupporting

confidence: 81%

MicroRNA-340 inhibits tumor cell proliferation, migration and invasion, and induces apoptosis in hepatocellular carcinoma

Wang

Song

Huang

2017

Molecular Medicine Reports

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“…For example, miR-101 decreases the abilities of invasion and migration in several tumor types containing osteosarcoma in vitro [29], gastric cancer [30], prostate cancer [31], and glioblastoma [32] in vitro and in vivo, through post-transcriptional down-regulation of EZH2 . Moreover, miR-26a [33,34], miR-138 [35,36,37], miR-124 [38,39,40], miR-98 [41,42], miR-214 [42], miR-30d [43], miR-298 [44], and miR-340 [45] also participate in the post-transcriptional regulation of EZH2 in different kinds of cancer cells. For example, miR-26a inhibits epithelial–mesenchymal transition (EMT) function and up-regulates tumor suppressor genes, DAB2IP and RUNX3, through post-transcriptional repression of EZH2 in human hepatocellular carcinoma and lung carcinoma cells in vitro [33].…”

Section: Molecular Regulations Of Ezh2mentioning

confidence: 99%

EZH2 in Cancer Progression and Potential Application in Cancer Therapy: A Friend or Foe?

Yan

Lin

Liao

et al. 2017

IJMS

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Enhancer of zeste homolog 2 (EZH2), a histone methyltransferase, catalyzes tri-methylation of histone H3 at Lys 27 (H3K27me3) to regulate gene expression through epigenetic machinery. EZH2 functions as a double-facet molecule in regulation of gene expression via repression or activation mechanisms, depending on the different cellular contexts. EZH2 interacts with both histone and non-histone proteins to modulate diverse physiological functions including cancer progression and malignancy. In this review article, we focused on the updated information regarding microRNAs (miRNAs) and long non coding RNAs (lncRNAs) in regulation of EZH2, the oncogenic and tumor suppressive roles of EZH2 in cancer progression and malignancy, as well as current pre-clinical and clinical trials of EZH2 inhibitors.

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“…Overexpression of EZH2 has been found to be associated with tumor aggressiveness, metastasis, and poor prognosis in multiple cancers [17-20], including lung cancer [21, 22]. MiR-26a was documented to suppress tumor growth by targeting EZH2 in some tumors [23-25].…”

Section: Resultsmentioning

confidence: 99%

MiRNA-26a Contributes to the Acquisition of Malignant Behaviors of Doctaxel-Resistant Lung Adenocarcinoma Cells through Targeting EZH2

Chen

Tao

et al. 2017

Cell Physiol Biochem

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Background/Aims: Accumulating evidence revealed that microRNAs (miRNAs) have been demonstrated as critical molecules in tumor development and progression. MiR-26a, located in a fragile chromosomal region associated with various human cancer, has been reported to be involved in regulating various cellular process, such as proliferation, apoptosis and invasion through targeting multiple oncogene. Docetaxel-mediated chemotherapy has been applied in improving the survival and prognosis of patients with advanced lung adenocarcinoma (LAD). However, chemoresistance remains a major impediment to clinical application of this agent. It has been presented that decreased miR-26a expression lead to cisplatin resistance and promoted growth and migration in human lung cancer. Enhancer of zeste homolog 2 (EZH2) is the target of miR-26a. The present study aimed to investigate the function of miR-26a/EZH2 in the acquisition of malignant behaviors of LAD. Methods: MiR-26a and EZH2 expression levels in the dcetaxel-insensitive groups (n = 19) and the docetaxel-sensitive groups (n = 18) were assessed by qRT-PCR. Colony formation assay, flow cytometric analysis, wound healing assay, cell transwell assays and western blotting were performed to assess the effects of miR-26a on proliferation, apoptosis and epithelial-to-mesenchymal (EMT) phenotypes in docetaxel resistant LAD cells in vitro. Xenograft transplantation, immunohistochemistry, tunel assays and western blotting assays were employed to demonstrate the role of miR-26a in docetaxel resistant LAD cells in vivo. The expression level of EZH2 in docetaxel-resistant LAD cells and corresponding parental cells was detected by qRT-PCR and western blotting. The relationship between miR-26a and EZH2 was confirmed by luciferase reporter assay. And rescue assays were performed to further confirm that miRNA-26a contributes to the acquisition of malignant behaviors of docetaxel-resistant LAD cells through targeting EZH2. Results: MiR-26a was significantly down-regulated in the dcetaxel-insensitive groups (n = 19) compared with the docetaxel-sensitive groups (n = 18) assessed by qRT-PCR. MiR-26a decreased the proliferation, increased the apoptosis rate and reversed EMT to MET of docetaxel-resistant LAD cells both in vivo and vitro. EZH2 was confirmed as target of miR-26a. Rescue assays further verified that the function of miR-26a exerts in docetaxel-resistant LAD cells is through targeting EZH2. Conclusions: Our data revealed that overexpression of miR-26a in docetaxel-resistant LAD cells could decrease the proliferation, increase the apoptosis rate and reverse EMT to MET of docetaxel-resistant LAD cells both in vivo and vitro and such function is partially exerted via downregulating EZH2. MiR-26a/EZH2 signal pathway makes contribute to the malignant phenotype of docetaxel-resistant of LAD cells which indicated that miR-26a exerts pivotal functions in the molecular etiology of chemoresistant lung adenocarcinoma.

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miR-340 impedes the progression of laryngeal squamous cell carcinoma by targeting EZH2

Cited by 32 publications

References 29 publications

MicroRNA-340 inhibits tumor cell proliferation, migration and invasion, and induces apoptosis in hepatocellular carcinoma

MicroRNA-340 inhibits tumor cell proliferation, migration and invasion, and induces apoptosis in hepatocellular carcinoma

EZH2 in Cancer Progression and Potential Application in Cancer Therapy: A Friend or Foe?

MiRNA-26a Contributes to the Acquisition of Malignant Behaviors of Doctaxel-Resistant Lung Adenocarcinoma Cells through Targeting EZH2

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