Expression and function of miR-27b in human glioma

Chen, Lingchao; Li, Huibing; Han, Lihua; Zhang, Kailiang; Wang, Guangxiu; Wang, Yongzhi; Liu, Yanwei; Zheng, Yongri; Jiang, Tao; Pu, Peiyu; Jiang, Chuanlu; Kang, Chunsheng

doi:10.3892/or.2011.1458

Cited by 25 publications

(24 citation statements)

References 14 publications

(17 reference statements)

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“…MiR-23b has been reported to function as a renal cancer oncogene [25], similar to ovarian cancer seen in the present study, whereas it functions as a tumor suppressor in hepatocellular carcinoma [26]. The introduction of pre-miR-27b stimulates invasion in breast cancer cells by targeting the ST14 tumor suppressor [27], and is upregulated in glioma cells and tumor tissues [28]. However, it is downregulated in lung cancer tissue [29].…”

Section: Discussionsupporting

confidence: 64%

MicroRNAs overexpressed in ovarian ALDH1-positive cells are associated with chemoresistance

et al. 2013

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BackgroundOvarian carcinoma is the leading cause of cancer death worldwide among gynecological malignancies, and the majority of cases are related with recurrence and chemoresistance. Cancer stem cells (CSCs) are believed to be one of the causes of recurrent or chemoresistant ovarian cancer, and microRNAs are regulatory molecules newly implicated to control a variety of cellular processes, including CSCs. Therefore, we identified ovarian CSC-specific microRNAs and investigated their clinicopathological implication in ovarian carcinomas.MethodsWe isolated ALDH1 (+) cell population using the Aldefluor assay, and examined the differential expression pattern of miRNAs between ALDH1 (+) and ALDH1 (−) cells using a high-throughput microRNA microarray. We further investigated the expression patterns of differentially expressed miRNAs in human ovarian cancer samples using the real-time reverse transcription-polymerase chain reaction and analyzed their clinical impact in patients with ovarian cancer.ResultsWe found that high ALDH1 expression was associated with chemoresistance in in vitro and ex vivo samples (p = 0.024). We identified six miRNAs, including miR-23b, miR-27a, miR-27b, miR-346, miR-424, and miR-503, overexpressed in ALDH1 (+) cells, and they were significantly upregulated in chemoresistant ovarian cancer cells (1.4 ~ 3.5-fold) and tumor samples (2.8 ~ 5.5-fold) compared with chemosensitive group. Upregulation of ALDH1 (p = 0.019) and miR-503 (p = 0.033) correlated with high clinical stage, and upregulation of miR-27a was related with distant metastasis (p = 0.046) in patients with ovarian cancer.ConclusionOur findings indicate that ALDH1 is a useful marker for enriching ovarian CSCs, and high expression of ALDH1 and its related miRNAs, particularly miR-23b, miR-27b, miR-424, and miR-503, are significantly implicated in chemoresistance and tumor progression in ovarian cancer.

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Section: Discussionsupporting

confidence: 64%

MicroRNAs overexpressed in ovarian ALDH1-positive cells are associated with chemoresistance

et al. 2013

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“…miRNA expression alterations have been reported to be involved in several physiological and pathological processes such as aging, tumorigenesis, metabolism and inflammation, 8 , 49 , 50 , 51 and several studies have demonstrated differential expression of miR-27 in various diseases. miR-27 is upregulated in breast cancer, oral cancer, glioma and peripheral arterial disease 41 , 52 , 53 , 54 , 55 and is downregulated in prostate cancer and head and neck squamous cancer. 56 , 57 Several reports have shown that mitochondrial fusion can inhibit cell death, whereas mitochondrial fission is involved in the promotion of apoptosis.…”

Section: Discussionmentioning

confidence: 99%

miR-27 regulates mitochondrial networks by directly targeting the mitochondrial fission factor

et al. 2014

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Mitochondrial morphology is dynamically regulated by forming small, fragmented units or interconnected networks, and this is a pivotal process that is used to maintain mitochondrial homeostasis. Although dysregulation of mitochondrial dynamics is related to the pathogenesis of several human diseases, its molecular mechanism is not fully elucidated. In this study, we demonstrate the potential role of miR-27 in the regulation of mitochondrial dynamics. Mitochondrial fission factor (MFF) mRNA is a direct target of miR-27, whose ectopic expression decreases MFF expression through binding to its 3′-untranslated region. Expression of miR-27 results in the elongation of mitochondria as well as an increased mitochondrial membrane potential and mitochondrial ATP level. Our results suggest that miR-27 is a novel regulator affecting morphological mitochondrial changes by targeting MFF.

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“…14 It has reported that marked downregulation of miRNA-27b-3p in tamoxifen-resistant cells compared with parental MCF-7 cells. 14 Recently, several studies have identified miR-27b-3p (also known as miR-27b) promotes cell proliferation and invasion in glioma and breast cancer, 15, 16 and blocks paclitaxel-induced apoptosis in cervical cancer. 17 MiR-27b-3p also reportedly plays a cancer-promoting role and is associated with poor prognosis in triple-negative breast cancer patients.…”

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confidence: 99%

Downregulation of microRNA-27b-3p enhances tamoxifen resistance in breast cancer by increasing NR5A2 and CREB1 expression

et al. 2016

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Estrogen-dependent breast cancer is often treated with the aromatase inhibitors or estrogen receptor (ER) antagonists. Tamoxifen as a major ER antagonist is usually used to treat those patients with ERα-positive breast cancer. However, a majority of patients with ERα positive fail to respond to tamoxifen due to the presence of intrinsic or acquired resistance to the drug. Altered expression and functions of microRNAs (miRNAs) have been reportedly associated with tamoxifen resistance. In this study, we investigated the role of miR-27b-3p in resistance of breast cancer to tamoxifen. MiR-27b-3p levels were remarkably reduced in the tamoxifen-resistant breast cancer cells compared with their parental cells. In addition, miR-27b-3p was also significantly downregulated in breast tumor tissues relative to adjacent non-tumor tissues. Moreover, the expression levels of miR-27b-3p were lower in the breast cancer tissues from tamoxifen-resistant patients compared with that from untreated-tamoxifen patients. Notably, tamoxifen repressed miR-27b-3p expression, whereas estrogen induced miR-27b-3p expression in breast cancer cells. Besides, we provided experimental evidences that miR-27b-3p enhances the sensitivity of breast cancer cells to tamoxifen in vitro and in vivo models. More importantly, we validated that miR-27b-3p directly targeted and inhibited the expression of nuclear receptor subfamily 5 group A member 2 (NR5A2) and cAMP-response element binding protein 1 (CREB1) and therefore augmented tamoxifen-induced cytotoxicity in breast cancer. Lastly, miR-27b-3p levels were found to be significantly negatively correlated with both NR5A2 and CREB1 levels in breast cancer tissues. Our findings provided further evidence that miR-27b-3p might be considered as a novel and potential target for the diagnosis and treatment of tamoxifen-resistant breast cancer.

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Expression and function of miR-27b in human glioma

Cited by 25 publications

References 14 publications

MicroRNAs overexpressed in ovarian ALDH1-positive cells are associated with chemoresistance

MicroRNAs overexpressed in ovarian ALDH1-positive cells are associated with chemoresistance

miR-27 regulates mitochondrial networks by directly targeting the mitochondrial fission factor

Downregulation of microRNA-27b-3p enhances tamoxifen resistance in breast cancer by increasing NR5A2 and CREB1 expression

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