MiR-135a functions as a selective killer of malignant glioma

Wu, Sihan; Lin, Yongcheng; Xu, Danyan; Chen, J; Shu, Minfeng; Zhu, Wenbo; Su, Xingwen; Zhou, Yi; Qiu, Pengxin; Gao, Yan

doi:10.1038/onc.2011.551

Cited by 86 publications

(65 citation statements)

References 39 publications

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“…MiR135a is downregulated in androgene-dependent versus androgene-independent prostate cancer cells [18]. Though miR-135a functions in a tumor suppressor in several cancer cells such as renal cell carcinoma [19] or glioma cell [20], it has not fully investigated in prostate cancer cells. Thus, in the present study, the underlying apoptotic mechanism by combination of Tanshinone I and TRAIL was studied mainly in highly aggressive DU145 and PC-3 prostate cancer cells in association with upregulation of death receptors and microRNA 135a-3p.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of microRNA135a-3p and death receptor 5 plays a critical role in Tanshinone I sensitized prostate cancer cells to TRAIL induced apoptosis

et al. 2014

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Though tumor necrosis factor related apoptosis inducing ligand (TRAIL) has been used as a potent anticancer agent, TRAIL resistance is a hot-issue in cancer therapy. We investigated the antitumor mechanism of Tanshinone I to sensitize prostate cancer cells to TRAIL. Comibination of Tanshinone I and TRAIL exerted synergistic cytotoxicity, increased cleaved PARP, sub G1 population, the number of TUNELpositive cells, activated caspase 8, 9 and ROS production in PC-3 and DU145 cells. Of note, combination of Tanshinone I and TRAIL enhanced the protein expression of death receptor 5 (DR5) and attenuated anti-apoptotic proteins. RT-PCR and RT-qPCR analyses confirmed that co-treatment of Tanshinone I and TRAIL up-regulated DR5 and microRNA 135a-3p at mRNA level or activity of DR5 promoter and attenuated phosphorylation of extracellular signal regulated kinases in PC-3. Conversely, the silencing of DR5 blocked the increased cytotoxicity, sub G1 population and PARP cleavages induced by co-treatment of Tanshinone I and TRAIL. Interestingly, miR135a-3p mimic enhanced DR5 at mRNA, increased PARP cleavage, Bax and the number of TUNEL positive cells in Tanshinone I and TRAIL cotreated PC-3. Overall, our findings suggest that Tanshinone I enhances TRAIL mediated apoptosis via upregulation of miR135a-3p mediated DR5 in prostate cancer cells as a potent TRAIL sensitizer.

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Section: Introductionmentioning

confidence: 99%

Upregulation of microRNA135a-3p and death receptor 5 plays a critical role in Tanshinone I sensitized prostate cancer cells to TRAIL induced apoptosis

et al. 2014

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“…Furthermore, to increase the efficiency of this kind of treatment, nucleic acid drugs can be modified to be more lipophilic that improves their intracellular penetration. Although modest compared with pretreatment model, the intratumoral injection of cholesterylated tumor suppressor miRNA mimics has been successful in regression of tumors in the post treatment xenograft model (18). Nonetheless, combined with the ease and simplicity of the drug delivery to a given tumor site in oral cavity, the use of antagomir-155 could have enormous potential to evolve for further drug development.…”

Section: Discussionmentioning

confidence: 99%

“…Being a multigenic disease, the single gene-based therapy of OSCC may fall short in therapy (18). Recent studies have shown that a growing class of noncoding RNAs called microRNAs (miRNAs) are involved in posttranscriptional regulation of genes (19).…”

mentioning

confidence: 99%

Oncogenic MicroRNA-155 Down-regulates Tumor Suppressor CDC73 and Promotes Oral Squamous Cell Carcinoma Cell Proliferation

Rather

Nagashri

Swamy

et al. 2013

Journal of Biological Chemistry

112

110

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Background: Cause of the complete loss of CDC73 in a subset of parathyroid tumors remains to be elucidated in the absence of a second mutation and promoter methylation. Results: Oncogenic miR-155 causes down-regulation of tumor suppressor CDC73 in OSCC. Conclusion: miR-155 up-regulation adds yet another mechanism for CDC73 down-regulation in tumors. Significance: Targeting miR-155 adds novelty to OSCC therapeutics.

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“…(33) According to this report, miR-135a is frequently downregulated in malignant glioma, with its expression negatively correlated to pathological grading, and can induce mitochondria-dependent apoptosis targeting STAT6, SMAD5, and BMPR2. These results are consistent with our current data.…”

Section: Discussionmentioning

confidence: 99%

Tumor‐suppressive microRNA‐135a inhibits cancer cell proliferation by targeting the c‐MYC oncogene in renal cell carcinoma

et al. 2012

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Recently, many studies have suggested that microRNAs (miRNAs) are involved in cancer cell development, invasion, and metastasis of various types of human cancers. In a previous study, miRNA expression signatures from renal cell carcinoma (RCC) revealed that expression of microRNA-135a (miR-135a) was significantly reduced in cancerous tissues. The aim of this study was to investigate the functional significance of miR-135a and to identify miR-135a-mediated molecular pathways in RCC cells. Restoration of mature miR-135a significantly inhibited cancer cell proliferation and induced G 0 ⁄ G 1 arrest in the RCC cell lines caki2 and A498, suggesting that miR-135a functioned as a potential tumor suppressor. We then examined miR-135a-mediated molecular pathways using genome-wide gene expression analysis and in silico analysis. A total of 570 downregulated genes were identified in miR-135a transfected RCC cell lines. To investigate the biological significance of potential miR-135a-mediated pathways, we classified putative miR-135a-regulated genes according to the Kyoto Encyclopedia of Genes and Genomics pathway database. From our in silico analysis, 25 pathways, including the cell cycle, pathways in cancer, DNA replication, and focal adhesion, were significantly regulated by miR-135a in RCC cells. Moreover, based on the results of this analysis, we investigated whether miR-135a targeted the c-MYC gene in RCC. Gain-of-function and luciferase reporter assays showed that c-MYC was directly regulated by miR-135a in RCC cells. Furthermore, c-MYC expression was significantly upregulated in RCC clinical specimens. Our data suggest that elucidation of tumor-suppressive miR-135a-mediated molecular pathways could reveal potential therapeutic targets in RCC. (Cancer Sci 2013; 104: 304-312) R enal cell carcinoma (RCC) is the most common neoplasm of the adult kidney, and approximately 80% of RCC patients are diagnosed with the clear cell RCC (ccRCC) subtype.(1) In the USA, the incidence and mortality rates of RCC have increased in recent years, with approximately 58 000 new cases and 13 000 deaths in 2010.(2) Although surgery is curative for localized disease, a significant percentage of patients developed relapses or metastases with poor prognosis.(3,4) Therefore, researchers have become interested in elucidating the molecular mechanisms of RCC oncogenesis and metastasis, which could lead to development of better prognostic, diagnostic, and therapeutic interventions for the disease.RNA can be divided into two categories, protein-coding RNAs and non-coding RNAs (ncRNAs). It is important to examine the functions of ncRNAs in both normal and diseased tissues and to elucidate their involvement in human diseases, including cancer. MicroRNAs (miRNAs) are endogenous small ncRNA molecules (19-22 bases) that regulate protein-coding gene expression by repressing translation of RNA or cleaving RNA transcripts in a sequence-specific manner.(5) A growing body of evidence suggests that miRNAs are aberrantly expressed in many human cancers and ...

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MiR-135a functions as a selective killer of malignant glioma

Cited by 86 publications

References 39 publications

Upregulation of microRNA135a-3p and death receptor 5 plays a critical role in Tanshinone I sensitized prostate cancer cells to TRAIL induced apoptosis

Upregulation of microRNA135a-3p and death receptor 5 plays a critical role in Tanshinone I sensitized prostate cancer cells to TRAIL induced apoptosis

Oncogenic MicroRNA-155 Down-regulates Tumor Suppressor CDC73 and Promotes Oral Squamous Cell Carcinoma Cell Proliferation

Tumor‐suppressive microRNA‐135a inhibits cancer cell proliferation by targeting the c‐MYC oncogene in renal cell carcinoma

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