miR-20a-directed regulation of BID is associated with the TRAIL sensitivity in colorectal cancer

Huang, Guiqian; Chen, Xiangjian; Cai, Yefeng; Wang, Xiaobo; Chen, Xing

doi:10.3892/or.2016.5278

Cited by 46 publications

(53 citation statements)

References 36 publications

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“…Subsequently, the mitochondrial permeability transition pore is open and then cytochrome c and Smac/DIABLO which are apoptotic inducers derived from mitochondria will be released into cytoplasm. Finally, caspase-9 and caspase-3 are cleaved and apoptosis occurs in cancer cells [19,21,31,32]. Consistent with these reports, our results emphasized the importance of TRAIL and FasL in γδ T cells-mediated cell lysis in HCC.…”

Section: Mir-382-overexpressed Hcc Model Is Sensitive To γδ T Cells Tsupporting

confidence: 81%

“…We found that co-treatment with miR-382 and γδ T cells induced significant translocation of tBid to mitochondria through the c-FLIP/caspase 8 pathway ( Figure 5C). Since the translocation of tBid induced opening of mitochondrial permeability transition pore (mPTP) [21], we found that combination with miR-382 and γδ T cells induced release of cytochrome c and Smac/DIABLO, which were the apoptotic inducer [22], from mitochondria into the cytoplasm. As the results, caspase 9 and its substrate caspase 3 were significantly activated ( Figure 5D).…”

Section: Mir-382 Promotes γδ T Cells-induced Activation Of Caspases Tmentioning

confidence: 99%

“…Bid is the substrate of caspase 8. It can be cleaved by caspase 8 and then translocated from the cytosolic fraction to mitochondria as the form of truncated Bid (tBid) [21]. We therefore separated the mitochondria from the HepG2 and PLC cells to detect the level of tBid.…”

Section: Mir-382 Promotes γδ T Cells-induced Activation Of Caspases Tmentioning

confidence: 99%

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WITHDRAWN: Overexpression of miR-382 sensitizes hepatocellular carcinoma cells to γδ T cells through inhibiting the expression of c-FLIP

Hou¹,

Chen²,

Zheng³

et al. 2018

Oncotarget

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Section: Mir-382-overexpressed Hcc Model Is Sensitive To γδ T Cells Tsupporting

confidence: 81%

Section: Mir-382 Promotes γδ T Cells-induced Activation Of Caspases Tmentioning

confidence: 99%

See 1 more Smart Citation

WITHDRAWN: Overexpression of miR-382 sensitizes hepatocellular carcinoma cells to γδ T cells through inhibiting the expression of c-FLIP

Hou¹,

Chen²,

Zheng³

et al. 2018

Oncotarget

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show abstract

“…Here, we reported that miR-20a is downregulated in osteosarcoma and indicated that miR-20a is a tumorsupressor in osteosarcoma cell growth. miR-20a downregulation was reported in cutaneous squamous cell carcinoma, future science group www.futuremedicine.com hepatocellular carcinoma and pancreatic cancer cells [18][19][20], whereas its upregulation was shown in uveal melanoma, colorectal cancer and cervical cancer [21][22][23]. These controversial data indicate that the function of miR-20a is possibly tumor specific and highly dependent on its downstream target in various cancers.…”

Section: Discussionmentioning

confidence: 95%

MiRNA-20A Upregulates TAK1 and Increases Proliferation in Osteosarcoma Cells

Yuan

Zhao

et al. 2018

Future Oncol.

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Aim:The aim of this study is to explore the function of miR-20a in osteosarcoma. Materials & methods: miR-20a expression was measured by real-time PCR. miR-20a mimics, inhibitor and scramble siRNA were transfected into osteosarcoma cells to observe effects on colony formation and tumor growth. Moreover, relationships of miR-20a with TAK1 were investigated by western blot and luciferase activity. Results: We found that miR-20a was downregulated in osteosarcoma, and overexpression of miR-20a reduced colony formation and tumor growth. Furthermore, the data revealed that the function of miR-20a was probably exerted via targeting the TAK1 expression. Overexpression of miR-20a sensitizes the osteosarcoma cells to chemotherapeutic drugs. Conclusion: Our data identify the role of miR-20a in osteosarcoma growth, indicating its potential application in chemotherapy. Osteosarcoma is the most common primary malignant bone tumor with high morbidity in young adults and children, comprising 2.4% of all malignancies in pediatric patients and about 20% of all primary bone tumors [1]. It occurs mainly around regions with active bone growth and reparation. Osteosarcoma is highly aggressive and responded poorly to chemotherapy, and the 5-year survival rate for patients with metastatic osteosarcoma is only 14% [2]. Therefore, it is of extreme significance to elucidate novel molecular targets to develop alternative therapeutic target for this disease.miRNAs are a small family of noncoding RNAs that play important roles in the development of human diseases by negatively regulating gene expression at either post-transcriptional or translational levels [3,4]. Over the last decade, many miRNAs have been showed in regulating diverse biological events such as cell proliferation, differentiation and apoptotic processes [5][6][7], which are important in the development of cancer. Accumulated evidence indicated that aberrant expression of miRNAs associates with various types of cancer. These dysregulated miRNAs function as either oncogenes or tumor suppressors in carcinogenesis and progression of cancers [8,9]. Thus, to explore the aberrant miRNAs expression in osteosarcoma might lead to the discovery of novel miRNAs biomarkers.In this study, we found that miR-20a was downregulated in osteosarcoma samples and osteosarcoma cell lines, and the ectopic expression of miR-20a reduced cell colony formation in vitro and tumor growth in vivo. Furthermore, bioinformatic prediction and experimental validation revealed that the function of miR-20a was probably exerted via targeting the TAK1 expression. To translate these findings, overexpression of miR-20a sensitizes the osteosarcoma cells to chemotherapeutic drugs. Collectively, our data identify the key role of miR-20a in osteosarcoma growth, indicating its potential application in cancer chemotherapy.

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“…MiRNAs have been observed to be dysregulated in almost all human cancers [13,14]. Correcting the aberrant expression of miRNAs has been shown to inhibit cell proliferation, metastasis, invasion, and chemoresistance in cancers [15,16]. As recent studies have demonstrated the association between the miRNA expression profile and TRAIL sensitivity in some cancers [17,18], we aimed to explore the ability of the combination of TRAIL with miR-128 to enhance TRAIL-induced cytotoxicity against CRC.…”

Section: Introductionmentioning

confidence: 99%

miR-128 Targets the SIRT1/ROS/DR5 Pathway to Sensitize Colorectal Cancer to TRAIL-Induced Apoptosis

Liu

Yang

Liu

et al. 2018

Cell Physiol Biochem

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Background/Aims: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is an ideal anti-tumor drug because it exhibits selective cytotoxicity against cancer cells. However, certain cancer cells are resistant to TRAIL, and the potential mechanisms are still unclear. The aim of this study was to reduce the resistance of colorectal cancer (CRC) cells to TRAIL. Methods: Quantitative real-time PCR analysis was performed to detect the expression of microRNA-128 (miR-128) in tissues from patients with CRC and CRC cell lines. MTT assays were used to evaluate the effect of miR-128 on TRAIL-induced cytotoxicity against CRC cell lines. The distribution of death receptor 5 (DR5) and the production of reactive oxygen species (ROS) were detected by flow cytometry analysis. Western blot, flow cytometry, and luciferase reporter assays were performed to evaluate the potential mechanism and pathway of miR-128-promoted apoptosis in TRAIL-treated CRC cells. Results: MiR-128 expression was downregulated in tumor tissues from patients with CRC as well as in CRC cell lines in vitro. The enforced expression of miR-128 sensitized CRC cells to TRAIL-induced cytotoxicity by inducing apoptosis. Mechanistically, bioinformatics, western blot analysis, and luciferase reporter assays showed that miR-128 directly targeted sirtuin 1 (SIRT1) in CRC cells. miR-128 overexpression suppressed SIRT1 expression, which promoted the production of ROS in TRAIL-treated CRC cells. This increase of ROS subsequently induced DR5 expression, and thus increased TRAIL-induced apoptosis in CRC cells. Conclusion: The combination of miR-128 with TRAIL may represent a novel approach for the treatment of CRC.

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miR-20a-directed regulation of BID is associated with the TRAIL sensitivity in colorectal cancer

Cited by 46 publications

References 36 publications

WITHDRAWN: Overexpression of miR-382 sensitizes hepatocellular carcinoma cells to γδ T cells through inhibiting the expression of c-FLIP

WITHDRAWN: Overexpression of miR-382 sensitizes hepatocellular carcinoma cells to γδ T cells through inhibiting the expression of c-FLIP

MiRNA-20A Upregulates TAK1 and Increases Proliferation in Osteosarcoma Cells

miR-128 Targets the SIRT1/ROS/DR5 Pathway to Sensitize Colorectal Cancer to TRAIL-Induced Apoptosis

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