Tumor‐targeting TRAIL expression mediated by miRNA response elements suppressed growth of uveal melanoma cells

Liu, Jia; Ma, Leina; Li, Caixin; Zhang, Ziyu; Yang, Guanghua; Zhang, Wenwei

doi:10.1016/j.molonc.2013.08.003

Cited by 46 publications

(33 citation statements)

References 41 publications

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“…Finally, in vivo data revealed that Ad-TRAIL-MRE-7-122 suppressed the growth of Bcap37 tumors in mice as potent as Ad-TRAIL and had no hepatotoxicity to the animals. In fact, the similar effects have been verified in some other types of cancers using MRE-based strategy, such as melanoma, glioma and bladder carcinoma [11][12][13].…”

Section: Discussionsupporting

confidence: 60%

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Breast cancer-specific TRAIL expression mediated by miRNA response elements of let-7 and miR-122

Yan¹,

Zhang²,

Fan³

et al. 2014

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Breast cancer is a highly aggressive malignancy and always has a poor prognosis. The current therapeutic strategies including surgery, chemotherapy and radiotherapy benefit little for patients survival. Although tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can induce apoptosis in a wide range of cancer cells, such as breast cancer, it also has cytotoxicity to normal cells. To improve the selectivity of TRAIL expression to breast cancer cells, we inserted miRNA response elements (MREs) of let-7 and miR-122 into a TRAIL-expressing adenoviral vector (Ad-TRAIL-MRE-7-122) to restrict its expression within breast cancer cells. qPCR assay confirmed that the levels of let-7 and miR-122 were downregulated in breast cancer samples and cell lines, compared with normal tissues and cell lines. Luciferase assay indicated that MREs of let-7 and miR-122 was able to confer luciferase expression with the selectivity to breast cancer. Ad-TRAIL-MRE-7-122 highly expressed TRAIL in breast cancer cells, but not in normal cells. The breast cancer-specific apoptosis was detected after the infection of Ad-TRAIL-MRE-7-122. The viability of breast cancer cells, rather than normal cells, was reduced by the treatment of Ad-TRAIL-MRE-7-122. Animal experiments further confirmed that Ad-TRAIL-MRE-7-122 and Ad-TRAIL both greatly impeded the growth of breast cancer xenograft in mice. Taken together, we constructed a TRAIL-expressing recombinant adenovirus regulated by MREs of let-7 and miR-122 and showed evidences that this strategy may be promising for breast cancer treatment.

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Section: Discussionsupporting

confidence: 60%

“…More importantly, the expression of inserted genes can be suppressed in normal cells because of the overexpression of selected miRNAs. However, no publication that focuses on the MRE-regulated gene therapy for breast cancer is available, although this strategy has been tested for some other types of cancer [11][12][13][14].…”

mentioning

confidence: 99%

Breast cancer-specific TRAIL expression mediated by miRNA response elements of let-7 and miR-122

Yan¹,

Zhang²,

Fan³

et al. 2014

neo

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“…Northern blot analysis was performed to determine the levels of miR-155 in the indicated samples and cell lines, according to previously described procedures (13). Briefly, total RNA was isolated from the tissues and cells using TRIzol reagent (Invitrogen Life Technologies, Carlsbad, CA, USA), which was then separated using 15% urea-PAGE (8 M; 480 g urea/liter; Sigma-Aldrich).…”

Section: Reverse Transcription-quantitative Polymerase Chain Reactionmentioning

confidence: 99%

MicroRNA-155 enhances the activation of Wnt/β-catenin signaling in colorectal carcinoma by suppressing HMG-box transcription factor 1

Wan

Han

et al. 2016

Molecular Medicine Reports

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Abstract. Colorectal carcinoma (CRC) is a malignant solid tumor arising from the large intestine and is associated with an increasing incidence and poor prognosis. Further understanding of the molecular mechanisms underlying CRC may contribute to the development of novel effective therapeutic strategies. MicroRNAs (miRs), including miR-155, have been reported to be associated with the etiology and biology of CRC; however, the molecular mechanisms by which miR-155 affect CRC remain to be fully elucidated. The present study used a multidisciplinary approach, involving reverse transcription-quantitative polymerase chain reaction, northern blotting, MTT assay, cell cycle progression analysis, immunoblotting, and animal experiments, to determine the possible targets of miR-155 in CRC cells. miR-155 was found to be overexpressed in CRC tissue samples, compared with paired normal colon tissue samples. In addition, the inhibition of miR-155 induced a deceleration in CRC cell proliferation and inactivation of the Wnt/β-catenin signaling pathway. miR-155 suppression also reduced the growth of CRC xenografts in an animal model. HMG-box transcription factor 1 (HBP1) was identified as a novel target of miR-155, which mediated its effect on CRC via the Wnt/β-catenin pathway. Furthermore, patients with CRC exhibiting higher serum levels of miR-155 exhibited reduced survival rates. In conclusion, the present study demonstrated that miR-155 may contribute to the progression and growth of CRC by enhancing the Wnt/β-catenin pathway in an HBP1-associated mechanism. Therefore, miR-155 may be considered a promising therapeutic target for the treatment of CRC.

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“…Northern blot analysis was performed according to the procedures previously described [9]. miR-155 inhibitor and mimics mirVana™ miRNA inhibitors and mimics specific for miR-155 (Invitrogen, USA) were used to increase and silence the expression of miR-155, respectively, in glioma cell lines and primary astrocytes.…”

Section: Quantitative Pcrmentioning

confidence: 99%

miR-155 contributes to the progression of glioma by enhancing Wnt/β-catenin pathway

et al. 2015

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As the most common brain tumor, glioma is featured with poor prognosis due to its resistance to current therapeutic strategies. The elucidation of etiology is believed to facilitate the development of novel effective anti-glioma treatment modalities. As a confirmed oncogenic microRNA (miRNA) in many other types of cancers, the role of miR-155 in glioma is still unknown. This study is aimed to study the role of miR-155 in the progression of glioma. Our results revealed that miR-155 was overexpressed in the collected glioma specimen, compared with noncancerous brain tissues. The suppression of miR-155 attenuated the proliferation of glioma cells and the activation of Wnt pathway. Silencing miR-155 was also able to suppress the growth of U-87 MG glioma xenografts in mice. Pearson analysis indicated that miR-155 level was inversely correlated with the abundance of HMG-box transcription factor 1 (HBP1), a strong Wnt pathway inhibitor, in glioma samples. Further experiments confirmed that miR-155 suppressed the expression of HBP1 by targeting the putative miRNA recognition elements (MREs) within its messenger RNA (mRNA) 3' untranslated region (UTR). Furthermore, HBP1 small interfering RNA (siRNA) abolished the effect of miR-155 suppression on the proliferation of glioma and the activation of Wnt pathway. Taken together, miR-155 promoted the progression of glioma by enhancing the activation of Wnt pathway. Thus, targeting miR-155 may be an effective strategy for glioma treatment.

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Tumor‐targeting TRAIL expression mediated by miRNA response elements suppressed growth of uveal melanoma cells

Cited by 46 publications

References 41 publications

Breast cancer-specific TRAIL expression mediated by miRNA response elements of let-7 and miR-122

Breast cancer-specific TRAIL expression mediated by miRNA response elements of let-7 and miR-122

MicroRNA-155 enhances the activation of Wnt/β-catenin signaling in colorectal carcinoma by suppressing HMG-box transcription factor 1

miR-155 contributes to the progression of glioma by enhancing Wnt/β-catenin pathway

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