microRNA response elements-regulated TRAIL expression shows specific survival-suppressing activity on bladder cancer

Zhao, Youguang; Liu, Ying; Wang, Liang; Yang, Hang; Wang, Qingtang; Qi, Haiyan; Li, Shadan; Zhou, Peng; Liang, Ping; Wang, Qiwu; Li, Xiaowei

doi:10.1186/1756-9966-32-10

Cited by 20 publications

(17 citation statements)

References 46 publications

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“…It is well documented that TRAIL induces apoptosis via microRNA regulation [45] including miR34a/ [46] or miR-494 [47] in cancer cells. Thus, Farooqi et al [3] suggested that miRNA regulation of TRAIL-mediated signaling in prostate cancer cells can provide potential biomarkers for the characterization of patients as responders and non-responders for TRAIL-based therapy.…”

Section: Discussionmentioning

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: Discussionmentioning

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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“…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: Discussionmentioning

confidence: 59%

“…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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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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“…It is appropriate to mention that miRNA subsets under-expressed in cervical cancer cells can be used to regulate the proficiency of cancer-specific adenoviral vector that expressed TRAIL based on miRNA response elements (MREs) of miRNAs whose levels were reduced in cervical cancer. Similar approaches have been tested using in bladder cancer and glioma using adenoviral vector expressing TRAIL and introducing MREs of miRNA subsets down-regulated in respective cancer cells [185,186]. …”

Section: Resultsmentioning

confidence: 99%

Nip the HPV encoded evil in the cancer bud: HPV reshapes TRAILs and signaling landscapes

2013

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HPV encoded proteins can elicit ectopic protein–protein interactions that re-wire signaling pathways, in a mode that promotes malignancy. Moreover, accumulating data related to HPV is now providing compelling substantiation of a central role played by HPV in escaping immunosurveillance and impairment of apoptotic response. What emerges is an intricate network of Wnt, TGF, Notch signaling cascades that forms higher-order ligand–receptor complexes routing downstream signaling in HPV infected cells. These HPV infected cells are regulated both extracellularly by ligand receptor axis and intracellularly by HPV encoded proteins and impair TRAIL mediated apoptosis. We divide this review into different sections addressing how linear signaling pathways integrate to facilitate carcinogenesis and compounds that directly or indirectly reverse these aberrant interactions offer new possibilities for therapy in cancer. Although HPV encoded proteins mediated misrepresentation of pathways is difficult to target, improved drug-discovery platforms and new technologies have facilitated the discovery of agents that can target dysregulated pathways in HPV infected cervical cancer cells, thus setting the stage for preclinical models and clinical trials.

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microRNA response elements-regulated TRAIL expression shows specific survival-suppressing activity on bladder cancer

Cited by 20 publications

References 46 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

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

Nip the HPV encoded evil in the cancer bud: HPV reshapes TRAILs and signaling landscapes

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