miRNA-556-3p promotes human bladder cancer proliferation, migration and invasion by negatively regulating DAB2IP expression

Chen, Feng; Sun, Ping; Hu, Jing; Feng, Hao; Li, Mingqiu; Liu, Guibo; Pan, Yanming; Feng, Yanjun; Xu, Yipeng; Feng, Kejian; Feng, Yukuan

doi:10.3892/ijo.2017.3969

Cited by 30 publications

(18 citation statements)

References 47 publications

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“…MiR-217 has been reported to inhibit the proliferation and migration of bladder cancer cells through targeting KMT2D 36 . MiR-556-3p can exacerbate the capacity of proliferation, migration and invasion of human bladder cancer cells via negatively regulating the expression of DAB2IP 37 . Xie et al have revealed that downregulation of miR-532-5p can signi cantly promote the proliferation and invasion of bladder cancer cells by activating the HMGB3/Wnt/β-catenin signaling pathway 38 .…”

Section: Discussionmentioning

confidence: 99%

Magnesium Isoglycyrrhizinate Suppresses the Progression of Bladder Cancer by Modulating miR-26b/Nox4 Axis

Yuan

Guancheng

Sun

et al. 2020

Preprint

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Background: Magnesium Isoglycyrrhizinate (MI), a magnesium salt of 18α-GA stereoisomer, has been reported to exert efficient hepatoprotective activity. However, its effect in bladder cancer remain unclear.Methods: The effect of MI in the growth, colony formation, apoptosis, invasion and migration of bladder cancer cells (HTB9 and BIU87 cells) was evaluated in vitro. Typical apoptotic changes of bladder cancer cells such as nuclear concentration and fragmentation was observed by Hoechst staining. The effect of MI in the expression of miR-26b, Nox4, NF-κB and HIF-1α was detected by qRT-PCR and western blot in vitro. Targetscan was used to predict the potential targets of miR-26b, then their interaction was determined by the luciferase reporter assay. Finally, the xenograft model of mice was established to evaluate the anti-tumor effects of MI in vivo. Results: MI significantly suppressed the proliferation, colony formation, invasion, migration and induced apoptosis of human bladder cancer cells. Nox4 was identified to be a direct target of miR-26b, and MI significantly increased the expression of miR-26b. MiR-26b mimics significantly decreased the relative luciferase activity of wild type (WT) Nox4, while exhibited no obvious change in mutant type (MUT) Nox4. Meanwhile, MI markedly downregulated the expression of Nox4, NF-κB and HIF-1α both in vitro and in vivo. Moreover, MI could efficiently inhibit the growth of xenograft tumor in vivo, and also obviously decreased the expression of Nox4, NF-κB and HIF-1α. Conclusion: In summary, MI showed a potent anti-tumor effect against bladder cancer partially through modulating miR-26b/Nox4 axis.

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Section: Discussionmentioning

confidence: 99%

Magnesium Isoglycyrrhizinate Suppresses the Progression of Bladder Cancer by Modulating miR-26b/Nox4 Axis

Yuan

Guancheng

Sun

et al. 2020

Preprint

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“…Several miRNAs of the miR-92a family were reported to target DAB2IP in multiple tumors [ 86 , 91 , 92 , 93 ]. DAB2IP inhibition by miR-556 in bladder and esophageal cancer fosters cells proliferation and sustains tumor progression via aberrant Ras-MAPK signaling activation [ 94 , 95 ]. Intriguingly, miR-556 was detected in the plasma of bladder cancer patients, suggesting that this miRNA could repress DAB2IP in a cell non-autonomous manner.…”

Section: Post-transcriptional Inhibition Of Rasgaps In Cancermentioning

confidence: 99%

Cutting the Brakes on Ras—Cytoplasmic GAPs as Targets of Inactivation in Cancer

Bellazzo

Collavin

2020

Cancers

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The Ras pathway is frequently deregulated in cancer, actively contributing to tumor development and progression. Oncogenic activation of the Ras pathway is commonly due to point mutation of one of the three Ras genes, which occurs in almost one third of human cancers. In the absence of Ras mutation, the pathway is frequently activated by alternative means, including the loss of function of Ras inhibitors. Among Ras inhibitors, the GTPase-Activating Proteins (RasGAPs) are major players, given their ability to modulate multiple cancer-related pathways. In fact, most RasGAPs also have a multi-domain structure that allows them to act as scaffold or adaptor proteins, affecting additional oncogenic cascades. In cancer cells, various mechanisms can cause the loss of function of Ras inhibitors; here, we review the available evidence of RasGAP inactivation in cancer, with a specific focus on the mechanisms. We also consider extracellular inputs that can affect RasGAP levels and functions, implicating that specific conditions in the tumor microenvironment can foster or counteract Ras signaling through negative or positive modulation of RasGAPs. A better understanding of these conditions might have relevant clinical repercussions, since treatments to restore or enhance the function of RasGAPs in cancer would help circumvent the intrinsic difficulty of directly targeting the Ras protein.

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“…miRNAs may modulate the expressions of different coding genes by inducing translational repression or the degradation of target mRNAs via base pairing with the specific sequences in the 3′UTRs . In fact, the deregulations of many carcinogenic or antitumor miRNA have been verified to be associated with tumor initiation and progression . For example, miR‐133b/135a induced human renal carcinoma cell apoptosis via the JAK2/STAT3 signaling pathway; miR‐21 promoted triple‐negative breast cancer cell proliferation and invasion via targeting PTEN; and miR‐4317 suppressed human gastric cancer cell proliferation via the regulation of ZNF322 .…”

Section: Introductionmentioning

confidence: 99%

microRNA‐100 functions as a tumor suppressor in non‐small cell lung cancer via regulating epithelial‐mesenchymal transition and Wnt/β‐catenin by targeting HOXA1

et al. 2020

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Background: Non-small cell lung cancer (NSCLC) is a leading subtype in lung cancer, with high morbidities and mortalities worldwide. microRNA (miRNA) has appeared to play indispensable roles in a variety of solid carcinomas. The current study focused on the functions of miR-100 in NSCLC. Methods: qRT-PCR was performed to detect miR-100 and HOXA1 expressions in NSCLC tissues and cells. MTT and transwell assays were used to determine the functions of miR-100 in NSCLC cell proliferation, invasion and migration abilities. Western blot was used to measure related protein expressions. Results: qRT-PCR results showed that miR-100 expressions were dramatically decreased in NSCLC tissues. MTT assays indicated that miR-100 restoration inhibited NSCLC cell proliferation. Furthermore, transwell assay was performed to determine the impacts of miR-100 on NSCLC invasion and migration abilities. As expected, the invasion and migration capacities were significantly repressed. Direct interactions between HOXA1 and miR-100 were also verified via dualluciferase reporter assays. Western blot analysis demonstrated that miR-100 exerted suppressive functions via regulating EMT and Wnt/β-catenin in NSCLC cells. Conclusions: Our results showed that miR-100 served antitumor roles in NSCLC, providing new evidence of miR-100 as a promising therapeutic biomarker in NSCLC.

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miRNA-556-3p promotes human bladder cancer proliferation, migration and invasion by negatively regulating DAB2IP expression

Cited by 30 publications

References 47 publications

Magnesium Isoglycyrrhizinate Suppresses the Progression of Bladder Cancer by Modulating miR-26b/Nox4 Axis

Magnesium Isoglycyrrhizinate Suppresses the Progression of Bladder Cancer by Modulating miR-26b/Nox4 Axis

Cutting the Brakes on Ras—Cytoplasmic GAPs as Targets of Inactivation in Cancer

microRNA‐100 functions as a tumor suppressor in non‐small cell lung cancer via regulating epithelial‐mesenchymal transition and Wnt/β‐catenin by targeting HOXA1

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