Tumor suppressor microRNA-34a inhibits cell proliferation by targeting Notch1 in renal cell carcinoma

Zhang, Changcun; Mo, Ren; Yin, Binde; Zhou, Libin; Liu, Yongchao; Fan, Jia

doi:10.3892/ol.2014.1931

Cited by 26 publications

(21 citation statements)

References 31 publications

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“…with the normal tissues, which suggested that dysregulation of miR-34a may be involved in the development of human esophageal cancer. Moreover, studies have reported that miR-34a can affect the growth of proneural glioma and renal cell carcinoma cells (13,24). In the present study, we found that TE-1 cells grew slowly following transfection with .…”

Section: Discussionsupporting

confidence: 63%

“…It has been reported that miR-34a expression was significantly reduced in non-small cell lung cancer compared with normal tissues (12). miR-34a induces G1 arrest, apoptosis and senescence by repressing the expression of Notch1 in RCC cell lines, and inhibit gastric cancer tumorigenesis by targeting PDGFR and MET through the PI3K/Akt pathway (13,14). miR-34a, which is located at chromosome 1p36, is a well-known tumor-suppressor miRNA present in various types of human cancer (15,16).…”

Section: Introductionmentioning

confidence: 99%

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miR-34a inhibits the migration and invasion of esophageal squamous cell carcinoma by targeting Yin Yang-1

Nie

Geng

et al. 2015

Oncology Reports

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Esophageal squamous cell carcinoma (ESCC), one of the most common gastrointestinal tumors, is known for its high mortality rate. microRNAs (miRNAs) have been reported to play important regulatory roles in cancer metastasis and progression. miR-34a has been demonstrated to be associated with the development of and metastasis in certain types of cancer via various target genes, but its function and targets in ESCC are unknown. The aim of this study was to examine whether the expression of miR-34a was significantly decreased in ESCC tissues, compared with normal esophageal tissues using RT-PCR and western blot analysis. The results showed that miR-34a overexpression increased apoptosis and decreased clonogenic formation, but inhibited invasion and migration in ESCC cells by suppressing MMP-2 and -9 expression. Yin Yang-1 (YY1), a widely distributed transcription factor that belongs to the GLI-Kruppel class of zinc finger proteins, was found to be a direct target of miR-34a in ESCC cell lines. Rescue experiments indicated that the suppressive effect of miR-34a on invasion and migration was mediated by activating YY1 expression. Results of the present study showed that miR-34a is associated with ESCC migration and provides a potential therapeutic and diagnostic target for ESCC.

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Section: Discussionsupporting

confidence: 63%

Section: Introductionmentioning

confidence: 99%

miR-34a inhibits the migration and invasion of esophageal squamous cell carcinoma by targeting Yin Yang-1

Nie

Geng

et al. 2015

Oncology Reports

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“…In 5 and 20 mM metformin-treated cells, the levels of miRNA34a expression were 1.66- and 2.46-fold greater, respectively, compared with the levels in the control group (Figure 4B). In some previous studies, miRNA34a has been shown to be capable of inhibiting cell proliferation in renal cancer cells [15,16]. These data implied that the upregulation of miRNA34a induced by metformin probably contributed to the inhibitory effect of metformin on cell proliferation in ACHN cells.…”

Section: Resultsmentioning

confidence: 64%

Metformin Induces Growth Inhibition and Cell Cycle Arrest by Upregulating MicroRNA34a in Renal Cancer Cells

et al. 2017

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BackgroundMetformin is a widely used biguanide drug for the treatment of type 2 diabetes. It has been revaluated as a potential anti-cancer drug with promising activity in various tumors. However, the precise mechanisms underlying the suppression of cancer cells by metformin remain not well understood.Material/MethodsIn this study, human renal cell carcinoma cell line ACHN was used to investigate the anti-proliferation effect of metformin. A cell counting kit-8 assay was used to detect the cell viability. The cell cycle distribution and apoptosis were analyzed by flow cytometry. The expression of cyclin D1 and p27KIP1 was detected by Western blot. The underlying mechanism involving miRNA34a was further investigated by quantitative RT-PCR and transfection with miRNA inhibitor specific for miRNA34a in ACHN, 769-P, and A498 cells.ResultsMetformin could significantly inhibit the proliferation of ACHN cells in a dose- and time-dependent manner. In addition, the results showed that metformin induced G0/G1 phase arrest and delayed entry into S phase in ACHN cells. It was shown that metformin downregulates the expression of cyclin D1 and increases the p27KIP1 level. Furthermore, metformin increased ACHN cell death. Lastly, miRNA34a was found to be upregulated by metformin in ACHN, 769-P, and A498 cells. Subsequently, it was demonstrated that inhibition of miRNA34a could partially attenuate the suppressive effect of metformin on renal cancer cell proliferation.ConclusionsThe study data revealed that metformin induced cell growth inhibition and cell cycle arrest partially by upregulating miRNA34a in renal cancer cells.

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“…28,29 Beyond that, a report's analysis articulated that miR-34a inhibited cell proliferation by targeting Notch1 in renal cell carcinoma. 30 Meanwhile, other reports suggested that P53 could combine with the promoter of miR-34a and activate its transcription. P53 mutate could inhibit miR-34a transcription activation and result in a lower expression of miR-34a.…”

Section: Discussionmentioning

confidence: 99%

The influence of miR-34a expression on stemness and cytotoxic susceptibility of breast cancer stem cells

Zhang

et al. 2016

Cancer Biology & Therapy

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In this study, we investigate the effect of miR-34a expression and biological characteristics of breast cancer stem cells (BCSCs). The mammospheres were formed from murine breast cancer cell line 4T1 and regarded as murine BCSCs. Identification of stemness molecules and cloning experiments validate the biological characteristics of BCSCs we have established. We showed that miR-34a, as a tumor suppressor, could separately reduce the stemness of BCSCs and activate the cytotoxic susceptibility of BCSCs to natural killer (NK) cells in vitro via down regulating the expression of Notch1 signaling molecules. Moreover, miR-34a could completely restrain established mice breast tumor xenografts in vivo in the NOD/SCID mice that have functional NK cells at a normal level, whereas it was less effective in NOD/SCID/ CD122/IL-2Rβ mice that do not have functional NK cells. We conclude that miR-34a is a crucial, dual tumor suppressor and BCSCs-targeting immunotherapeutic agent and has shown efficacy in the treatment of murine breast cancer. The results also suggest that impaired NK cells could contribute to the resistance to therapies.

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Tumor suppressor microRNA-34a inhibits cell proliferation by targeting Notch1 in renal cell carcinoma

Cited by 26 publications

References 31 publications

miR-34a inhibits the migration and invasion of esophageal squamous cell carcinoma by targeting Yin Yang-1

miR-34a inhibits the migration and invasion of esophageal squamous cell carcinoma by targeting Yin Yang-1

Metformin Induces Growth Inhibition and Cell Cycle Arrest by Upregulating MicroRNA34a in Renal Cancer Cells

The influence of miR-34a expression on stemness and cytotoxic susceptibility of breast cancer stem cells

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