The identification of novel targets of miR-16 and characterization of their biological functions in cancer cells

Yan, Xin; Liang, Hongwei; Deng, Ting; Zhu, Kegan; Zhang, Suyang; Wang, Nan; Jiang, Xueyuan; Wang, Xueliang; Li, Rui; Zen, Ke; Zhang, Chen Yu; Ba, Yi; Chen, Xi

doi:10.1186/1476-4598-12-92

Cited by 53 publications

(35 citation statements)

References 21 publications

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“…Well-growing U251 cells in the logarithmic growth phase were seeded at a density of 1x10 6 cells/well in 6-well plates (Corning) and cultured for 12 h. The following groups were established for the experiment: the blank group (without any treatment), the control group (transfected with siRNA-NC), the siRNA-1 group (transfected with siRNA-1), the siRNA-2 group (transfected with siRNA-2) and the siRNA-3 group (transfected with siRNA-3). Transfection was carried out according to the instructions for the Lipofectamine™ 2000 reagent (Invitrogen) as previously described (14).…”

Section: Genementioning

confidence: 99%

Expression of neonatal Nav1.5 in human brain astrocytoma and its effect on proliferation, invasion and apoptosis of astrocytoma cells

Xing

Wang

et al. 2014

Oncology Reports

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Abstract. In the present study, we designed and conducted a series of assays to determine the expression of voltage-gated sodium channel (VGSC) neonatal isoform Nav1.5 (nNav1.5) in human brain astrocytoma and its effect on the proliferation, migration, invasion and apoptosis of astrocytoma U251 cells. The results showed that nNav1.5 mRNA and protein were expressed in both human brain astrocytoma and normal brain tissues, but their expression levels in astrocytoma were significantly higher (P<0.05). In astrocytomas, nNav1.5 mRNA and protein levels were also different (P<0.05) and were correlated with pathological grades. The immunofluorescence confocal microscopy observations demonstrated that nNav1.5 protein was expressed in the nucleus, cytoplasm and membrane of the astrocytoma cells. After transfection, the small interfering RNA (siRNA) targeted to nNav1.5 significantly reduced the expression levels of SCN5A/nNav1.5 mRNA and protein by 57.2% (P<0.05) and 66.6% (P<0.05), respectively. The MTT, wound healing, Matrigel invasion and flow cytometric assays confirmed that following siRNA downregulation of the expression of the SCN5A/nNav1.5 gene, the in vitro proliferation and in vitro invasiveness of the U251 cells were significantly reduced (P<0.05 for both comparisons), and the apoptosis rate was significantly increased (P<0.05). These results revealed that nNav1.5 expression in human brain astrocytoma was upregulated, and its expression was positively correlated with the degree of malignancy. Additionally, reduced nNav1.5 expression significantly suppressed the proliferation and invasiveness of astrocytoma cells, indicating a new target in the molecular diagnosis and therapy of astrocytoma.

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Section: Genementioning

confidence: 99%

Expression of neonatal Nav1.5 in human brain astrocytoma and its effect on proliferation, invasion and apoptosis of astrocytoma cells

Xing

Wang

et al. 2014

Oncology Reports

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“…MAP7 was reported to be engaged into the function of neuron cell [6]. MAP7 was reported to be upregulated and correlated with the prognosis of cancers [7,8]. The function and mechanism of MAP7 in CC was still unknow.…”

Section: Introductionmentioning

confidence: 99%

MAP7 promotes migration and invasion and progression of human cervical cancer through modulating the autophagy

et al. 2020

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Background: Microtubule-associated proteins 7(MAP7) was reported to be engaged into the function of neuronal function. The function of MAP7 in human cervical cancer (CC) was unknown. We aimed to uncover the function and mechanism of MAP7 on CC. Methods: We applied qRT-PCR, western blot and immunochemistry to detect the expression difference between normal tissue and CC. In vitro, we establish MAP7 stable knocking down and overexpression cell lines and investigated the function and underlying mechanism of MAP7 in CC. Results: Both mRNA and protein of MAP7 were upregulated in CC compared with the normal tissue. MAP7 was correlated with the clinical stage and tumor size and lymph node metastasis. MAP7 promotes the invasion and migration of CC cell lines. We next detected EMT pathway and autophagy associated pathway. MAP7 promotes the EMT through modulating the autophagy. Conclusion: Taken above, our results showed that MAP7 promotes the migration and invasion and EMT through modulating the autophagy.

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“…This was accompanied by a rearrangement of actin filaments from a cortical to a stress-fiber pattern (Figure 3) [10]. Transfection of Pre-miR™ miRNA Precursor Molecules for miR-183 and miR-666-5p inhibited the appearance of these changes (Figure 4).…”

Section: Resultsmentioning

confidence: 99%

A useful method of identifying of miRNAs which can down-regulate Zeb-2

et al. 2013

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BackgroundAlthough identification of the target mRNAs of micro RNAs (miRNAs) is essential to understanding their function, the low complementarity between miRNAs and their target mRNAs has complicated this process. In this study, we sought to identify miRNAs which reduce the expression of the transcription factor Zeb-2, a transcriptional repressor of E-cadherin which is known to be down regulated by members of the miR-200 family (miR-200a,b,c miR-429, and miR-141).FindingsWe first used a computational target predicting system to identify 82 candidate miRNAs which bound the 3′UTR region of the Zeb-2 mRNA. Of these 82 miRNAs, precursors for 51 were available in our miRNA precursor library. Pre-miR™ Precursor Molecules for these 51 miRNAs were co-transfected into NIH3T3 cells with a luciferase reporter vector containing the 3′UTR region of the Zeb-2 mRNA. Seven miRNAs (miR-141, mi-183, miR-200a, miR-200b, miR-200c, miR-429 and miR-666-5p) were shown to down-regulate luciferase activity and Western blotting analysis confirmed that Pre-miR™ Precursor Molecules for these seven miRNAs induced expression of E-cadherin and miScript target protector against miR-183 and miR-666-5p abrogated this effect. Moreover, an Anti-miR™ miRNA Inhibitor targeting miR-183 and miR-666-5p repressed expression of E-cadherin.ConclusionsWe have established a method to identify miRNAs that bind the 3′UTR region of the Zeb-2 mRNA and that induce expression of E-cadherin, possibly by down-regulating the expression of Zeb-2. Our method may be more widely applicable for identifying miRNAs that bind target mRNA 3′UTR regions and down-regulate the expression of proteins encoded by these mRNAs.

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The identification of novel targets of miR-16 and characterization of their biological functions in cancer cells

Cited by 53 publications

References 21 publications

Expression of neonatal Nav1.5 in human brain astrocytoma and its effect on proliferation, invasion and apoptosis of astrocytoma cells

Expression of neonatal Nav1.5 in human brain astrocytoma and its effect on proliferation, invasion and apoptosis of astrocytoma cells

MAP7 promotes migration and invasion and progression of human cervical cancer through modulating the autophagy

A useful method of identifying of miRNAs which can down-regulate Zeb-2

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