Analysis of TP53 gene expression and p53 level of human hypopharyngeal FaDu (HTB-43) head and neck cancer cell line after microRNA-181a inhibition

Cheah, Yoke Kqueen; Cheng, Ri Wen; Yeap, Swee Keong; Khoo, Chai Hoon; See, Hui Shien

doi:10.4238/2014.january.22.4

Cited by 5 publications

(2 citation statements)

References 17 publications

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“…As the samples in the current study were collected from the archive with limited number and type of nasopharynx samples, some inevitable differences existed between the current and previous study, which were clinical material (formalin instead of RNAlater fixation) and type of tissues used for non-NPC control group (normal, lymphoma and inflammation instead of normal only). Even though the clinical material used in the current study was slightly different with the previous study, several studies showed that miRNA expression in FFPE samples was highly correlated to miRNA expression in fresh frozen samples, which is comparable to RNAlater fixed samples [28][29][30]. Another study by Vojtechova et al [33] could not find a better correlation values of miRNA expression profiles in fresh frozen with FFPE samples.…”

Section: Discussioncontrasting

confidence: 56%

“…In Malaysia, so far, there was one published study by Nurul-Syakima et al [25] that profiled the miRNA expression in head and neck cancers using human biopsies, in which NPC biopsies were included. However, detailed analyses in that study was only limited to investigate the roles of miRNAs in HSCC, excluding the NPC [28,29]. In this study, we took the initiative to determine the expression of miR-101 and miR-744, the miRNAs that were found to be miR-101 and miR-744 in Nasopharyngeal Carcinoma Azmir AHMAD et al http://wjst.wu.ac.th differentially expressed in the study by Nurul-Syakima et al [25], in NPC biopsies and analyse statistically on their performance to be biomarkers for NPC.…”

Section: Discussionmentioning

confidence: 99%

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Differential Expression of miR-101 and miR-744 in Nasopharyngeal Carcinoma in Pahang State of Malaysia

AHMAD¹,

WAHID²,

LEMAN³

et al. 2018

Walailak J Sci & Tech

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Previous study found that microRNA-101 (miR-101) and microRNA-744 (miR-744) were deregulated in head and neck cancers and were implicated in nasopharyngeal carcinoma (NPC) carcinogenesis. Thus, this study aimed to determine the expression of miR-101 and miR-744 in NPC and analyse the utility of these microRNAs (miRNAs) as diagnostic biomarkers. Total RNA was extracted from 31 NPC and 7 non-NPC control formalin-fixed paraffin-embedded (FFPE) samples. Complementary DNA (cDNA) was synthesized from the total RNA and proceeded with quantitative real-time polymerase chain reaction. Differential expression of miR-101 and miR-744 were calculated from quantification cycle (Cq) data using 2-ΔΔCq calculation. The performance of these miRNAs were calculated using receiver operating characteristic (ROC) curve analysis. The differential expression for miR-101 and miR-744 were -1.39 (p < 0.05) and 2.48 (p > 0.05), respectively, where the deregulations were consistent with the previous report. The area under curve for miR-101, miR-744 and combination of miR-101 and miR-744 were 0.654 (95 % CI: 0.465 - 0.844), 0.588 (95 % CI: 0.368 - 0.808) and 0.626 (95 % CI: 0.481 - 0.771), respectively. However, re-analysis using balanced sample size between NPC and non-NPC control group showed the value decreased to 0.653 (95 % CI: 0.347 - 0.959) for miR-101 but increased to 0.827 (95 % CI: 0.601 - 1.000) for miR-744 and 0.758 (95 % CI: 0.576 - 0.939) for the combination of miR-101 and miR-744, indicating the importance of having a balanced sample size. We have successfully determined the expression of miR-101 and miR-744 in NPC samples. We also demonstrated statistically the utility of these miRNAs as diagnostic biomarkers.

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Section: Discussioncontrasting

confidence: 56%

Section: Discussionmentioning

confidence: 99%

Differential Expression of miR-101 and miR-744 in Nasopharyngeal Carcinoma in Pahang State of Malaysia

AHMAD¹,

WAHID²,

LEMAN³

et al. 2018

Walailak J Sci & Tech

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miR-30c and miR-181a synergistically modulate p53–p21 pathway in diabetes induced cardiac hypertrophy

et al. 2016

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p53-p21 pathway mediates cardiomyocyte hypertrophy and apoptosis and is upregulated in diabetic cardiomyopathy (DbCM). We investigated role of microRNAs in regulating p53-p21 pathway in high glucose (HG)-induced cardiomyocyte hypertrophy and apoptosis. miR-30c and miR-181a were identified to target p53. Cardiac expression of microRNAs was measured in diabetic patients, diabetic rats, and in HG-treated cardiomyocytes. Effect of microRNAs over-expression and inhibition on HG-induced cardiomyocyte hypertrophy and apoptosis was examined. Myocardial expression of p53 and p21 genes was increased and expression of miR-30c and miR-181a was significantly decreased in diabetic patients, DbCM rats, and in HG-treated cardiomyocytes. Luciferase assay confirmed p53 as target of miR-30c and miR-181a. Over-expression of miR-30c or miR-181a decreased expression of p53, p21, ANP, cardiomyocyte cell size, and apoptosis in HG-treated cardiomyocytes. Concurrent over-expression of these microRNAs resulted in greater decrease in cardiomyocyte hypertrophy and apoptosis, suggesting a synergistic effect of these microRNAs. Our results suggest that dysregulation of miR-30c and miR-181a may be involved in upregulation of p53-p21 pathway in DbCM.

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Gga-miR-181a modulates ANP32A expression and inhibits MDCC-MSB-1 cell

Zhao

Han

et al. 2021

In Vitro Cell.Dev.Biol.-Animal

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Analysis of TP53 gene expression and p53 level of human hypopharyngeal FaDu (HTB-43) head and neck cancer cell line after microRNA-181a inhibition

Cited by 5 publications

References 17 publications

Differential Expression of miR-101 and miR-744 in Nasopharyngeal Carcinoma in Pahang State of Malaysia

Differential Expression of miR-101 and miR-744 in Nasopharyngeal Carcinoma in Pahang State of Malaysia

miR-30c and miR-181a synergistically modulate p53–p21 pathway in diabetes induced cardiac hypertrophy

Gga-miR-181a modulates ANP32A expression and inhibits MDCC-MSB-1 cell

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