Upregulation of BTF3 affects the proliferation, apoptosis, and cell cycle regulation in hypopharyngeal squamous cell carcinoma

Zhang, Yang; Gross, Neil D.; Li, Zufei; Yin, Gaofei; Liu, Chuan; Huang, Zhigang

doi:10.1016/j.biopha.2019.109211

Cited by 14 publications

(7 citation statements)

References 27 publications

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“…A positive correlation between low expression of PCDH20 (as an independent prognostic factor) with T staging and lymph node metastasis has been established, although the sample size was small (7). Zhang (8) corroborated the upregulated BTF3 expression in HSCC, which is positively correlated with HSCC lymph node metastasis. Upregulated S100A4 expression in HSCC was substantiated by Xu (9) and was positively correlated with neck lymph node metastasis.…”

Section: Introductionmentioning

confidence: 84%

Molecular Markers of MDR of Chemotherapy for HSCC: Proteomic Screening With High-Throughput Liquid Chromatography-Tandem Mass Spectrometry

et al. 2021

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BackgroundHypopharyngeal squamous cell cancer (HSCC) is a head and neck tumor with a poor prognosis. Chemotherapy lacks effectiveness because of multidrug resistance (MDR), which has increased toxic side effects. Thus, there is an urgent need to identify the molecular markers of MDR of chemotherapy for HSCC.MethodsFifty clinical samples of HSCC were derived from patients including 12 sensitive or resistant to chemotherapy drugs. Proteomic screening was performed using liquid chromatography-tandem mass spectrometry (LC-MS), which was based on data-independent acquisition. Molecular markers of MDR of chemotherapy in patients with HSCC were identified with clinical data and validated with ELISA.ResultsA total of 673 differentially expressed proteins were identified in HSCC samples, where 172 were upregulated and 501 were downregulated. A total of 183 differentially expressed proteins including 102 upregulated and 81 downregulated proteins, were identified by comparing cancer sensitive to chemotherapy with cancer resistant to chemotherapy. Clinical HSCC samples had significantly higher expression of FADD and significantly lower expression of RIPK1. Expressions of FADD and RIPK1 proteins were significantly lower in the chemotherapy-sensitive group. These expression differences were not correlated with clinical data. RIPK1 and FADD are involved in necroptosis and the signaling pathway of PRRs. Using ELISA, the low expression of RIPK1 and FADD was found in the patients sensitive to chemotherapy.ConclusionLC-MS proteomics is an effective method to identify the molecular markers of HSCC. FADD and RIPK1 can act as molecular markers of MDR of chemotherapy in patients with HSCC and may function through necroptosis and the PRR signaling pathway.

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Section: Introductionmentioning

confidence: 84%

Molecular Markers of MDR of Chemotherapy for HSCC: Proteomic Screening With High-Throughput Liquid Chromatography-Tandem Mass Spectrometry

et al. 2021

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“…The KDM2A loss of function inhibits the proliferation of 3T3-L1 preadipocytes, and this is assessed using three biased techniques (CCK-8 assay, EdU and Ki67 staining). It is well known that the occurrence of cell cycle regulation and apoptosis are the classical molecular mechanisms for cell proliferation and growth [ 26 , 27 , 28 ]. Consistent with our finding, the knockout of KDM2A in HEK293T cell lines significantly inhibited this cell proliferation through the downregulation of TGF-β signaling, leading to more cells being blocked in the G2/M phase [ 29 ].…”

Section: Discussionmentioning

confidence: 99%

Ablation of KDM2A Inhibits Preadipocyte Proliferation and Promotes Adipogenic Differentiation

Hua

Yue

Zhao

et al. 2021

IJMS

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Epigenetic signals and chromatin-modifying proteins play critical roles in adipogenesis, which determines the risk of obesity and which has recently attracted increasing interest. Histone demethylase 2A (KDM2A) is an important component of histone demethylase; however, its direct effect on fat deposition remains unclear. Here, a KDM2A loss of function was performed using two unbiased methods, small interfering RNA (siRNA) and Cre-Loxp recombinase systems, to reveal its function in adipogenesis. The results show that the knockdown of KDM2A by siRNAs inhibited the proliferation capacity of 3T3-L1 preadipocytes. Furthermore, the promotion of preadipocyte differentiation was observed in siRNA-treated cells, manifested by the increasing content of lipid droplets and the expression level of adipogenic-related genes. Consistently, the genetic deletion of KDM2A by Adipoq-Cre in primary adipocytes exhibited similar phenotypes to those of 3T3-L1 preadipocytes. Interestingly, the knockdown of KDM2A upregulates the expression level of Transportin 1(TNPO1), which in turn may induce the nuclear translocation of PPARγ and the accumulation of lipid droplets. In conclusion, the ablation of KDM2A inhibits preadipocyte proliferation and promotes its adipogenic differentiation. This work provides direct evidence of the exact role of KDM2A in fat deposition and provides theoretical support for obesity therapy that targets KDM2A.

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“…mir, microrna; nc, negative control; BTF3, basic transcription factor 3; MMP, matrix metallopeptidase. example, Zhang et al (32) reported that the genetic knockdown of BTF3 impaired the regulation of proliferation, the cell cycle and apoptosis in hypopharyngeal squamous cell carcinoma via the serine-protein kinase aTM signaling pathway (32). BTF3 also promoted prostate cancer progression through modeling stem-like traits (33).…”

Section: Discussionmentioning

confidence: 99%

“…TargetScan 7.2 software was used to predict that the signal transductor and transcriptional activator BTF3 was a potential target gene of miR-802; this was further validated in the present study using a dual-luciferase reporter assay, whereby miR-802 inhibited the activity of the BTF3 3′-UTR reporter gene. Several studies have previously reported that BTF3 regulated tumor cell migration and invasion ( 29 – 31 ); for example, Zhang et al ( 32 ) reported that the genetic knockdown of BTF3 impaired the regulation of proliferation, the cell cycle and apoptosis in hypopharyngeal squamous cell carcinoma via the serine-protein kinase ATM signaling pathway ( 32 ). BTF3 also promoted prostate cancer progression through modeling stem-like traits ( 33 ).…”

Section: Discussionmentioning

confidence: 99%

miR‑802 inhibits the epithelial‑mesenchymal transition, migration and invasion of cervical cancer by regulating BTF3

Liu

Zhang

2020

Mol Med Rep

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Microrna (mir)-802 has been discovered to be involved in the occurrence and development of numerous types of tumor; however, studies into the role of mir-802 in cervical cancer are limited. Therefore, the present study aimed to investigate the regulatory effects of mir-802 in cervical cancer cells. mir-802 expression levels in cervical cancer tissue and cells were analyzed using reverse transcription-quantitative (rT-q) Pcr, a dual-reporter luciferase activity assay was used to identify the direct target gene of mir-802, and rT-qPcr and western blotting were performed to determine the relationship between mir-802 and basic transcription factor 3 (BTF3). cell viability, and migration and invasion were analyzed using cell counting Kit-8 and Transwell assays, respectively. Finally, the expression levels of metastasis-associated proteins, n-cadherin and e-cadherin, were determined using rT-qPcr and western blotting. decreased expression levels of mir-802 were found in cervical cancer tissues and cells, and the overexpression of mir-802 inhibited cell viability, migration and invasion. Moreover, mir-802 was discovered to directly target BTF3 to inhibit its expression. notably, the overexpression mir-802 markedly reversed the promotive effect of BTF3 on cell viability, in addition to the migratory and invasive abilities of the cells. Simultaneously, the overexpression of mir-802 significantly suppressed epithelial-mesenchymal transition, and the expression levels of matrix metallopeptidase (MMP)2 and MMP9 in cells through regulating BTF3. in conclusion, the present study revealed that mir-802 may suppress cervical cancer progression by decreasing BTF3 expression levels, indicating that it may represent a potential therapeutic target for the treatment and prognosis of patients with cervical cancer.

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Upregulation of BTF3 affects the proliferation, apoptosis, and cell cycle regulation in hypopharyngeal squamous cell carcinoma

Cited by 14 publications

References 27 publications

Molecular Markers of MDR of Chemotherapy for HSCC: Proteomic Screening With High-Throughput Liquid Chromatography-Tandem Mass Spectrometry

Molecular Markers of MDR of Chemotherapy for HSCC: Proteomic Screening With High-Throughput Liquid Chromatography-Tandem Mass Spectrometry

Ablation of KDM2A Inhibits Preadipocyte Proliferation and Promotes Adipogenic Differentiation

miR‑802 inhibits the epithelial‑mesenchymal transition, migration and invasion of cervical cancer by regulating BTF3

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