TBX3 knockdown suppresses the proliferation of hypopharyngeal carcinoma FaDu cells by inducing G1/S cell cycle arrest and apoptosis

Huang, Yongjiu; Zhu, Hongmei; Ji, Xiaohui; Yin, Chang; Zhang, Yanhui; Huang, Ruixuan; Xie, Jin; Dong, Pin

doi:10.3892/ol.2019.11089

Cited by 7 publications

(6 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, the expression of TBX3 was positively correlated with the level of PVT1, which was further confirmed by the result that knockdown of TBX3 visibly reduced the level of PVT1. Thus, these results indicate that transcription factor TBX3 promoted the transcriptional expression of PVT1.The dysregulation of TBX3 has been displayed in breast cancer [30], gastric cancer [31], hypopharyngeal carcinoma [32], and papillary thyroid carcinoma [16]. The present results also showed that the transcriptional and translational expressions of TBX3 were prominently highly expressed in both ATC tissues and FRO cells.…”

Section: Discussionsupporting

confidence: 72%

TBX3 activating PVT1 accelerates proliferation, migration, and invasion by modulating the miR-30a/LOX axis in anaplastic thyroid carcinoma

et al. 2022

View full text Add to dashboard Cite

Introduction: Anaplastic thyroid carcinoma (ATC) is a nearly chemo-resistant malignancy with high invasion and mortality. Long non-coding RNAs (lncRNAs) have been demonstrated to be dysregulated and play a crucial role in the development and process of ATC. The present study aimed to explore the mechanism of PVT1 dysregulation in ATC. Material and methods:The mRNA levels of PVT1 and T-box3 (TBX3), and the protein levels of TBX3 in ATC and paracancerous tissues, and FRO and Nthy-ori 3-1 cells were determined by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) and western blot, respectively. The transcriptional factor binding site was predicted and validated between TBX3 and PVT1 promoter through the JASPAR website, and ChIP and luciferase analysis. The proliferation, migration, and invasion of FRO cells were assessed by MTT, colony formation, and transwell assays. Results: PVT1 expression was upregulated in ATC, which was positively correlative with the level of transcription factor TBX3. Downregulation of PVT1 inhibited the proliferation, migration, and invasion of FRO cells. Moreover, TBX3 targeting the promoter region of PVT1 promoted the expression level of PVT1 and modulated the downstream signalling axis of PVT1, miR-30a/LOX. Also, interference of PVT1 reversed the stimulative role of overexpression of TBX3 in the progress of FRO cells. Conclusion: TBX3 enhanced proliferation, migration, and invasion of ATC cells via activation of PVT1 and modulation of the miR-30a/LOX signalling axis.

show abstract

Section: Discussionsupporting

confidence: 72%

TBX3 activating PVT1 accelerates proliferation, migration, and invasion by modulating the miR-30a/LOX axis in anaplastic thyroid carcinoma

et al. 2022

View full text Add to dashboard Cite

show abstract

“…Our present data suggested that overexpression of miR-107 promoted the apoptosis. In line with this result, knockdown of TBX3 enhanced the apoptosis of FaDu cells [ 34 ]. In addition, in vivo , we found that miR-107 overexpression reduced tumor volume and weight, and improved the histopathological changes, probably implying the anti-tumor role of miR-107 in FaDu HSCC.…”

Section: Discussionmentioning

confidence: 65%

“…Herein, the overexpression of miR-107 significantly was found to inhibit FaDu cell migration and invasion, consistent with a previous report [ 10 ]. Moreover, cell adhesion molecule E-cadherin acts as a prognostic factor of HPCC [ 34 ]. Active MMP2 and active MMP9 are biomarkers of invasion in tumors.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of microRNA-107 suppressed proliferation, migration, invasion, and the PI3K/Akt signaling pathway and induced apoptosis by targeting Nin one binding (NOB1) protein in a hypopharyngeal squamous cell carcinoma cell line (FaDu)

et al. 2022

View full text Add to dashboard Cite

Hypopharyngeal squamous cell carcinoma (HSCC) is one of the most common head and neck cancers, with a worst prognosis owing to its aggressivity. MicroRNA-107 (miR-107) is reported to regulate the progression of various cancers. Nevertheless, its implied function in HSCC remains unclear. This study is aimed to exploring the roles and potential mechanisms of miR-107 in HSCC. We found that miR-107 expression was significantly decreased in HSCC tissues compared with the para-cancer tissues. Moreover, miR-107 overexpression by miR-107 mimics decreased FaDu cell viability, led to cell cycle arrest in G1/S phase, accelerated apoptosis, and reduced cell migration and invasion. MiR-107 possibly resulted in deactivation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway, evidenced by the decrease of phosphorylated (p-) PI3K and p-Akt. Besides, dual-luciferase reporter assay confirmed that miR-107 might bind to the 3’UTR of Nin one binding protein 1 (NOB1), and elevated NOB1 expression in HSCC tissues and a negative correlation between miR-107 and NOB1 were found. Rescue assays demonstrated the significant roles of miR-107 in FaDu cell behavior by modulating NOB1. In addition, the tumorigenic potential of miR-107 in vivo was conducted. It was found that miR-107 overexpression in FaDu cells significantly inhibited tumor growth and led to inactivation of the PI3K/Akt signaling. The above findings revealed that miR-107 could suppress FaDu cell proliferation, migration, invasion and induced apoptosis by targeting NOB1 through the PI3K/Akt pathway, suggesting that miR-107/NOB1 axis may exert a key role in FaDu HSCC development.

show abstract

“…The above selected four genes have been described as potential oncogenes in hypopharyngeal carcinoma [ 10 ], breast cancer [ 11 ], osteosarcoma [ 12 ], and adrenocortical adenomas [ 13 ]. Bisulfite pyrosequencing was used to verify their promoter methylation profiles.…”

Section: Resultsmentioning

confidence: 99%

Alterations of DNA methylation were associated with the rapid growth of cortisol-producing adrenocortical adenoma during pregnancy

et al. 2021

View full text Add to dashboard Cite

Background Cortisol-producing adrenocortical adenoma (CPA) during pregnancy rarely occurs in clinic. Growing evidence suggests that DNA methylation plays a key role in adrenocortical adenomas. The present study aims to examine the genome-wide DNA methylation profiles and identify the differences in DNA methylation signatures of non-pregnant and pregnant patients with CPA. Results Four pregnant and twelve non-pregnant patients with CPA were enrolled. The pregnant patients with CPA had higher serum cortisol, Estradiol, Progesterone, and human chorionic gonadotropin concentration, while having lower serum FSH (follicle-stimulating hormone) and luteinizing hormone concentrations (P < 0.01). Compared with the non-pregnant patients, the duration is shorter, and the growth rate of the tumor is faster in pregnant patients with CPA (P < 0.05). Morphology and cell proliferation assay showed that the percentage of Ki-67 positive cells in CPA were higher in pregnant group than non-pregnant group (8.0% vs 5.5%, P < 0.05). The DNA methylation analysis showed that Genome-wide DNA methylation signature difference between pregnant and non-pregnant with CPA, that the pregnant group had more hypermethylated DMPs (67.94% vs 22.16%) and less hypomethylated DMPs (32.93% vs 77.84%). The proportion of hypermethylated DMPs was relatively high on chromosomes 1 (9.68% vs 8.67%) and X (4.99% vs 3.35%) but lower on chromosome 2(7.98% vs 12.92%). In pregnant patients with CPA, 576 hypomethylated DMPs and 1109 hypermethylated DMPs were identified in the DNA promoter region. Bioinformatics analysis indicated that the Wnt/β-Catenin pathway, Ras/MAPK Pathway and PI3K-AKT Pathway were associated with the development of CPA during pregnancy. Conclusions Genome-wide DNA methylation profiling of CPA in non-pregnant and pregnant patients was identified in the present study. Alterations of DNA methylation were associated with the pathogenesis and exacerbation of CPA during pregnancy.

show abstract

TBX3 knockdown suppresses the proliferation of hypopharyngeal carcinoma FaDu cells by inducing G1/S cell cycle arrest and apoptosis

Cited by 7 publications

References 38 publications

TBX3 activating PVT1 accelerates proliferation, migration, and invasion by modulating the miR-30a/LOX axis in anaplastic thyroid carcinoma

TBX3 activating PVT1 accelerates proliferation, migration, and invasion by modulating the miR-30a/LOX axis in anaplastic thyroid carcinoma

Overexpression of microRNA-107 suppressed proliferation, migration, invasion, and the PI3K/Akt signaling pathway and induced apoptosis by targeting Nin one binding (NOB1) protein in a hypopharyngeal squamous cell carcinoma cell line (FaDu)

Alterations of DNA methylation were associated with the rapid growth of cortisol-producing adrenocortical adenoma during pregnancy

Contact Info

Product

Resources

About