Inhibition of ZNF746 suppresses invasion and epithelial to mesenchymal transition in H460 non-small cell lung cancer cells

Kim, Bonglee; Sohn, Eun Jung; Jung, Ji Hoon; Shin, Eun Ah; You, Ok Heui; Im, Jinwon

doi:10.3892/or.2013.2801

Cited by 22 publications

(20 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…3a, b ). This fits wells with published data from human tumor research, showing that migration and epithelial to mesenchymal transition (EMT) are increased in hypoxic areas by the release of different proteins [ 32 – 36 ]. If each of these enzymes/proteins act in concert together or if each of these factors can act independently is presently unknown.…”

Section: Tumor Establishment and Cell Migrationsupporting

confidence: 89%

Progression and metastasis of lung cancer

Popper

2016

Cancer Metastasis Rev

397

298

View full text Add to dashboard Cite

Metastasis in lung cancer is a multifaceted process. In this review, we will dissect the process in several isolated steps such as angiogenesis, hypoxia, circulation, and establishment of a metastatic focus. In reality, several of these processes overlap and occur even simultaneously, but such a presentation would be unreadable. Metastasis requires cell migration toward higher oxygen tension, which is based on changing the structure of the cell (epithelial-mesenchymal transition), orientation within the stroma and stroma interaction, and communication with the immune system to avoid attack. Once in the blood stream, cells have to survive trapping by the coagulation system, to survive shear stress in small blood vessels, and to find the right location for extravasation. Once outside in the metastatic locus, tumor cells have to learn the communication with the “foreign” stroma cells to establish vascular supply and again express molecules, which induce immune tolerance.

show abstract

Section: Tumor Establishment and Cell Migrationsupporting

confidence: 89%

Progression and metastasis of lung cancer

Popper

2016

Cancer Metastasis Rev

397

298

View full text Add to dashboard Cite

show abstract

“…Also Kim et al . reported that silencing of the zinc finger protein 756 (ZNF756) gene in H460 non-small-cell lung carcinoma (NSCLC) led to suppression of NANOG and three MMP genes ( MMP-1, MMP-2 and MMP-9 ) [ 40 ]. Imai et al .…”

Section: Discussionmentioning

confidence: 99%

Silencing expression of the NANOG gene and changes in migration and metastasis of urinary bladder cancer cells

Gawlik-Rzemieniewska¹,

Galilejczyk²,

Krawczyk³

et al. 2016

aoms

View full text Add to dashboard Cite

IntroductionIt has been proved that expression of the NANOG gene is observed not only in embryonic-derived malignancies, but also in breast cancer, ovarian cancer, cervix cancer and bladder cancer. NANOG overexpression is correlated with high activity of MMP-2 and MMP-9. The aim of the study was to evaluate the changes in the malignant phenotype of T24 bladder cancer cells with modulated expression of the NANOG gene.Material and methodsHuman urinary bladder cancer cells T24 (HTB-4) were cultivated under standard conditions. Transfection of the cells with silencing constructions was performed with the application of Lipofectamine 2000 (Invitrogen) reagent. Evaluation of changes in the expression level of individual genes was performed using qRTPCR. Changes in the protein level were evaluated using the Human ELISA Kit (Abcam). The invasion capability of transfected cells was tested using Matrigel Invasion Chambers (BD Biosciences). The changes in cell migration were assessed with a wound-healing assay.ResultsThe qRTPCR evaluation showed that silencing the NANOG gene in T24 cells led to the decrease of mRNA for the MMP-2 gene to the level of 62.4% and the MMP-9 gene to the level of 76%. The cells with modulated expression of the NANOG gene migrated slower in the Matrigel invasion assay and in the wound-healing assay. The immunoenzymatic test showed a decrease in the protein level of MMP-9.ConclusionsThe transcriptional activity of the NANOG gene might be connected with some aspects of bladder cancer cell metastasis in vitro and has an influence on MMP-2 and MMP-9 expression levels.

show abstract

“…A recent study showed that Twist 1 interacted with PGC-1α, which was important in mitochondria synthesis and function and could inhibit UCP1 in brown adipocytes, which was involved in the mitochondrial oxidative metabolism and uncoupling process 12 . Additionally, Twist 1 knockdown was found to induce the expression of UCP1 and CPT-1, which are related to oxidative metabolism, and to increase PGC-1α expression and mediate mitochondrial biogenesis in brown adipocytes 15 , 16 . These findings indicate the role of Twist 1 in IR and mitochondria-mediated adipocyte metabolism.…”

Section: Introductionmentioning

confidence: 96%

Reduced expression of Twist 1 is protective against insulin resistance of adipocytes and involves mitochondrial dysfunction

Wang

Ren

et al. 2018

Sci Rep

View full text Add to dashboard Cite

Insulin resistance (IR) has become a global epidemic that represents a serious hazard to public health. However, the precise mechanisms modulating IR have not been fully elucidated. The present study aimed to investigate the role of transcriptional factor Twist 1 in adipocyte IR and to further explore the molecular mechanism. An in vitro IR model based on cultured 3T3-L1 adipocytes was established under high glucose/insulin stimulation and an in vivo IR model in C57/BL6J mice induced by a high fat diet (HFD) was also developed. Lentivirus targeting Twist 1 silencing was introduced. The relationships between Twist 1 expression and IR state, mitochondrial dysfunction and the downstream insulin signaling pathway were assayed. Our results firstly showed the elevation of Twist 1 in IR adipocytes, and Twist 1 silencing attenuated IR. Then mitochondrial ultra-structural damage, elevated ROS, decreased MMP and ATP, and changes in mitochondrial biosynthesis-related genes in IR group indicated mitochondrial dysfunction. Further, the downstream IRS/PI3K/AKT/GluT4 pathway was showed involved in Twist 1-mediated IR. In total, we provide evidence of a protective role of Twist 1 silencing in relieving the IR state of adipocytes. Mitochondrial dysfunction and the downstream IRS/PI3K/AKT/GluT4 pathway were involved in this Twist 1-mediated IR.

show abstract

Inhibition of ZNF746 suppresses invasion and epithelial to mesenchymal transition in H460 non-small cell lung cancer cells

Cited by 22 publications

References 32 publications

Progression and metastasis of lung cancer

Progression and metastasis of lung cancer

Silencing expression of the NANOG gene and changes in migration and metastasis of urinary bladder cancer cells

Reduced expression of Twist 1 is protective against insulin resistance of adipocytes and involves mitochondrial dysfunction

Contact Info

Product

Resources

About