Quercetin reverses EGF-induced epithelial to mesenchymal transition and invasiveness in prostate cancer (PC-3) cell line via EGFR/PI3K/Akt pathway

Bhat, Firdous Ahmad; Sharmila, Govindaraj; Solaimuthu, Balakrishnan; Ramachandran, A.; Elumalai, Perumal; Suganya, S.; Singh, Pratibha; Srinivasan, N.; Arunakaran, J.

doi:10.1016/j.jnutbio.2014.06.008

Cited by 114 publications

(72 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These data indicate that EGF may induce EMT and promote cell viability by interfering with the cell cycle. Similar results have been published previously (19).…”

Section: Egf Induces Emt and Promotes Cell Viability Different Tumorsupporting

confidence: 93%

Role of Annexin A2 in the EGF-induced epithelial-mesenchymal transition in human CaSki cells

Cui

Jiang

et al. 2016

Oncology Letters

View full text Add to dashboard Cite

Abstract. The epidermal growth factor receptor (EGF-R) signaling pathway is thought to have an important role in the development and progression of several carcinomas, as it is associated with cell proliferation, differentiation and migration. Activation of EGF-R signaling regulates epithelial-mesenchymal transition (EMT)-associated invasion and migration in normal and malignant epithelial cells. However, the specific mechanisms have not yet been fully elucidated. The present study utilized wound healing assays, western blotting, flow cytometry and MTT assays to demonstrate that Annexin A2 (ANXA2) is a key regulatory factor in EGF-induced EMT in CaSki cervical cancer cells. Moreover, the increased expression levels of ANXA2 promoted cell viability and migration in human CaSki cells. It was also found that silencing ANXA2 partially reverses EGF-induced EMT and inhibits cell viability and migration in CaSki cells. These findings suggest that ANXA2 is a key regulator of EGF-induced EMT in CaSki cervical cancer cells.

show abstract

“…These data indicate that EGF may induce EMT and promote cell viability by interfering with the cell cycle. Similar results have been published previously (19).…”

Section: Egf Induces Emt and Promotes Cell Viability Different Tumorsupporting

confidence: 93%

Role of Annexin A2 in the EGF-induced epithelial-mesenchymal transition in human CaSki cells

Cui

Jiang

et al. 2016

Oncology Letters

View full text Add to dashboard Cite

show abstract

“…Studies have shown that quercetin prevented epidermal growth factor (EGF)-induced EMT, migration, and invasion of prostate cancer cells by suppressing the expression of vimentin and N-cadherin [80]. Genistein, an isolavone found in soybeans, fava beans, and lupine, has been shown to downregulate mesenchymal markers ZEB1, slug, and vimentin and therefore cause reversal of EMT in gemcitabine-resistant pancreatic cancer cells [81].…”

Section: Anti-vimentin Agentsmentioning

confidence: 99%

Targeting the Cytoskeleton with Plant-Bioactive Compounds in Cancer Therapy

Ardelean¹

2017

Cytoskeleton - Structure, Dynamics, Function and Disease

View full text Add to dashboard Cite

In this overview we describe the main plant-derived bioactive compounds used in cancer therapy which has the cell cytoskeleton as therapeutic target. Three major classes of these compounds are described: antimitotics with microtubule-destabilizing and-stabilizing efects, plant-bioactive compounds that interact with intermediate ilaments/actin, and plant-bioactive compounds that interact with intermediate ilaments like keratins and vimentin. We also focus on the molecular aspects of interactions with their cellular targets: microtubules, intermediate ilaments, and microilaments. Some critical aspects of cardiac side efects of cancer chemotherapy are also discussed, focusing on cardiac cytoskeleton and protective efect of plant-derived compounds. The application of plant bioactives in the treatment of cancer has resulted in increased therapeutic eicacy through targeting the cytoskeleton, respectively, prevention of the injury of cytoskeletal components elicited by chemotherapeutics.

show abstract

“…Transcriptional repressors Snail, Slug and Twist regulate the expression of mesenchymal and epithelial markers and, hence, play a critical role in EMT [24] . Therefore, to completely understand the mechanism of physcion's action, the effect of physcion on these regulatory molecules was examined.…”

Section: Physcion Inhibits Epithelial-mesenchymal Transition (Emt) Prmentioning

confidence: 99%

Physcion inhibits the metastatic potential of human colorectal cancer SW620 cells in vitro by suppressing the transcription factor SOX2

et al. 2015

View full text Add to dashboard Cite

Aim: Physcion, an anthraquinone derivative, exhibits hepatoprotective, anti-inflammatory, anti-microbial and anti-cancer activities. In this study we examined whether and how physcion inhibited metastatic potential of human colorectal cancer cells in vitro. Methods: Human colorectal cancer cell line SW620 was tested. Cell migration and invasion were assessed using a wound healing and Transwell assay, respectively. The expression levels of transcription factor SOX2 in the cells were modulated with shRNA targeting SOX2 and SOX2 overexpressing plasmid. The expression of target molecules involved in epithelial-mesenchymal transition (EMT) process and the signaling pathways was determined with Western blots or qRT-PCR. ROS levels were measured using DCF-DA. Results: Physcion (2.5, 5 mol/L) did not affect the cell viability, but dose-dependently inhibited the cell adhesion, migration and invasion. Physcion also inhibited the EMT process in the cells, as evidenced by the increased epithelial marker E-cadherin expression, and by decreased expression of mesenchymal markers N-cadherin, vimentin, fibronectin and α-SMA, as well as transcriptional repressors Snail, Slug and Twist. Physcion suppressed the expression of SOX2, whereas overexpression of SOX2 abrogated the inhibition of physcion on metastatic behaviors. Physcion markedly increased ROS production and phosphorylation of AMPK and GSK3β in the cells, whereas the AMPK inhibitor compound C or the ROS inhibitor NAC abolished the inhibition of physcion on metastatic behaviors. Conclusion: Physcion inhibits the metastatic potential of human colorectal cancer cells in vitro via activating ROS/AMPK/GSK3β signaling pathways and suppressing SOX2.

show abstract

Quercetin reverses EGF-induced epithelial to mesenchymal transition and invasiveness in prostate cancer (PC-3) cell line via EGFR/PI3K/Akt pathway

Cited by 114 publications

References 38 publications

Role of Annexin A2 in the EGF-induced epithelial-mesenchymal transition in human CaSki cells

Role of Annexin A2 in the EGF-induced epithelial-mesenchymal transition in human CaSki cells

Targeting the Cytoskeleton with Plant-Bioactive Compounds in Cancer Therapy

Physcion inhibits the metastatic potential of human colorectal cancer SW620 cells in vitro by suppressing the transcription factor SOX2

Contact Info

Product

Resources

About