Aquaporin3 Is Required for FGF-2-Induced Migration of Human Breast Cancers

Cao, Xu; Zhang, Wei Ran; Cao, Wen; Liu, Bo Wen; Zhang, Fei; Zhao, Hong; Meng, Ran; Zhang, Lin; Niu, Rui; Hao, Xi Shan; Zhang, Bin

doi:10.1371/journal.pone.0056735

Cited by 63 publications

(53 citation statements)

References 27 publications

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“…Our findings support AQP8 positive contribution to carcinogenesis. There are consistent discoveries about the roles of other subtypes of AQPs in tumorigenesis, such as that AQP1 increases the migration speed of B16F10 melanoma cells and 4T1 mammary gland tumor cells, and AQP3 is favor of FGF-2-induced migration of human breast cancers (Hu et al, 2006;Cao et al, 2013). Our results suggest that upregulation of AQP8, in response to EGF accelerates human SiHa cell migration by enhancing plasma-membrane water permeability, which in turn boosts transmembrane water fluxes that occur during cell migration.…”

Section: Discussionsupporting

confidence: 76%

Aquaporin 8 Involvement in Human Cervical Cancer SiHa Migration via the EGFR-Erk1/2 Pathway

Shi¹,

Tuokan²,

Chen³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Overexpression of aquaporins (AQPs) has been reported in several human cancers. Epidermal growth factor receptor (EGFR)-extracellular signal-regulated kinases 1/2 (Erk1/2) are associated with tumorigenesis and cancer progression and may upregulate AQP expression. In this study, we demonstrated that EGF (epidermal growth factor) induces SiHa cells migration and AQP8 expression. Wound healing results showed that cell migration was increased by 2.79-1.50-fold at 24h and 48h after EGF treatment. AQP8 expression was significantly increased (3.33-fold) at 48h after EGF treatment in SiHa cells. An EGFR kinase inhibitor, PD153035, blocked EGFinduced AQP8 expression and cell migration and AQP8 expression was decreased from 1.59-fold (EGF-treated) to 0.43-fold (PD153035-treated) in SiHa. Furthermore, the MEK (MAPK (mitogen-activated protein kinase)/ Erk (extracellular signal regulated kinase)/Erk inhibitor U0126 also inhibited EGF-induced AQP8 expression and cell migration. AQP8 expression was decreased from 1.21-fold (EGF-treated) to 0.43-fold (U0126-treated). Immunofluorescence microscopy further confirmed the results. Collectively, our findings show that EGF induces AQP8 expression and cell migration in human cervical cancer SiHa cells via the EGFR/Erk1/2 signal transduction pathway.

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Section: Discussionsupporting

confidence: 76%

Aquaporin 8 Involvement in Human Cervical Cancer SiHa Migration via the EGFR-Erk1/2 Pathway

Shi¹,

Tuokan²,

Chen³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…16 Both apoptosis and autophagy are genetically-regulated, evolutionarily-conserved processes that regulate cell fate. 19 In this study, we detected the anticancer effects of apigenin on human papillary thyroid carcinoma BCPAP cells. 17 However, there are only few reports concerning the autophagy-inducing effects of apigenin as well as its underlying molecular mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Apigenin induces autophagic cell death in human papillary thyroid carcinoma BCPAP cells

et al. 2015

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Apigenin, abundantly present in fruits and vegetables, is recognized as a flavonoid with anti-inflammatory, antioxidant and anticancer properties. In this study, we first investigated the anti-neoplastic effects of apigenin on papillary thyroid carcinoma (PTC) cell line BCPAP cells. Our results show that apigenin inhibited the viability of BCPAP cells in a dose-dependent manner. A large body of evidence demonstrates that autophagy contributes to cell death in certain contexts. In the present study, autophagy was induced by apigenin treatment in BCPAP cells, as evidenced by Beclin-1 accumulation, conversion of LC3 protein, p62 degradation as well as the significantly increased formation of acidic vesicular organelles (AVOs) compared to the control group. 3-MA, an autophagy inhibitor, rescued the cells from apigenin-induced cell death. Notably, apigenin enhanced production of reactive oxygen species (ROS), and subsequent induction of significant DNA damage as monitored by the TUNEL assay. In addition, apigenin treatment caused a significant accumulation of cells in the G2/M phase via down-regulation of Cdc25C expression. Our findings reveal that apigenin inhibits papillary thyroid cancer cell viability by the stimulation of reactive oxygen species (ROS) production, induction of DNA damage, leading to G2/M cell cycle arrest followed by autophagic cell death. Thus, our results provide new insights into the molecular mechanisms underlying apigenin-mediated autophagic cell death and suggest apigenin as a potential chemotherapeutic agent which is able to fight against papillary thyroid cancer.

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“…Migration of breast cancer cells was tested as described by Cao et al [50]. Briefly, ~1 X 10 6 cells were plated in each well of a 6-well plate and cultured as a monolayer to confluence overnight in RPMI-1640 and DMEM for MCF 7 and MDA-MB-231, respectively prior to serum starvation (5% Fetal Bovine Serum) for 24 h. Next day, the monolayers were wounded by scratching with a sterile 10 μl pipette tip [51] and treated with compounds 13 , 14 , or cisplatin for 24 h. The concentrations of the compounds used were their respective IC 50 values.…”

Section: Methodsmentioning

confidence: 99%

Synthesis, characterization, and evaluation of cis-diphenyl pyridineamine platinum(II) complexes as potential anti-breast cancer agents

et al. 2014

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Although cisplatin is considered as an effective anti-cancer agent, it has shown limitations and may produce toxicity in patients. Therefore, we synthesized two cis-dichlorideplatinum(II) compounds (13 and 14) composed of meta- and para-N,N-diphenyl pyridineamine ligands through a reaction of the amine precursors and PtCl2 with respective yields of 16% and 47%. We hypothesized that compounds 13 and 14, with lipophilic ligands, should transport efficiently in cancer cells and demonstrate more effectiveness than cisplatin. When tested for biological activity, compounds 13 and 14 were found to inhibit the growth of MCF 7 and MDA-MB-231 cells (IC50s 1 ± 0.4 μM and 1 ± 0.2 μM for 13 and 14, respectively, and IC50 7.5 ± 1.3 μM for compound 13 and 1 ± 0.3 μM for compound 14). Incidentally, these doses were found to be lower than cisplatin doses (IC50 5 ± 0.7 μM for MCF 7 and 10 ± 1.1 μM for MDA-MB-231). Similar to cisplatin, 13 and 14 interacted with DNA and induced apoptosis. However, unlike cisplatin, they blocked the migration of MDA-MB-231 cells suggesting that in addition to apoptotic and DNA-binding capabilities, these compounds are useful in blocking the metastatic migration of breast cancer cells. To delineate the mechanism of action, computer-aided analyses (DFT calculations) were conducted for compound 13. Results indicate that in vivo, the pyridineamine ligands are likely to dissociate from the complex, forming a platinum DNA adduct with anti-proliferative activity. These results suggest that complexes 13 and 14 hold promise as potential anti-cancer agents.

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Aquaporin3 Is Required for FGF-2-Induced Migration of Human Breast Cancers

Cited by 63 publications

References 27 publications

Aquaporin 8 Involvement in Human Cervical Cancer SiHa Migration via the EGFR-Erk1/2 Pathway

Aquaporin 8 Involvement in Human Cervical Cancer SiHa Migration via the EGFR-Erk1/2 Pathway

Apigenin induces autophagic cell death in human papillary thyroid carcinoma BCPAP cells

Synthesis, characterization, and evaluation of cis-diphenyl pyridineamine platinum(II) complexes as potential anti-breast cancer agents

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