Aromatase induction in tamoxifen-resistant breast cancer: Role of phosphoinositide 3-kinase-dependent CREB activation

Phuong, Nguyen Thi Thuy; Lim, Sung Chul; Kim, Young Mi; Kang, Keon Wook

doi:10.1016/j.canlet.2014.05.003

Cited by 27 publications

(21 citation statements)

References 46 publications

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“…14-3-3ζ has been shown to directly bind to Raf and activate MEK/ERK [23–25], which directly phosphorylate p90 ribosomal S6 kinase, that in turn activates and phosphorylates of CREB at Ser-133 [26, 27]. Thus, we tested whether CREB-mediated transcriptional upregulation of LDHA could be modulated through the 14-3-3ζ-ERK-RSK signaling axis.…”

Section: Resultsmentioning

confidence: 99%

Upregulation of lactate dehydrogenase a by 14-3-3ζ leads to increased glycolysis critical for breast cancer initiation and progression

Chang

Zhang

et al. 2016

Oncotarget

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Metabolic reprogramming is a hallmark of cancer. Elevated glycolysis in cancer cells switches the cellular metabolic flux to produce more biological building blocks, thereby sustaining rapid proliferation. Recently, new evidence has emerged that metabolic dysregulation may occur at early-stages of neoplasia and critically contribute to cancer initiation. Here, our bioinformatics analysis of microarray data from early-stages breast neoplastic lesions revealed that 14-3-3ζ expression is strongly correlated with the expression of canonical glycolytic genes, particularly lactate dehydrogenase A (LDHA). Experimentally, increasing 14-3-3ζ expression in human mammary epithelial cells (hMECs) up-regulated LDHA expression, elevated glycolytic activity, and promoted early transformation. Knockdown of LDHA in the 14-3-3ζ-overexpressing hMECs significantly reduced glycolytic activity and inhibited transformation. Mechanistically, 14-3-3ζ overexpression activates the MEK-ERK-CREB axis, which subsequently up-regulates LDHA. In vivo, inhibiting the activated the MEK/ERK pathway in 14-3-3ζ-overexpressing hMEC-derived MCF10DCIS.COM lesions led to effective inhibition of tumor growth. Therefore, targeting the MEK/ERK pathway could be an effective strategy for intervention of 14-3-3ζ-overexpressing early breast lesions. Together, our data demonstrate that overexpression of 14-3-3ζ in early stage pre-cancerous breast epithelial cells may trigger an elevated glycolysis and transcriptionally up-regulating LDHA, thereby contributes to human breast cancer initiation.

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Section: Resultsmentioning

confidence: 99%

Upregulation of lactate dehydrogenase a by 14-3-3ζ leads to increased glycolysis critical for breast cancer initiation and progression

Chang

Zhang

et al. 2016

Oncotarget

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“…The results from these experiments showed that PKD1 directly phosphorylated CREB and that the selenite-induced de-phosphorylation of PKD1 led to the inhibition of CREB phosphorylation in CRC cells. Moreover, studies conducted by Nguyen et al [36] and Huang et al [37] concluded that CREB can promote cancer cell survival via PI3K/AKT-dependent activation. Our previous study also provided evidence that selenite can induce CRC cells apoptosis by inhibiting the PI3K/AKT survival pathway [7].…”

Section: Discussionmentioning

confidence: 97%

The p38 MAPK-regulated PKD1/CREB/Bcl-2 pathway contributes to selenite-induced colorectal cancer cell apoptosis in vitro and in vivo

et al. 2014

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Supranutritional selenite has anti-cancer therapeutic effects in vivo; however, the detailed mechanisms underlying these effects are not clearly understood. Further studies would broaden our understanding of the anti-cancer effects of this compound and provide a theoretical basis for its clinical application. In this study, we primarily found that selenite exposure inhibited phosphorylation of cyclic adenosine monophosphate (cAMP)-response element binding protein (CREB), leading to suppression of Bcl-2 in HCT116 and SW480 colorectal cancer (CRC) cells. Moreover, the selenite-induced inhibitory effect on PKD1 activation was involved in suppression of the CREB signalling pathway. Additionally, we discovered that selenite treatment can upregulate p38 MAPK phosphorylation, which results in inhibition of the PKD1/CREB/Bcl-2 survival pathway and triggers apoptosis. Finally, we established a colorectal cancer xenograft model and found that selenite treatment markedly inhibits tumour growth through the MAPK/PKD1/CREB/Bcl-2 pathway in vivo. Our results demonstrated that a supranutritional dose of selenite induced CRC cell apoptosis through inhibition of the PKD1/CREB/Bcl-2 axis both in vitro and in vivo.

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“…In line with the increase in cell viability we observed in the 11b-PGF2a treated MCF-FP cell line in response to serum starved conditions, the downstream pathways we identified in this manuscript are already documented survival pathways in breast cancer. ERK is a well-known pathway that affects cancer cell biology and up-regulates a variety of oncogenes including Slug (Chen et al, 2009) while, recent studies demonstrated the involvement of CREB in the induction of aromatase expression (Phuong et al, 2014;Samarajeewa et al, 2013). Thus activation of these oncogenic pathways by 11b-PGF2a treatment provides potential underlying mechanisms for the increase of MCF-FP viability in both an ER-dependent and -independent manner.…”

Section: Discussionmentioning

confidence: 93%

11β-Prostaglandin F2α, a bioactive metabolite catalyzed by AKR1C3, stimulates prostaglandin F receptor and induces slug expression in breast cancer

Yoda

Kikuchi

Miki

et al. 2015

Molecular and Cellular Endocrinology

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Aromatase induction in tamoxifen-resistant breast cancer: Role of phosphoinositide 3-kinase-dependent CREB activation

Cited by 27 publications

References 46 publications

Upregulation of lactate dehydrogenase a by 14-3-3ζ leads to increased glycolysis critical for breast cancer initiation and progression

Upregulation of lactate dehydrogenase a by 14-3-3ζ leads to increased glycolysis critical for breast cancer initiation and progression

The p38 MAPK-regulated PKD1/CREB/Bcl-2 pathway contributes to selenite-induced colorectal cancer cell apoptosis in vitro and in vivo

11β-Prostaglandin F2α, a bioactive metabolite catalyzed by AKR1C3, stimulates prostaglandin F receptor and induces slug expression in breast cancer

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