TGF-β1–ROS–ATM–CREB signaling axis in macrophage mediated migration of human breast cancer MCF7 cells

Singh, Rishi Pal; Shankar, Bhavani S.; Sainis, Krishna B.

doi:10.1016/j.cellsig.2014.03.028

Cited by 61 publications

(44 citation statements)

References 52 publications

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“…Note that knockdown of CREB1 using at least two shRNAs (Fig S5C) did not affect the ability of CTx to induce an MET in the N8 cells (Fig 3B). Moreover, loss of CREB1 alone induced a partial MET in N8 cells (Fig 3B), consistent with previous reports of its role in the induction of an EMT (39, 40). From these observations, it was obvious that CREB1 did not play an important role in the PKA-induced MET.…”

Section: Resultssupporting

confidence: 92%

Activation of PKA leads to mesenchymal-to-epithelial transition and loss of tumor-initiating ability

Pattabiraman

Bierie

Kober

et al. 2016

Science

295

247

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The epithelial-to-mesenchymal transition (EMT) enables carcinoma cells to acquire malignancy-associated traits and properties of tumor-initiating cells (TICs). TICs have emerged in recent years as important targets for cancer therapy owing to their ability to drive clinical relapse and enable metastasis. Here we propose a strategy to eliminate mesenchymal TICs by inducing their conversion to more epithelial counterparts that have lost tumor-initiating ability. We report that increases in intracellular levels of the second messenger, cAMP, and the subsequent activation of protein kinase A (PKA) induce a mesenchymal-to-epithelial transition (MET) in mesenchymal human mammary epithelial cells. Activation of PKA triggers PHF2-mediated epigenetic reprogramming of TICs, promoting their differentiation that leads to loss of tumor-initiating ability. This study provides proof-of-principle for inducing an MET as differentiation therapy for TICs and uncovers a novel role for PKA in enforcing and maintaining the epithelial state.

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Section: Resultssupporting

confidence: 92%

Activation of PKA leads to mesenchymal-to-epithelial transition and loss of tumor-initiating ability

Pattabiraman

Bierie

Kober

et al. 2016

Science

295

247

View full text Add to dashboard Cite

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“…CREB plays a major role in the regulation of cell migration and proliferation during development and disease processes [22,23]. In fact, CREB-mediated IL-6 expression was required for 15-HETE-induced VSMC migration and proliferation [4].…”

Section: Discussionmentioning

confidence: 99%

“…CREB regulates cell migration and proliferation [22,23]. To examine whether 15-HETE treatment activates CREB, we performed Western blot analysis using phosphor-specific antibodies.…”

Section: Creb Activation Is Essential For 15-hete-induced Vaf Migrationmentioning

confidence: 99%

STAT3-mediated MMP-2 expression is required for 15-HETE-induced vascular adventitial fibroblast migration

Zhang

Liu

et al. 2015

The Journal of Steroid Biochemistry and Molecular Biology

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“…Hepatic cells infected with hepatitis virus have been shown to express a high level of HLA-E, which inhibits NK-cell cytotoxicity in abnormal hepatic cells and stimulates NK cells to release cytokines, including interleukin (IL)-10 and transforming growth factor (TGF)-β1 [10]. In breast cancer and lung adenocarcinoma, IL-10 and TGF-β1 have been confirmed to promote tumor growth through pathways including tumor migration and invasion [11–12]. NB is an aggressive tumor.…”

Section: Introductionmentioning

confidence: 99%

Involvement of IL-10 and TGF-β in HLA-E-mediated neuroblastoma migration and invasion

et al. 2016

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Human leukocyte antigen (HLA)-E is highly expressed in a variety of tumors and, in addition to immune escape, may promote tumor growth via other mechanisms. However, the role of HLA-E in neuroblastoma (NB) migration and invasion is unknown. In the present study, HLA-E expression in human NB tumors was measured by immunohistochemistry. The effect of HLA-E on NB cell migration and invasion was studied in vitro and in vivo, as well as the effect of HLA-E on natural killer (NK)-cell cytotoxicity. HLA-E was expressed in 70.2% of the NB tumor tissues examined. HLA-E expression by NB cells inhibited NK-cell cytotoxicity and induced the release of interleukin (IL)-10 and transforming growth factor (TGF)-β1. HLA-E and the released cytokines enhanced the ability of NB cells migration and invasion. NK cell infusion did not inhibit the growth of NB cells with high HLA-E expression but instead increased the number of metastatic cells in the bone marrow. Taken together, the results indicate that IL-10 and TGF-β are involved in HLA-E-mediated NB migration and invasion. Thus, HLA-E may be a new treatment target in NB.

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TGF-β1–ROS–ATM–CREB signaling axis in macrophage mediated migration of human breast cancer MCF7 cells

Cited by 61 publications

References 52 publications

Activation of PKA leads to mesenchymal-to-epithelial transition and loss of tumor-initiating ability

Activation of PKA leads to mesenchymal-to-epithelial transition and loss of tumor-initiating ability

STAT3-mediated MMP-2 expression is required for 15-HETE-induced vascular adventitial fibroblast migration

Involvement of IL-10 and TGF-β in HLA-E-mediated neuroblastoma migration and invasion

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