The PPARβ agonist L-165041 promotes VEGF mRNA stabilization in HPV18-harboring HeLa cells through a receptor-independent mechanism

Roche, Emmanuelle; Lascombe, Isabelle; Bittard, Hugues; Mougin, Christiane; Fauconnet, Sylvie

doi:10.1016/j.cellsig.2013.10.006

Cited by 6 publications

(6 citation statements)

References 47 publications

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“…However, mTOR signaling activation was also shown to be activated in the absence of E6 or p53 under the influence of the transcriptional factor PPARbeta. It was shown that PPARbeta acts as an agonist for VEGF in CC cell lines and did not require target nuclear receptors for higher levels of VEGF mRNA [40].…”

Section: Carcinogenesis In Presence and Absence Of Hpvmentioning

confidence: 99%

The Communication between the PI3K/AKT/mTOR Pathway and Y-Box Binding Protein-1 in Gynecological Cancer

Sobočan

Bračič

Knez

et al. 2020

Cancers

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Studies of the mechanistic (mammalian) target of rapamycin inhibitors (mTOR) represent a step towards the targeted treatment of gynecological cancers. It has been shown that women with increased levels of mTOR signaling pathway targets have worse prognosis compared to women with normal mTOR levels. Yet, targeting mTOR alone has led to unsatisfactory outcomes in gynecological cancer. The aim of our review was therefore to provide an overview of the most recent clinical results and basic findings on the interplay of mTOR signaling and cold shock proteins in gynecological malignancies. Due to their oncogenic activity, there are promising data showing that mTOR and Y-box-protein 1 (YB-1) dual targeting improves the inhibition of carcinogenic activity. Although several components differentially expressed in patients with ovarian, endometrial, and cervical cancer of the mTOR were identified, there are only a few investigated downstream actors in gynecological cancer connecting them with YB-1. Our analysis shows that YB-1 is an important player impacting AKT as well as the downstream actors interacting with mTOR such as epidermal growth factor receptor (EGFR), Snail or E-cadherin.

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Section: Carcinogenesis In Presence and Absence Of Hpvmentioning

confidence: 99%

The Communication between the PI3K/AKT/mTOR Pathway and Y-Box Binding Protein-1 in Gynecological Cancer

Sobočan

Bračič

Knez

et al. 2020

Cancers

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“…However, there is currently no consensus on how PPARβ/δ influences angiogenesis (reviewed in [4, 5, 6, 7, 8]). Two recent studies suggest that PPARβ/δ agonists can increase expression of VEGF mRNA modestly in cancer cells, but these studies did not measure angiogenic endpoints, and the effects were independent of PPARβ/δ, and therefore likely due to off-target effects of the agonists used (GW501516, L165041) [38, 39]. In contrast, secretion of VEGF was increased in a human colon cancer cell line by knockdown of PPARβ/δ, and ligand activation of PPARβ/δ inhibited secretion of VEGF, an effect that was mitigated by knockdown of PPARβ/δ [20].…”

Section: Modulating Hallmarks and Enabling Characteristics Of Cancer mentioning

confidence: 99%

Establishing the Role of PPARβ/δ in Carcinogenesis

Peters

Gonzalez

Müller

2015

Trends in Endocrinology & Metabolism

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The role of the nuclear hormone receptor peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) in carcinogenesis is controversial because conflicting studies indicate that PPARβ/δ inhibits and promotes tumorigenesis. This review focuses on recent studies on PPARβ/δ including: 1) the significance of increased or decreased PPARβ/δ expression in cancers, 2) a range of opposing mechanisms describing how PPARβ/δ agonists, antagonists and inverse agonists regulate tumorigenesis and/or whether there may be cell context-specific mechanisms, and 3) whether activating or inhibiting PPARβ/δ is feasible for cancer chemoprevention and/or therapy. Research questions that need to be addressed will be highlighted in order to establish whether PPARβ/δ can be effectively targeted for cancer chemoprevention.

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“…For example, in colon carcinoma cells, the phosphorylation of ELAVL1 by PKC isozymes promotes COX2 overexpression through increased mRNA stability [72]. In hypoxic conditions, cytoplasmic localization and ARE-binding activity of ELAVL1 increases, leading to expression of pro-angiogenic mRNAs, likely due to activation of ELAVL1 by PKC and other kinases [73–77]. Moreover, ELAVL1 promotes chemo-resistance by binding to and stabilizing HIF1a and other hypoxia-associated mRNAs [78–80].…”

Section: Are-bps In Cancermentioning

confidence: 99%

Post-transcriptional regulation of cytokine and growth factor signaling in cancer

Louis

Bohjanen

2017

Cytokine & Growth Factor Reviews

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Cytokines and growth factors regulate cell proliferation, differentiation, migration and apoptosis, and play important roles in coordinating growth signal responses during development. The expression of cytokine genes and the signals transmitted through cytokine receptors are tightly regulated at several levels, including transcriptional and post-transcriptional levels. A majority of cytokine mRNAs, including growth factor transcripts, contain AU-rich elements (AREs) in their 3’ untranslated regions that control gene expression by regulating mRNA degradation and changing translational rates. In addition, numerous proteins involved in transmitting signals downstream of cytokine receptors are regulated at the level of mRNA degradation by GU-rich elements (GREs) found in their 3’ untranslated regions. Abnormal stabilization and overexpression of ARE or GRE-containing transcripts had been observed in many malignancies, which is a consequence of the malfunction of RNA-binding proteins. In this review, we briefly summarize the role of AREs and GREs in regulating mRNA turnover to coordinate cytokine and growth factor expression, and we describe how dysregulation of mRNA degradation mechanisms contributes to the development and progression of cancer.

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The PPARβ agonist L-165041 promotes VEGF mRNA stabilization in HPV18-harboring HeLa cells through a receptor-independent mechanism

Cited by 6 publications

References 47 publications

The Communication between the PI3K/AKT/mTOR Pathway and Y-Box Binding Protein-1 in Gynecological Cancer

The Communication between the PI3K/AKT/mTOR Pathway and Y-Box Binding Protein-1 in Gynecological Cancer

Establishing the Role of PPARβ/δ in Carcinogenesis

Post-transcriptional regulation of cytokine and growth factor signaling in cancer

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