The MEK5/ERK5 signalling pathway in cancer: a promising novel therapeutic target

Simões, André E.; Rodrigues, Cecília M. P.; Borralho, Pedro M.

doi:10.1016/j.drudis.2016.06.010

Cited by 64 publications

(61 citation statements)

References 103 publications

(157 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The mitogen-activated protein kinase (MAPK) cascade, is the best characterized of the four conventional subfamilies of MAPK cascades transducing a large number of signals, and that lead, as the last step, to the activation of four different MAPK or groups of MAPK: ERK1/2; JNK 1,2 and 3; p38 α, β, γ and δ; and the recently discovered ERK5 [19]. As soon as they are activated, in turn, they phosphorylate a large variety of substrates involved in well-established cell responses, including cell proliferation, differentiation, apoptosis, and migration [19].…”

Section: Erk1/2 As An Emerging Target In Anti-cancer Therapymentioning

confidence: 99%

Modulation of Ras/ERK and Phosphoinositide Signaling by Long-Chain n-3 PUFA in Breast Cancer and Their Potential Complementary Role in Combination with Targeted Drugs

Serini

Calviello

2017

Nutrients

View full text Add to dashboard Cite

A potential complementary role of the dietary long-chain n-3 polyunsaturated fatty acids (LCn-3 PUFA) in combination with innovative mono-targeted therapies has recently been proposed. These compounds are thought to act pleiotropically to prevent the development and progression of a variety of cancers, including breast cancer. We hereinafter critically analyze the reports investigating the ability of LCn-3 PUFA to modulate the Ras/ERK and the phosphoinositide survival signaling pathways often aberrantly activated in breast cancer and representing the main targets of innovative therapies. The in vitro or in vivo animal and human interventional studies published up to January 2017 investigating the effects of LCn-3 PUFA on these pathways in normal and cancerous breast cells or tissues were identified through a systematic search of literature in the PubMed database. We found that, in most cases, both the in vitro and in vivo studies demonstrated the ability of LCn-3 PUFA to inhibit the activation of these pro-survival pathways. Altogether, the analyzed results strongly suggest a potential role of LCn-3 PUFA as complementary agents in combination with mono-targeted therapies. Moreover, the results indicate the need for further in vitro and human interventional studies designed to unequivocally prove the potential adjuvant role of these fatty acids.

show abstract

Section: Erk1/2 As An Emerging Target In Anti-cancer Therapymentioning

confidence: 99%

Modulation of Ras/ERK and Phosphoinositide Signaling by Long-Chain n-3 PUFA in Breast Cancer and Their Potential Complementary Role in Combination with Targeted Drugs

Serini

Calviello

2017

Nutrients

View full text Add to dashboard Cite

show abstract

“…In comparison with the other sub-pathways, the ERK5 sub-pathway has been less intensively investigated (30). It is associated with a variety of stimuli, including mitogens (for example, epithermal growth factor) and cellular stresses (including oxidation and osmotic stress) (31).…”

Section: Mapk Signaling Sub-pathwaysmentioning

confidence: 99%

Mitogen-activated protein kinase signaling pathway in oral cancer (Review)

et al. 2017

View full text Add to dashboard Cite

Abstract. The mitogen-activated protein kinase (MAPK) signaling pathway is associated with tumor cell proliferation, differentiation, apoptosis, angiogenesis, invasion and metastasis. The present review assesses the involvement of the MAPK signaling pathway in oral cancer progression and invasion based on analysis of individual sub-pathways and their mechanisms of action. The regulation of this pathway for targeted oral cancer therapy is explored and the challenges confronting this, as well as corresponding potential solutions, are discussed. Exploring this pathway with an emphasis on its components, subfamilies, sub-pathways, interactions with other pathways and clinical practice modes may improve oral cancer treatment.

show abstract

“…ERK5, also known as big MAPK, is activated by oxidative stress, hyperosmolarity and certain growth factors (29). Unlike other MAPK members, ERK5 has a unique large C-terminal region, whose function has not been fully elucidated (30).…”

Section: Mir-143 Downregulates the Expression Of Erk5 And C-fosmentioning

confidence: 99%

“…Unlike other MAPK members, ERK5 has a unique large C-terminal region, whose function has not been fully elucidated (30). It has been shown that ERK5 directly interacts with, phosphorylates and activates a number of transcription factors, including c-Myc, Sap1a, c-Fos, Fos-related antigen 1 and myocyte enhancer factor-2 family members (29). ERK5 is important for promoting cell proliferation, differentiation and neuronal survival (30).…”

Section: Mir-143 Downregulates the Expression Of Erk5 And C-fosmentioning

confidence: 99%

miR-143 is associated with proliferation and apoptosis involving ERK5 in HeLa cells

et al. 2016

View full text Add to dashboard Cite

Abstract. Inappropriate expression of microRNA (miR) is strongly associated with carcinogenesis. miR-143 was reported to be one of the most prominent miRs implicated in the genesis and progression of human cancer. However, its correlation with cell proliferation and apoptosis in cervical cancer remains to be fully elucidated. In the present study, it was demonstrated that miR-143 is able to suppress the proliferation of cervical cancer HeLa cells and induce cell apoptosis in a time-and dose-dependent manner. The present study also investigated the potential targets of miR-143, extracellular-signal-regulated kinase 5 (ERK5) and its downstream substrate oncoprotein c-Fos, both of which are involved in cell proliferation and apoptosis. Upon increasing the miR-143 level, the ERK5 and c-Fos protein expression was significantly decreased without the effect of ERK5 transcription. Therefore, miR-143 is able to suppress cell proliferation and induce apoptosis in HeLa cells, potentially through negative regulation of ERK5 at its post-transcriptional stage.

show abstract

The MEK5/ERK5 signalling pathway in cancer: a promising novel therapeutic target

Cited by 64 publications

References 103 publications

Modulation of Ras/ERK and Phosphoinositide Signaling by Long-Chain n-3 PUFA in Breast Cancer and Their Potential Complementary Role in Combination with Targeted Drugs

Modulation of Ras/ERK and Phosphoinositide Signaling by Long-Chain n-3 PUFA in Breast Cancer and Their Potential Complementary Role in Combination with Targeted Drugs

Mitogen-activated protein kinase signaling pathway in oral cancer (Review)

miR-143 is associated with proliferation and apoptosis involving ERK5 in HeLa cells

Contact Info

Product

Resources

About