Dual specificity phosphatase (DUSP)-4 is induced by platelet-derived growth factor -BB in an Erk1/2-, STAT3- and p53-dependent manner

Yin, Runsheng; Eger, Glenda; Sarri, Niki; Rorsman, Charlotte; Heldin, Carl‐Henrik; Lennartsson, Johan

doi:10.1016/j.bbrc.2019.09.014

Cited by 4 publications

(2 citation statements)

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“…DUSP4/6, encoding MAPK phosphatases 2/3 (MKP2/3), were negative feedback regulators of the MAPK pathway through dephosphorylation of ERK, p38, and C-Jun Nterminal kinase (JNK) [29,30]. Interestingly, Ito et al [31] developed a CRISPR paralog targeting library screen and uncovered a novel synthetic lethal interaction between DUSP4/6 and oncogenic neuroblastoma RAS viral oncogene homolog (NRAS) in melanoma cells.…”

Section: Synthetic Lethality Of Dual-specificity Phosphatase 4 (Dusp4...mentioning

confidence: 99%

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Protein tyrosine phosphatases: emerging role in cancer therapy resistance

Zhao,

Shuai,

et al. 2024

Cancer Communications

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BackgroundTyrosine phosphorylation of intracellular proteins is a post‐translational modification that plays a regulatory role in signal transduction during cellular events. Dephosphorylation of signal transduction proteins caused by protein tyrosine phosphatases (PTPs) contributed their role as a convergent node to mediate cross‐talk between signaling pathways. In the context of cancer, PTP‐mediated pathways have been identified as signaling hubs that enabled cancer cells to mitigate stress induced by clinical therapy. This is achieved by the promotion of constitutive activation of growth‐stimulatory signaling pathways or modulation of the immune‐suppressive tumor microenvironment. Preclinical evidences suggested that anticancer drugs will release their greatest therapeutic potency when combined with PTP inhibitors, reversing drug resistance that was responsible for clinical failures during cancer therapy.Areas coveredThis review aimed to elaborate recent insights that supported the involvement of PTP‐mediated pathways in the development of resistance to targeted therapy and immune‐checkpoint therapy.Expert opinionThis review proposed the notion of PTP inhibition in anticancer combination therapy as a potential strategy in clinic to achieve long‐term tumor regression. Ongoing clinical trials are currently underway to assess the safety and efficacy of combination therapy in advanced‐stage tumors.

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Section: Synthetic Lethality Of Dual-specificity Phosphatase 4 (Dusp4...mentioning

confidence: 99%

“…DUSP4/6 , encoding MAPK phosphatases 2/3 (MKP2/3), were negative feedback regulators of the MAPK pathway through dephosphorylation of ERK, p38, and C‐Jun N‐terminal kinase (JNK) [ 29 , 30 ]. Interestingly, Ito et al.…”

Section: Ptps Mediate Resistance To Targeted Therapymentioning

confidence: 99%