Figure S6 from Inhibiting ERK5 Overcomes Breast Cancer Resistance to Anti-HER2 Therapy By Targeting the G1–S Cell-Cycle Transition

Zhang, Jingwei; Pearson, Adam J.; Sabherwal, Nitin; Telfer, Brian A.; Ali, Nisha; Kan, Karmern; Xu, Qiuping; Zhang, Wei; Chen, Fuhui; Li, Shiyang; Wang, Jinhua; Gray, Nathanael S.; Risa-Ebrí, Blanca; Finegan, Katherine G.; Cross, Michael J.; Giurisato, Emanuele; Whitmarsh, Alan J.; Tournier, Cathy

doi:10.1158/2767-9764.22544291.v1

Figure S6 from Inhibiting ERK5 Overcomes Breast Cancer Resistance to Anti-HER2 Therapy By Targeting the G₁–S Cell-Cycle Transition

journal contribution

posted on 2023-04-04, 01:22 authored by Jingwei Zhang, Adam J. Pearson, Nitin Sabherwal, Brian A. Telfer, Nisha Ali, Karmern Kan, Qiuping Xu, Wei Zhang, Fuhui Chen, Shiyang Li, Jinhua Wang, Nathanael S. Gray, Blanca Risa-Ebrí, Katherine G. Finegan, Michael J. Cross, Emanuele Giurisato, Alan J. Whitmarsh, Cathy Tournier

The effect of lapatinib and JWG-045 as single treatments was compared to that achieved in combination therapy on the cell cycle profile of sensitive and resistant breast cancer cell lines.

Funding

Worldwide Cancer Research (WCR)

UKRI | Medical Research Council (MRC)

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ARTICLE ABSTRACT

Here we demonstrate that targeting ERK5 in HER2-positive breast cancer cells reduces the level of phosphorylation of RB, an important mediator of the G1–S transition. This effect is associated with increased antitumor activity of lapatinib in combination therapy with ERK5 silencing. Collectively, these findings reveal that ERK5 constitutes a relevant therapeutic target for the many patients with resistant HER2-positive breast cancer.

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Keywords

Breast Cancer Cell Signaling Growth factors Protein serine-threonine kinases Cell Cycle Control of cell cycle progression CDKs and CDK inhibitors Drug Resistance Novel mechanisms Drug Mechanisms Cellular responses to anticancer drugs Oncogenes & Tumor Suppressors Rb and family

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