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Transglutaminase-2 mediates acquisition of neratinib resistance in metastatic breast cancer
Journal article   Open access   Peer reviewed

Transglutaminase-2 mediates acquisition of neratinib resistance in metastatic breast cancer

Aparna Shinde, Eylem Kulkoyluoglu Cotul, Hao Chen, Andrew Smith, Sarah Libring, Luis Solorio and Michael K. Wendt
Molecular biomedicine, Vol.3(1), pp.19-19
06/22/2022
DOI: 10.1186/s43556-022-00079-y
PMCID: PMC9213622
PMID: 35729402
url
https://doi.org/10.1186/s43556-022-00079-yView
Published (Version of record) Open Access

Abstract

Acquisition of resistance to targeted therapies remains a major clinical obstacle for the HER2 + subtype of breast cancer. Using an isogeneic progression series of HER2 + breast cancer metastasis we demonstrate that metastatic cells have an increased capacity to acquire resistance to the covalent, pan-ErbB inhibitor, neratinib. RNA sequencing analyses comparing parental and metastatic cells identified upregulation of transglutaminase 2 (TG2). Genetic depletion and overexpression approaches established that TG2 is both necessary and sufficient for acquisition of neratinib resistance. Mechanistically, we describe a pathway in which TG2-mediates activation of NF-κB signaling leading to upregulation of IL-6 in metastatic cells. This autocrine expression of IL-6 functions to maintain enhanced levels of TG2 via JAK:STAT3 signaling. This drug persistence feedback loop can be interrupted through the use of the JAK1/2 inhibitor ruxolitinib. In vivo application of ruxolitinib had no effect on tumor growth under non-treated conditions, but effectively prevented acquisition of resistance, leading to tumor regression upon coadministration with neratinib. Overall, our studies reveal a mechanism in metastatic breast cancer cells that predisposes them to acquisition of resistance to ErbB-targeted therapeutics. Clinically, immediate application of ruxolitinib could prevent acquisition of resistance and improve patient responses to HER2-targeted therapies.

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