Data on the evaluation of the relation between β-arrestin 2 and YAP phosphorylation in patient-derived colon cancer organoids
Minsuh Kim,
Ji Min Kim,
Eun Jeong Cho,
Chang Ohk Sung,
Joon Kim,
Se Jin Jang
Affiliations
Minsuh Kim
Asan Institute for Life Sciences, Asan Medical Center, Seoul, Republic of Korea; Department of Pathology, Asan Center for Cancer Genome Discovery, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea
Ji Min Kim
University of Ulsan College of Medicine, Seoul, Republic of Korea
Eun Jeong Cho
University of Ulsan College of Medicine, Seoul, Republic of Korea
Chang Ohk Sung
Department of Pathology, Asan Center for Cancer Genome Discovery, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea; University of Ulsan College of Medicine, Seoul, Republic of Korea
Joon Kim
Graduate School of Medical Science and Engineering, KAIST, Daejeon, Republic of Korea
Se Jin Jang
Department of Pathology, Asan Center for Cancer Genome Discovery, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea; University of Ulsan College of Medicine, Seoul, Republic of Korea; Corresponding author at: Department of Pathology, Asan Center for Cancer Genome Discovery, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
The data presented in this article is related to a rapid communication entitled “β-arrestin 2 suppresses the activation of YAP by promoting LATS kinase activity”. This article describes the correlation of β-arrestin 2 and YAP phosphorylation in patient-derived organoid models. Here, we analyzed 45 colon cancer organoids (CCOs) selected in the related research article to investigate the role of β-arrestin 2 in YAP phosphorylation. Hematoxylin and eosin (H&E) staining and immunohistochemistry data showed that the CCOs maintained tissue architecture and histological features of their original cancer tissues. Moreover, mutation data detected from RNA-seq (RNA-sequencing) analysis showed that these CCOs retained the genetic features of their original colon cancer tissues as well. We also confirmed at the protein level that organoids expressing β-arrestin 2 showed high expression of phosphorylated YAP. These organoid model studies strongly support the related research article that β-arrestin 2 suppresses the activation of YAP in colon cancer.
