Dysregulation of YAP by ARF Stimulated with Tea-derived Carbon Nanodots

Yingqiu Xie, Qinglei Sun, Ayan A. Nurkesh, Jiang Lu, Sholpan Kauanova, Jinhong Feng, Darkhan Tursynkhan, Qing Yang, Aishabibi Kassymbek, Mirat Karibayev, Korlan Duisenova, Haiyan Fan, Xiao Wang, Limara Manarbek, Aisulu Maipas, Zhenbang Chen, Mannix P. Balanay

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

YAP is a downstream nuclear transcription factor of Hippo pathway which plays an essential role in development, cell growth, organ size and homeostasis. It was previously identified that elevation of YAP in genomics of genetic engineered mouse (GEM) model of prostate cancer is associated with Pten/Trp53 inactivation and ARF elevation hypothesizing the essential crosstalk of AKT/mTOR/YAP with ARF in prostate cancer. However, the detailed function and trafficking of YAP in cancer cells remains unclear. Using GEM microarray model, we found ARF dysregulates Hippo and Wnt pathways. In particular, ARF knockdown reduced non-nuclear localization of YAP which led to an increase in F-actin. Mechanistically, ARF knockdown suppressed protein turnover of β-catenin/YAP, and therefore enhanced the activity of AKT and phosphorylation of YAP. Moreover, we found tea-derived carbon dots can interact with ARF in nucleus that may further lead to the non-nuclear localization of YAP. Thus, we reported a novel crosstalk of ARF/β-catenin dysregulated YAP in Hippo pathway and a new approach to stimulate ARF-mediated signaling to inhibit nuclear YAP using nanomaterials implicating an innovative avenue for treatment of cancer.

Original languageEnglish
Article number16441
JournalScientific Reports
Volume7
Issue number1
DOIs
Publication statusPublished - Dec 1 2017

Fingerprint

Catenins
Tea
Prostatic Neoplasms
Carbon
Wnt Signaling Pathway
Organ Size
Nanostructures
Genomics
Growth and Development
Actins
Neoplasms
Homeostasis
Transcription Factors
Phosphorylation

ASJC Scopus subject areas

  • General

Cite this

Dysregulation of YAP by ARF Stimulated with Tea-derived Carbon Nanodots. / Xie, Yingqiu; Sun, Qinglei; Nurkesh, Ayan A.; Lu, Jiang; Kauanova, Sholpan; Feng, Jinhong; Tursynkhan, Darkhan; Yang, Qing; Kassymbek, Aishabibi; Karibayev, Mirat; Duisenova, Korlan; Fan, Haiyan; Wang, Xiao; Manarbek, Limara; Maipas, Aisulu; Chen, Zhenbang; Balanay, Mannix P.

In: Scientific Reports, Vol. 7, No. 1, 16441, 01.12.2017.

Research output: Contribution to journalArticle

Xie, Y, Sun, Q, Nurkesh, AA, Lu, J, Kauanova, S, Feng, J, Tursynkhan, D, Yang, Q, Kassymbek, A, Karibayev, M, Duisenova, K, Fan, H, Wang, X, Manarbek, L, Maipas, A, Chen, Z & Balanay, MP 2017, 'Dysregulation of YAP by ARF Stimulated with Tea-derived Carbon Nanodots', Scientific Reports, vol. 7, no. 1, 16441. https://doi.org/10.1038/s41598-017-16441-y
Xie, Yingqiu ; Sun, Qinglei ; Nurkesh, Ayan A. ; Lu, Jiang ; Kauanova, Sholpan ; Feng, Jinhong ; Tursynkhan, Darkhan ; Yang, Qing ; Kassymbek, Aishabibi ; Karibayev, Mirat ; Duisenova, Korlan ; Fan, Haiyan ; Wang, Xiao ; Manarbek, Limara ; Maipas, Aisulu ; Chen, Zhenbang ; Balanay, Mannix P. / Dysregulation of YAP by ARF Stimulated with Tea-derived Carbon Nanodots. In: Scientific Reports. 2017 ; Vol. 7, No. 1.
@article{6a5c862a58424d8fb8fd2e4348259d84,
title = "Dysregulation of YAP by ARF Stimulated with Tea-derived Carbon Nanodots",
abstract = "YAP is a downstream nuclear transcription factor of Hippo pathway which plays an essential role in development, cell growth, organ size and homeostasis. It was previously identified that elevation of YAP in genomics of genetic engineered mouse (GEM) model of prostate cancer is associated with Pten/Trp53 inactivation and ARF elevation hypothesizing the essential crosstalk of AKT/mTOR/YAP with ARF in prostate cancer. However, the detailed function and trafficking of YAP in cancer cells remains unclear. Using GEM microarray model, we found ARF dysregulates Hippo and Wnt pathways. In particular, ARF knockdown reduced non-nuclear localization of YAP which led to an increase in F-actin. Mechanistically, ARF knockdown suppressed protein turnover of β-catenin/YAP, and therefore enhanced the activity of AKT and phosphorylation of YAP. Moreover, we found tea-derived carbon dots can interact with ARF in nucleus that may further lead to the non-nuclear localization of YAP. Thus, we reported a novel crosstalk of ARF/β-catenin dysregulated YAP in Hippo pathway and a new approach to stimulate ARF-mediated signaling to inhibit nuclear YAP using nanomaterials implicating an innovative avenue for treatment of cancer.",
author = "Yingqiu Xie and Qinglei Sun and Nurkesh, {Ayan A.} and Jiang Lu and Sholpan Kauanova and Jinhong Feng and Darkhan Tursynkhan and Qing Yang and Aishabibi Kassymbek and Mirat Karibayev and Korlan Duisenova and Haiyan Fan and Xiao Wang and Limara Manarbek and Aisulu Maipas and Zhenbang Chen and Balanay, {Mannix P.}",
year = "2017",
month = "12",
day = "1",
doi = "10.1038/s41598-017-16441-y",
language = "English",
volume = "7",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "Nature Publishing Group",
number = "1",

}

TY - JOUR

T1 - Dysregulation of YAP by ARF Stimulated with Tea-derived Carbon Nanodots

AU - Xie, Yingqiu

AU - Sun, Qinglei

AU - Nurkesh, Ayan A.

AU - Lu, Jiang

AU - Kauanova, Sholpan

AU - Feng, Jinhong

AU - Tursynkhan, Darkhan

AU - Yang, Qing

AU - Kassymbek, Aishabibi

AU - Karibayev, Mirat

AU - Duisenova, Korlan

AU - Fan, Haiyan

AU - Wang, Xiao

AU - Manarbek, Limara

AU - Maipas, Aisulu

AU - Chen, Zhenbang

AU - Balanay, Mannix P.

PY - 2017/12/1

Y1 - 2017/12/1

N2 - YAP is a downstream nuclear transcription factor of Hippo pathway which plays an essential role in development, cell growth, organ size and homeostasis. It was previously identified that elevation of YAP in genomics of genetic engineered mouse (GEM) model of prostate cancer is associated with Pten/Trp53 inactivation and ARF elevation hypothesizing the essential crosstalk of AKT/mTOR/YAP with ARF in prostate cancer. However, the detailed function and trafficking of YAP in cancer cells remains unclear. Using GEM microarray model, we found ARF dysregulates Hippo and Wnt pathways. In particular, ARF knockdown reduced non-nuclear localization of YAP which led to an increase in F-actin. Mechanistically, ARF knockdown suppressed protein turnover of β-catenin/YAP, and therefore enhanced the activity of AKT and phosphorylation of YAP. Moreover, we found tea-derived carbon dots can interact with ARF in nucleus that may further lead to the non-nuclear localization of YAP. Thus, we reported a novel crosstalk of ARF/β-catenin dysregulated YAP in Hippo pathway and a new approach to stimulate ARF-mediated signaling to inhibit nuclear YAP using nanomaterials implicating an innovative avenue for treatment of cancer.

AB - YAP is a downstream nuclear transcription factor of Hippo pathway which plays an essential role in development, cell growth, organ size and homeostasis. It was previously identified that elevation of YAP in genomics of genetic engineered mouse (GEM) model of prostate cancer is associated with Pten/Trp53 inactivation and ARF elevation hypothesizing the essential crosstalk of AKT/mTOR/YAP with ARF in prostate cancer. However, the detailed function and trafficking of YAP in cancer cells remains unclear. Using GEM microarray model, we found ARF dysregulates Hippo and Wnt pathways. In particular, ARF knockdown reduced non-nuclear localization of YAP which led to an increase in F-actin. Mechanistically, ARF knockdown suppressed protein turnover of β-catenin/YAP, and therefore enhanced the activity of AKT and phosphorylation of YAP. Moreover, we found tea-derived carbon dots can interact with ARF in nucleus that may further lead to the non-nuclear localization of YAP. Thus, we reported a novel crosstalk of ARF/β-catenin dysregulated YAP in Hippo pathway and a new approach to stimulate ARF-mediated signaling to inhibit nuclear YAP using nanomaterials implicating an innovative avenue for treatment of cancer.

UR - http://www.scopus.com/inward/record.url?scp=85036516487&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85036516487&partnerID=8YFLogxK

U2 - 10.1038/s41598-017-16441-y

DO - 10.1038/s41598-017-16441-y

M3 - Article

AN - SCOPUS:85036516487

VL - 7

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

IS - 1

M1 - 16441

ER -