Last update 01 Nov 2024

ELAVL1 x FOXQ1

Last update 01 Nov 2024

Basic Info

Related Targets

ELAVL1FOXQ1

Drugs associated with ELAVL1 x FOXQ1

KH-3

Target

ELAVL1 x FOXQ1

Mechanism

ELAVL1 inhibitors [+1]

Active Org.-

Originator Org.

University of Kansas

Active Indication-

Inactive Indication

Metastatic breast cancer

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ELAVL1 x FOXQ1

100 Translational Medicine associated with ELAVL1 x FOXQ1

0 Patents (Medical) associated with ELAVL1 x FOXQ1

Literatures (Medical) associated with ELAVL1 x FOXQ1

01 Feb 2024·iScience

circCD2AP promotes epithelial mesenchymal transition and stemness in bladder cancer by regulating FOXQ1/USP21 axis

Article

Author: Zhou, Lei ; Wang, Jinrong ; Zhang, Yichuan ; Tan, Jing ; Liu, Yuan

Bladder cancer (BC) is a prevalent and deadly disease. circCD2AP was suggested to be highly expressed in BC. However, the exact mechanism needs further investigation. In this study, circCD2AP was observed to be upregulated in BC and linked to poor prognosis in individuals. Functionally, circCD2AP or USP21 knockdown inhibited BC cell EMT and stemness both in vitro and in vivo. Mechanistically, circCD2AP interacted with ELAVL1 to enhance the stability of USP21 mRNA, which, in turn, inhibited the ubiquitination degradation of FOXQ1. Through rescue assay, USP21 or FOXQ1 knockdown was found to abolish the promoting effects of circCD2AP or USP21 overexpression on BC cell EMT and stemness. Overall, this study has unveiled the role of circCD2AP/ELAVL1/USP21/FOXQ1 axis in BC EMT and stemness regulation, offering insights into the mechanisms underlying BC progression, with potential implications for therapeutic strategies.

Communications Biology

Targeting the interaction between RNA-binding protein HuR and FOXQ1 suppresses breast cancer invasion and metastasis

Article

Author: Aubé, Jeffrey ; Marquez, Rebecca T ; Wood, Spencer ; Welch, Danny R ; Dixon, Dan A ; Wei, Lanjing ; Gardashova, Gulhumay ; Lan, Lan ; Roy, Sudeshna ; Xu, Liang ; Ji, Min ; Li, Ling ; Gao, Fei P ; Wu, Xiaoqing ; Han, Shuang ; Gowthaman, Ragul ; Zhong, Cuncong ; Karanicolas, John

AbstractPatients diagnosed with metastatic breast cancer have a dismal 5-year survival rate of only 24%. The RNA-binding protein Hu antigen R (HuR) is upregulated in breast cancer, and elevated cytoplasmic HuR correlates with high-grade tumors and poor clinical outcome of breast cancer. HuR promotes tumorigenesis by regulating numerous proto-oncogenes, growth factors, and cytokines that support major tumor hallmarks including invasion and metastasis. Here, we report a HuR inhibitor KH-3, which potently suppresses breast cancer cell growth and invasion. Furthermore, KH-3 inhibits breast cancer experimental lung metastasis, improves mouse survival, and reduces orthotopic tumor growth. Mechanistically, we identify FOXQ1 as a direct target of HuR. KH-3 disrupts HuR–FOXQ1 mRNA interaction, leading to inhibition of breast cancer invasion. Our study suggests that inhibiting HuR is a promising therapeutic strategy for lethal metastatic breast cancer.

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