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Ionizing radiation-induced long noncoding RNA CRYBG3 regulates YAP/TAZ through mechanotransduction. | LitMetric

Ionizing radiation-induced long noncoding RNA CRYBG3 regulates YAP/TAZ through mechanotransduction.

Cell Death Dis

State Key Laboratory of Radiation Medicine and Protection, School of Radiation Medicine and Protection, Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Medical College of Soochow University, Suzhou, China.

Published: March 2022

AI Article Synopsis

  • This study investigates the relationship between long noncoding RNAs (lncRNAs) and mechanotransduction in cancer, particularly how they affect cell behavior in response to tissue stiffness and environment.
  • The researchers discovered that ionizing radiation decreases tumor stiffness, which leads to the activation of lncRNA CRYBG3 that interferes with YAP/TAZ activity, effectively inhibiting lung cancer cell growth and spread.
  • Furthermore, their findings indicate that lncRNA CRYBG3 plays a crucial role in radiotherapy by regulating mechanotransduction and controlling tumor dynamics, highlighting its potential as a target for cancer treatment.

Article Abstract

Mechanotransduction sensing of tissue architecture and cellular microenvironment is a fundamental regulator of cell fate, including cancer. Meanwhile, long noncoding RNAs (lncRNAs) play multifunctions during cancer development and treatment. However, the link between lncRNAs and cellular mechanotransduction in the context of cancer progression has not yet been elucidated. In this study, using atomic force microscopy (AFM), we find that ionizing radiation reduces tumor stiffness. Ionizing radiation-induced lncRNA CRYBG3 can blunt YAP/TAZ activity through interference with mechanotransduction, resulting in the inhibition of cell proliferation, invasion, and metastasis of lung cancer cells. In vivo, we found that loss of lncRNA CRYBG3 could power the tumor initiation and metastasis ability, but this was abolished by concomitant deplete TAZ. At the molecular level, lncRNA CRYBG3 that in turn dysregulates F-actin organization, activates the LATS1/2 kinase, all in all resulting in YAP/TAZ nuclear exclusion. Our research proposes that lncRNA CRYBG3 is a mediator of radiotherapy through its control of cancer-tissue mechanotransduction and wiring YAP/TAZ activity to control tumor growth and metastasis.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8897501PMC
http://dx.doi.org/10.1038/s41419-022-04650-xDOI Listing

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