Deubiquitylase OTUD1 confers Erlotinib sensitivity in non-small cell lung cancer through inhibition of nuclear translocation of YAP1

Liu, Huafeng; Zhong, Liting; Lu, Yanjun; Li, Xuewen; Wei, Jiawang; Ding, Yuhai; Huang, Huiling; Nie, Qihong; Liao, Xiaohong

doi:10.1038/s41420-022-01119-w

Cited by 9 publications

(5 citation statements)

References 28 publications

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“…However, the precise mechanisms by which ubiquitination regulates these diverse biological processes remain unclear. Nevertheless, some evidence indicates that mechanical forces induce the ubiquitination of YAP1, which is implicated in tumorigenesis and angiogenesis [188][189][190][191].…”

Section: Ubiquitination: a Key Mechanism In The Pathways Of Cip And D...mentioning

confidence: 99%

The Role of Mechanotransduction in Contact Inhibition of Locomotion and Proliferation

Nakamura

2024

IJMS

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Contact inhibition (CI) represents a crucial tumor-suppressive mechanism responsible for controlling the unbridled growth of cells, thus preventing the formation of cancerous tissues. CI can be further categorized into two distinct yet interrelated components: CI of locomotion (CIL) and CI of proliferation (CIP). These two components of CI have historically been viewed as separate processes, but emerging research suggests that they may be regulated by both distinct and shared pathways. Specifically, recent studies have indicated that both CIP and CIL utilize mechanotransduction pathways, a process that involves cells sensing and responding to mechanical forces. This review article describes the role of mechanotransduction in CI, shedding light on how mechanical forces regulate CIL and CIP. Emphasis is placed on filamin A (FLNA)-mediated mechanotransduction, elucidating how FLNA senses mechanical forces and translates them into crucial biochemical signals that regulate cell locomotion and proliferation. In addition to FLNA, trans-acting factors (TAFs), which are proteins or regulatory RNAs capable of directly or indirectly binding to specific DNA sequences in distant genes to regulate gene expression, emerge as sensitive players in both the mechanotransduction and signaling pathways of CI. This article presents methods for identifying these TAF proteins and profiling the associated changes in chromatin structure, offering valuable insights into CI and other biological functions mediated by mechanotransduction. Finally, it addresses unanswered research questions in these fields and delineates their possible future directions.

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Section: Ubiquitination: a Key Mechanism In The Pathways Of Cip And D...mentioning

confidence: 99%

The Role of Mechanotransduction in Contact Inhibition of Locomotion and Proliferation

Nakamura

2024

IJMS

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“…The highly expressed MiR-135b in NSCLC directly binds to 3’-non-translational region of deubiquitination enzyme CYLD, regulates ubiquitination and activation of NF-κB signaling, which suggests that miR-135b is an effective therapeutic target for NSCLC ( 84 ). Deubiquitination enzyme OTUD1 acts as a cancer inhibitor and inhibits erlotinib resistance of NSCLC through YAP1-SOX9-SPP1 axis ( 85 ). The first DUB inhibitor VLX1570 is a dual inhibitor for USP14 and UCHL5, which started its clinical drug trials in 2015 ( 86 ).…”

Section: Ubiquitin-proteasome System Plays Important Roles In Pathoph...mentioning

confidence: 99%

“…Therefore, FAM188B might be an effective therapeutic target to inhibit the progression of LC (83). The highly expressed MiR-135b in NSCLC directly binds to 3'-non-translational region of deubiquitination enzyme CYLD, regulates ubiquitination and activation of NF-kB signaling, which suggests that miR-135b is an effective therapeutic target for NSCLC (84). Deubiquitination enzyme OTUD1 acts as a cancer inhibitor and inhibits erlotinib resistance of NSCLC through YAP1-SOX9-SPP1 axis (85).…”

Section: Deubiquitination and The Treatment Of Lcmentioning

confidence: 99%

The roles of protein ubiquitination in tumorigenesis and targeted drug discovery in lung cancer

Ye,

Yang,

Jiang

et al. 2023

Front. Endocrinol.

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The malignant lung cancer has a high morbidity rate and very poor 5-year survival rate. About 80% - 90% of protein degradation in human cells is occurred through the ubiquitination enzyme pathway. Ubiquitin ligase (E3) with high specificity plays a crucial role in the ubiquitination process of the target protein, which usually occurs at a lysine residue in a substrate protein. Different ubiquitination forms have different effects on the target proteins. Multiple short chains of ubiquitination residues modify substrate proteins, which are favorable signals for protein degradation. The dynamic balance adapted to physiological needs between ubiquitination and deubiquitination of intracellular proteins is beneficial to the health of the organism. Ubiquitination of proteins has an impact on many biological pathways, and imbalances in these pathways lead to diseases including lung cancer. Ubiquitination of tumor suppressor protein factors or deubiquitination of tumor carcinogen protein factors often lead to the progression of lung cancer. Ubiquitin proteasome system (UPS) is a treasure house for research and development of new cancer drugs for lung cancer, especially targeting proteasome and E3s. The ubiquitination and degradation of oncogene proteins with precise targeting may provide a bright prospect for drug development in lung cancer; Especially proteolytic targeted chimerism (PROTAC)-induced protein degradation technology will offer a new strategy in the discovery and development of new drugs for lung cancer.

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Section: Ubiquitination In CI and Mechanotransductionmentioning

confidence: 99%

Contact Inhibition and Mechanotransduction

Nakamura

2023

Preprint

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Contact inhibition (CI) represents a crucial tumor-suppressive mechanism responsible for controlling the unbridled growth of cells, thus preventing the formation of cancerous tissues. CI can be further categorized into two distinct yet interrelated components: CI of locomotion (CIL) and CI of proliferation (CIP). These two components of CI have historically been viewed as separate processes, but emerging research indicates that they share both distinctive and common pathways. Moreover, they exhibit intriguing intersections with mechanotransduction, a process that involves cells sensing and responding to mechanical forces. This review article describes the intricate interplay between mechanical forces and CI, shedding light on how these forces regulate CIL and CIP. Emphasis is placed on filamin A (FLNA)-mediated mechanotransduction, elucidating how FLNA senses mechanical forces and translates them into crucial biochemical signals that regulate cell locomotion and proliferation. In addition to FLNA, trans-acting factors (TAFs) emerge as sensitive players in both CI and the mechanotransduction process. This article presents methods for identifying these TAFs and profiling the associated changes in chromatin structure, offering valuable insights into CI and mechanotransduction regulation. Finally, it addresses unanswered research questions in these fields and delineates their possible future directions.

show abstract

Deubiquitylase OTUD1 confers Erlotinib sensitivity in non-small cell lung cancer through inhibition of nuclear translocation of YAP1

Cited by 9 publications

References 28 publications

The Role of Mechanotransduction in Contact Inhibition of Locomotion and Proliferation

The Role of Mechanotransduction in Contact Inhibition of Locomotion and Proliferation

The roles of protein ubiquitination in tumorigenesis and targeted drug discovery in lung cancer

Contact Inhibition and Mechanotransduction

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