NIR promotes progression of colorectal cancer through regulating RB

Li, Yuan; Wang, Ling; Liu, Xiaofeng; Zhang, Chunfeng; Du, Xiaojuan; Xing, Baocai

doi:10.1016/j.bbamcr.2020.118856

Cited by 5 publications

(19 citation statements)

References 37 publications

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“…Novel INHAT repressor (NIR), a nucleolar protein and novel histone acetyltransferase inhibitor (INHAT), was highly expressed in colorectal cancer tissues and significantly correlated with poor clinical outcome. It interacted with pRb via a LXCXE motif in its INHAT-2 domain and polyubiquitinated pRb for proteasomal degradation dependent on MDM2, giving rise to elevated G1/S phase transition and cell proliferation in colorectal cancer cells [ 42 ]. As NIR has not been reported to possess E3 ligase activity and can interact with MDM2 to inhibit MDM2 degradation [ 43 ], it would be interesting to further investigate whether NIR recruits MDM2 to form a ternary complex with pRb to promote pRb ubiquitination and degradation.…”

Section: Main Textmentioning

confidence: 99%

Post-translational modifications on the retinoblastoma protein

Zhou

Yam

et al. 2022

J Biomed Sci

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The retinoblastoma protein (pRb) functions as a cell cycle regulator controlling G1 to S phase transition and plays critical roles in tumour suppression. It is frequently inactivated in various tumours. The functions of pRb are tightly regulated, where post-translational modifications (PTMs) play crucial roles, including phosphorylation, ubiquitination, SUMOylation, acetylation and methylation. Most PTMs on pRb are reversible and can be detected in non-cancerous cells, playing an important role in cell cycle regulation, cell survival and differentiation. Conversely, altered PTMs on pRb can give rise to anomalies in cell proliferation and tumourigenesis. In this review, we first summarize recent findings pertinent to how individual PTMs impinge on pRb functions. As many of these PTMs on pRb were published as individual articles, we also provide insights on the coordination, either collaborations and/or competitions, of the same or different types of PTMs on pRb. Having a better understanding of how pRb is post-translationally modulated should pave the way for developing novel and specific therapeutic strategies to treat various human diseases.

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Section: Main Textmentioning

confidence: 99%

Post-translational modifications on the retinoblastoma protein

Zhou

Yam

et al. 2022

J Biomed Sci

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“…Based on the knowledge of the biological properties and function of NOC2L, further investigation was conducted to examine how NOC2L affects biological events. It has been proposed that NOC2L can participate in some key biological events, including the rRNA biogenesis [ 48 ], embryonic development [ 49 , 50 ], and cancer progression [ 9 , 51 ]. All these biological events affected by NOC2L can be contributed to its characteristic and function mentioned previously in this review.…”

Section: Noc2l Gene Cloning and Identificationmentioning

confidence: 99%

“…As a negative regulator of tumor suppressor P53 [ 7 ], NOC2L may promote tumorigenesis by counteracting the tumor suppression function of P53 [ 7 ]. In addition to P53-dependent pro-cancer effect of NOC2L [ 9 , 51 ], other P53-independent mechanisms of NOC2L-mediated tumorigenesis remain to be further addressed. As we all know, uncontrolled proliferation is a typical characteristic of malignant tumor [ 64 ].…”

Section: Noc2l Gene Cloning and Identificationmentioning

confidence: 99%

“…Furthermore, the level of NOC2L is significantly related to the poor outcome of CRC patients. These evidences imply that NOC2L may play an important role in the tumorigenesis and progression of CRC [ 9 ].…”

Section: Noc2l Gene Cloning and Identificationmentioning

confidence: 99%

“…In order to delineate the biological function of NOC2L, further studies were conducted to investigate NOC2L-targeted proteins and the underlying regulation mechanisms. NOC2L has been demonstrated to target TP53 [ 7 , 8 , 10 , 11 ], TP63 [ 11 ], Aurora B [ 10 ], Mouse double minute 2 homolog (MDM2) [ 8 ], retinoblastoma protein (RB) [ 9 ], Enhancer of zeste homolog 2 (EZH2) [ 12 ]. In this review, we summarize the biological function of NOC2L and the underlying mechanisms of how NOC2L interacts with its key targets.…”

Section: Introductionmentioning

confidence: 99%

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Unmasking the biological function and regulatory mechanism of NOC2L: a novel inhibitor of histone acetyltransferase

Chen

Liu

et al. 2023

J Transl Med

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NOC2 like nucleolar associated transcriptional repressor (NOC2L) was recently identified as a novel inhibitor of histone acetyltransferase (INHAT). NOC2L is found to have two INHAT function domains and regulates histone acetylation in a histone deacetylases (HDAC) independent manner, which is distinct from other INHATs. In this review, we summarize the biological function of NOC2L in histone acetylation regulation, P53-mediated transcription, ribosome RNA processing, certain development events and carcinogenesis. We propose that NOC2L may be explored as a potential biomarker and a therapeutic target in clinical practice.

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Patient‐derived xenograft model in colorectal cancer basic and translational research

Liu

Xin

Wang

2022

Anim Models and Exp Med

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Colorectal cancer (CRC), one of the most deadly cancers, is the fourth most common cause of cancer-related deaths. 1 Currently, surgery is the main treatment option for primary and metastatic CRC, and chemotherapy and targeted drugs are regularly used as adjuvant regimens. [2][3][4] Despite improvements in screening and treatment, the number of individuals newly diagnosed is increasing rapidly. Moreover, metastasis, recurrence, and chemoresistance are common in CRC patients after treatment, which leads to the dismal prognosis and high mortality of CRC patients. [5][6][7] These issues lead to the need for more advancements in CRC treatment. About 5% of CRCs are hereditary tumor syndromes, such as familial adenomatous polyposis (FAP) and Lynch syndrome. 8 Most of the CRCs are sporadic as the comprehensive effects of various factors, including somatic genetic alterations, chronic inflammation, lifestyle, and environmental stimuli. 9 These genetic and nongenetic risk factors work together to promote CRC development and progression. [10][11][12][13] To date, the mechanisms involved in the interactions of these factors driving CRC development and progression are

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NIR promotes progression of colorectal cancer through regulating RB

Cited by 5 publications

References 37 publications

Post-translational modifications on the retinoblastoma protein

Post-translational modifications on the retinoblastoma protein

Unmasking the biological function and regulatory mechanism of NOC2L: a novel inhibitor of histone acetyltransferase

Patient‐derived xenograft model in colorectal cancer basic and translational research

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