Expression of tripartite motif-containing 44 and its prognostic and clinicopathological value in human malignancies:a meta-analysis

Xiao, Guoliang; Yang, Qiuxi; Bao, Ziwei; Mao, Haixia; Zhang, Yi; Lin, Shibu

doi:10.1186/s12885-020-07014-w

Cited by 12 publications

(10 citation statements)

References 62 publications

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“…PRKAR2A is a camp-dependent type II regulatory subunit of protein kinase, and studies have shown that its expression is related to colorectal cancer, adipocyte differentiation, and other processes ( Spracklen et al., 2019 ). It was found that the mRNA expression level of Trim44 in most malignant tumor tissues was higher than that in corresponding normal tissues ( Xiao et al., 2020 ). Sash1 is an adaptor and signal transduction protein, which is considered as a tumor suppressor ( Ilnitskaya et al., 2020 ).…”

Section: Discussionmentioning

confidence: 99%

miR-1307 promotes hepatocarcinogenesis by CALR-OSTC-endoplasmic reticulum protein folding pathway

et al. 2021

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Summary miR-1307 is highly expressed in liver cancer and inhibits methyltransferase protein8. Thereby, miR-1307 inhibits the expression of KDM3A and KDM3B and increases the methylation modification of histone H3 lysine 9, which enhances the expression of endoplasmic-reticulum-related gene CALR. Of note, miR-1307 weakens the binding ability of OSTC to CDK2, CDK4, CyclinD1, and cyclinE and enhances the binding ability of CALR to CDK2, CDK4, CyclinD1, and cyclinE, decreasing of p21WAF1/CIP1, GADD45, pRB, and p18, and decreasing of ppRB. Furthermore, miR-1307 increases the activity of H-Ras, PKM2, and PLK1. Strikingly, miR-1307 reduces the binding ability of OSTC to ATG4 and enhances the binding ability of CALR to ATG4. Therefore, miR-1307 reduces the occurrence of autophagy based on ATG4-LC3-ATG3-ATG7-ATG5-ATG16L1-ATG12-ATG9- Beclin1. In particular, miR-1307 enhances the expression of PAK2, PLK1, PRKAR2A, MYBL1, and Trim44 and inhibits the expression of Sash1 and Smad5 via autophagy. Our observations suggest that miR-1307 promotes hepatocarcinogenesis by CALR-OSTC-endoplasmic reticulum protein folding pathway.

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Section: Discussionmentioning

confidence: 99%

miR-1307 promotes hepatocarcinogenesis by CALR-OSTC-endoplasmic reticulum protein folding pathway

et al. 2021

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“…TRIM44 is localized in the cytoplasmic compartment, contributing to diverse pathological conditions like tumors, growth disorders, and neurodegeneration ( Xiao et al 2020 ). TRIM44 is an atypical TRIM family protein that lacks the RING-finger domain but harbors a zinc-finger domain that is often found in ubiquitin-specific proteases (USPs).…”

Section: Rna-binding Protein Partners Of Rna Sensorsmentioning

confidence: 99%

Cytoplasmic RNA sensors and their interplay with RNA-binding partners in innate antiviral response: theme and variations

Chan

Jin

2022

RNA

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Sensing of pathogen-associated molecular patterns including viral RNA by innate immunity represents the first line of defense against viral infection. In addition to RIG-I-like receptors and NOD-like receptors, several other RNA sensors are known to mediate innate antiviral response in the cytoplasm. Double-stranded RNA-binding protein PACT interacts with prototypic RNA sensor RIG-I to facilitate its recognition of viral RNA and induction of host interferon response, but variations of this theme are seen when the functions of RNA sensors are modulated by other RNA-binding proteins to impinge on antiviral defense, proinflammatory cytokine production and cell death programs. Their discrete and coordinated actions are crucial to protect the host from infection. In this review, we will focus on cytoplasmic RNA sensors with an emphasis on their interplay with RNA-binding partners. Classical sensors such as RIG-I will be briefly reviewed. More attention will be brought to the new insights on how RNA-binding partners of RNA sensors modulate innate RNA sensing and how viruses perturb the functions of RNA-binding partners.

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“…Interestingly, in addition to known cardiac TRIMs, several other TRIMs were found to be differentially regulated in these disease conditions, and the expression of TRIM44 was increased under all the pathological conditions mentioned above. Accumulating evidence has shown that dysregulation of TRIM44 protein is associated with several diseases, such as cancer, developmental disorders, neurodegenerative disease, viral infection and aniridia ( Yang et al, 2013 ; Yamada et al, 2020 ; Xie et al, 2021 ; Wei et al, 2019 ; Xiao et al, 2020 ; Peng et al, 2018 ; Li et al, 2018 ; Liu et al, 2018 ; Yu et al, 2021 ; Kashevarova et al, 2014 ; Zhang et al, 2015a ; Samant et al, 2016 ; Lim et al, 2017 ; Landsend et al, 2018 ). Borlepawar et al’s analysis of upregulated expression of TRIM44 in cardiac pathology suggests that it may be involved in the regulation of cardiovascular pathological processes.…”

Section: Introductionmentioning

confidence: 99%

Cardiac-specific Trim44 knockout in rat attenuates isoproterenol-induced cardiac remodeling via inhibition of AKT/mTOR pathway

Jiang

Guan

et al. 2022

Disease Models &Amp; Mechanisms

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When pathological hypertrophy progresses to heart failure (HF), the prognosis is often very poor. Therefore, it is crucial to find new and effective intervention targets. Here, myocardium-specific Trim44 knockout rats were generated using CRISPR-Cas9 technology. Cardiac phenotypic observations revealed that Trim44 knockout affected cardiac morphology at baseline. Rats with Trim44 deficiency exhibited resistance to cardiac pathological changes in response to stimulation via isoproterenol (ISO) treatment, including improvement of cardiac remodeling and dysfunction by morphological and functional observations, reduced myocardial fibrosis and reduced expression of molecular markers of cardiac stress. Furthermore, signal transduction validation associated with growth and hypertrophy development in vivo and in vitro demonstrated that Trim44 deficiency inhibited the activation of signaling pathways involved in myocardial hypertrophy, especially response to pathological stress. In conclusion, the present study indicates that Trim44 knockout attenuates ISO-induced pathological cardiac remodeling through blocking the AKT/mTOR/GSK3β/P70S6K signaling pathway. This is the first study to demonstrate the function and importance of Trim44 in the heart at baseline and under pathological stress. Trim44 could be a novel therapeutic target for prevention of cardiac hypertrophy and HF.

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Expression of tripartite motif-containing 44 and its prognostic and clinicopathological value in human malignancies:a meta-analysis

Cited by 12 publications

References 62 publications

miR-1307 promotes hepatocarcinogenesis by CALR-OSTC-endoplasmic reticulum protein folding pathway

miR-1307 promotes hepatocarcinogenesis by CALR-OSTC-endoplasmic reticulum protein folding pathway

Cytoplasmic RNA sensors and their interplay with RNA-binding partners in innate antiviral response: theme and variations

Cardiac-specific Trim44 knockout in rat attenuates isoproterenol-induced cardiac remodeling via inhibition of AKT/mTOR pathway

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