TRIM37 deficiency induces autophagy through deregulating the MTORC1-TFEB axis

Wang, Wei; Xia, Zhi‐Jie; Farré, Jean‐Claude; Subramani, Suresh

doi:10.1080/15548627.2018.1463120

Cited by 40 publications

(33 citation statements)

References 64 publications

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“…Overexpression of RTL1 was detected in 30% of analyzed human HCC samples, indicating the potential relevance of this locus as a therapeutic target for patients [51]. RRAGB (Ras related GTP binding B) mediates mTOR (mechanistic target of rapamycin kinase) and TRIM37 (tripartite motif containing 37) pathways related to amino acid-stimulated MTORC1 (MTOR complex 1) signalling and autophagy [52]. In the current study, we found that RRAGB, RSPH9, RPS6KL1, RXFP1, and RTL1 are differentially expressed between NSCLC and ANTs.…”

Section: Discussionmentioning

confidence: 99%

A Six-Gene Signature Predicts Survival of Adenocarcinoma Type of Non-Small-Cell Lung Cancer Patients: A Comprehensive Study Based on Integrated Analysis and Weighted Gene Coexpression Network

Xie

2019

BioMed Research International

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Background and Goals. To identify a multigene signature model for prognosis of non-small-cell lung cancer (NSCLC) patients, we first found 2146 consensus differentially expressed genes (DEGs) in NSCLC overlapped in Gene Expression Omnibus (GEO) and TCGA lung adenocarcinoma (LUAD) datasets using integrated analysis. We constructed a weighted gene coexpression network (WGCN) using the consensus DEGs and identified the module significantly associated with pathological M stage and consisted of 61 genes. After univariate Cox regression analysis and subsequent stepwise model selection by the Akaike information criterion (AIC) and multivariate Cox hazard model analysis, an mRNA signature model which calculated prognostic score was generated: prognostic score = (−0.2491 × EXPRRAGB) + (−0.0679 × EXPRSPH9) + (−0.2317 × EXPRPS6KL1) + (−0.1035 × EXPRXFP1) + 0.1571 × EXPRRM2 + 0.1104 × EXPRTL1, where EXP is the fragments per kilobase million (FPKM) value of the mRNA included in the model. The prognostic model separated NSCLC patients in the TCGA-LUAD dataset into the low- and high-risk score groups with a median prognostic score of 0.972. Higher scores predicted higher risk. The area under ROC curve (AUC) was 0.994 or 0.776 in predicting the 1- to 10-year survival of NSCLC patients. The prognostic performance of this prognostic model was validated by an independent GSE11969 dataset of NSCLC adenocarcinoma with AUC values between 0.822 and 0.755 in predicting 1- to 10-year survival of NSCLC. These results suggested that the six-gene signature functioned as an independent biomarker to predict the overall survival of NSCLC adenocarcinoma.

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Section: Discussionmentioning

confidence: 99%

A Six-Gene Signature Predicts Survival of Adenocarcinoma Type of Non-Small-Cell Lung Cancer Patients: A Comprehensive Study Based on Integrated Analysis and Weighted Gene Coexpression Network

Xie

2019

BioMed Research International

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“…33 Furthermore, SIP1-mediated epithelial-mesenchymal transition and MTORC1-TFEB axis mediated autophagy were, respectively, found to be regulated by TRIM37. 21,36 However, there is no report about miRNA…”

Section: Mir-1236-3p Affected Cervical Cancer Cell Proliferation Cycle Progression and Migration By Inhibiting Trim37mentioning

confidence: 99%

Circular RNA circRNA_101996 promoted cervical cancer development by regulating miR‐1236‐3p/TRIM37 axis

Song

Chen

et al. 2021

The Kaohsiung J of Med Scie

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Circular RNAs (circRNAs) appear to be significant modulators in various physiological processes. Recently, it is found that circRNA_101996 exerts important roles in various cancers. Our previous studies showed that circRNA_101996 promoted cervical cancer growth and metastasis by regulating miR-8075/TPX2. However, the potential regulatory role of circRNA_101996 in cervical cancer still needs further investigation.Our results in this study suggested that circRNA_101996 was over-expressed in cervical cancer patients. circRNA_101996 up-regulation remarkably assisted cell proliferation, cell cycle progression, and cell migration in cervical cancer, while circRNA_101996 knockdown exerted the inverse effects. The molecular investigations indicated that circRNA_101996 could increase the expression level of miR-1236-3p, tripartite motif-containing 37 (TRIM37), through binding to miR-1236-3p and reducing its expression. Moreover, in vivo results demonstrated that circRNA_101996 shRNA can function as a tumor suppressor through downregulating TRIM37 in cervical cancer. In conclusion, our data indicated that circRNA_101996/miR-1236-3p/TRIM37 axis accelerated cervical cancer development, providing novel insights into cervical cancer diagnosis and treatment.

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“…Wang et al found that lysosomal protein mTOR interacts with TRIM37, leading to transcriptional activation of genes involved in lysosome biogenesis and macroautophagy/autophagy. Autophagy may thus be a way for the cell to survive the loss of TRIM37 [50].…”

Section: Trim37 Expression Is Strongly Associated With Cell Prolifmentioning

confidence: 99%

TRIMming down to TRIM37: Relevance to Inflammation, Cardiovascular Disorders, and Cancer in MULIBREY Nanism

Brigant

Meuth

Rochette

et al. 2018

IJMS

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TRIpartite motif (TRIM) proteins are part of the largest subfamilies of E3 ligases that mediate the transfer of ubiquitin to substrate target proteins. In this review, we focus on TRIM37 in the normal cell and in pathological conditions, with an emphasis on the MULIBREY (MUscle-LIver-BRain-EYe) genetic disorder caused by TRIM37 mutations. TRIM37 is characterized by the presence of a RING domain, B-box motifs, and a coiled-coil region, and its C-terminal part includes the MATH domain specific to TRIM37. MULIBREY nanism is a rare autosomal recessive caused by TRIM37 mutations and characterized by severe pre- and postnatal growth failure. Constrictive pericarditis is the most serious anomaly of the disease and is present in about 20% of patients. The patients have a deregulation of glucose and lipid metabolism, including type 2 diabetes, fatty liver, and hypertension. Puzzlingly, MULIBREY patients, deficient for TRIM37, are plagued with numerous tumors. Among non-MULIBREY patients affected by cancer, a wide variety of cancers are associated with an overexpression of TRIM37. This suggests that normal cells need an optimal equilibrium in TRIM37 expression. Finding a way to keep that balance could lead to potential innovative drugs for MULIBREY nanism, including heart condition and carcinogenesis treatment.

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TRIM37 deficiency induces autophagy through deregulating the MTORC1-TFEB axis

Cited by 40 publications

References 64 publications

A Six-Gene Signature Predicts Survival of Adenocarcinoma Type of Non-Small-Cell Lung Cancer Patients: A Comprehensive Study Based on Integrated Analysis and Weighted Gene Coexpression Network

A Six-Gene Signature Predicts Survival of Adenocarcinoma Type of Non-Small-Cell Lung Cancer Patients: A Comprehensive Study Based on Integrated Analysis and Weighted Gene Coexpression Network

Circular RNA circRNA_101996 promoted cervical cancer development by regulating miR‐1236‐3p/TRIM37 axis

TRIMming down to TRIM37: Relevance to Inflammation, Cardiovascular Disorders, and Cancer in MULIBREY Nanism

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