TRIM59 is a novel potential prognostic biomarker in patients with non-small cell lung cancer: A research based on bioinformatics analysis

Hao, Ling; Du, Bin; Xi, Xueyan

doi:10.3892/ol.2017.6467

Cited by 21 publications

(14 citation statements)

References 70 publications

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“…TriM67, located at chromosome 11q22-23, encodes a 783 amino acid protein with listBox zinc-finger motifs and an adjacent leucine-zipper motif. TRIM67 was identified to be significantly downregulated in NSCLC cell lines (11), which was additionally confirmed by Hao et al (20), who suggested that TriM67 may be a tumor suppressor gene. The functions of TriM67 are largely unclear.…”

Section: Discussionsupporting

confidence: 56%

TRIM67 promotes NF‑κB pathway and cell apoptosis in GA‑13315‑treated lung cancer cells

et al. 2019

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13-chlorine-3,15-dioxy-gibberellic acid methyl ester (Ga-13315), a gibberellin derivative, possesses strong anti-tumor activity in vitro and in vivo. The present study aimed to investigate the underlying mechanisms of Ga-13315-induced apoptosis in human non-small cell lung cancer cell lines. lung cancer cells were treated with different doses of Ga-13315 (4, 8, 16 and 32 ng/µl) for 48 h, and a ccK8 assay was performed to measure cell viability. alteration in gene expression was identified using rna-sequencing (rna-Seq). Quantitative polymerase chain reaction (qPcr) was used to confirm the differentially expressed genes (DEGs) identified in RNA-Seq. Gene expression plasmids or small interfering rna were used to overexpress or silence targeted genes, in order to investigate downstream signals. chromatin immunoprecipitation was conducted to evaluate the binding of transcription factors to the target genes. a Student's t-test or one-way analysis of variance followed by Tukey's honestly significant difference post-hoc test were performed to evaluate the significance between groups. P<0.05 was considered to indicate a statistically significant difference. GA-13315 significantly decreased the number of viable cells and induced apoptosis among lung cancer cells (median lethal dose =12-16 ng/µl). RNA-Seq identified 250 significant deGs, including 94 upregulated and 156 downregulated genes in A549 cells (P<0.05; fold change ≥1.5). Upregulation of TriM67, nF-κB subunit 2 (nF-κB2) and FaS was additionally confirmed using qPCR and western blot analysis in A549 and H460 cells. Apoptosis of A549 cells was significantly decreased following knockdown of TriM67. Ga-13315 promoted TriM67 expression to increase FaS expression and cell apoptosis. TriM67 promoted the processing of nF-κB2 into its active form, p52, which then enhanced the nF-κB pathway and Ga-13315-induced apoptosis.

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Section: Discussionsupporting

confidence: 56%

TRIM67 promotes NF‑κB pathway and cell apoptosis in GA‑13315‑treated lung cancer cells

et al. 2019

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“…TRIM59, a member of the TRIM family of proteins, serves a crucial role in the proliferation and metabolism of several types of cancer, such as lung (17,18) and gastric cancer (19). TRIM59 protein functions as an E3 ubiquitin ligase, and is comprised of an N-terminal really interesting RING-finger domain (1).…”

Section: Discussionmentioning

confidence: 99%

Blockade of TRIM59 enhances esophageal cancer cell chemosensitivity to cisplatin by upregulating p53

Liu

et al. 2020

Oncol Lett

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Human esophageal cancer (hESC) cell motility adopts various modes, resulting in hESC progression and poor survival. However, how tripartite motif 59 (TRIM59), as the ubiquitination machinery, participates in hESC metastasis is not completely understood. The results indicated that TRIM59 was aberrantly upregulated in hESC tissues compared with adjacent healthy esophageal tissues, which was associated with poor survival and advanced TNM state among patients with hESC. Moreover, patients with hESC with higher TRIM59 expression displayed undetectable p53 expression, which contributed to enhanced progression and motility of hESC. At the molecular level, TRIM59 was indicated to be an E3 putative ubiquitin ligase that targeted the p53 protein, leading to increased degradation of p53, which resulted in decreased chemosensitivity to cisplatin. TRIM59 knockdown reduced TRIM59 expression, increased p53 protein expression, and decreased hESC cell viability, clone formation and migration compared with the small interfering RNA negative control (siNC) group. Furthermore, hESC cell lines were more sensitive to cisplatin in the TRIM59-knockdown group compared with the siNC group. The results indicated a relationship between TRIM59, p53 and the chemosensitivity of cisplatin. The present study suggested that TRIM59 may serve as a promising prognostic indicator for patients with hESC.

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“…Interestingly, hypermethylation of TRIM58 in lung cancer may account for its down-regulation (Diaz-Lagares et al, 2016). Overexpression of TRIMs 11,22,44,47,59, and 65 were correlated with poor prognosis in lung cancers (Liu et al, 2013;Wang X.-L. et al, 2016;Xing et al, 2016;Han et al, 2017;Hao et al, 2017;Liu et al, 2017b;Huang et al, 2019;Yin et al, 2019). Overexpression of TRIM44 induced mTOR signaling, epithelial-mesenchymal transition, and cyclin/CDK upregulation in lung cancer cells (Xing et al, 2016).…”

Section: Lung Cancermentioning

confidence: 99%

The Tripartite Nexus: Autophagy, Cancer, and Tripartite Motif-Containing Protein Family Members

2020

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Autophagy is a cellular degradative process that has multiple important actions in cancer. Autophagy modulation is under consideration as a promising new approach to cancer therapy. However, complete autophagy dysregulation is likely to have substantial undesirable side effects. Thus, more targeted approaches to autophagy modulation may prove clinically beneficial. One potential avenue to achieving this goal is to focus on the actions of tripartite motif-containing protein family members (TRIMs). TRIMs have key roles in an array of cellular processes, and their dysregulation has been extensively linked to cancer risk and prognosis. As detailed here, emerging data shows that TRIMs can play important yet context-dependent roles in controlling autophagy and in the selective targeting of autophagic substrates. This review covers how the autophagyrelated actions of TRIM proteins contribute to cancer and the possibility of targeting TRIMdirected autophagy in cancer therapy.

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TRIM59 is a novel potential prognostic biomarker in patients with non-small cell lung cancer: A research based on bioinformatics analysis

Cited by 21 publications

References 70 publications

TRIM67 promotes NF‑κB pathway and cell apoptosis in GA‑13315‑treated lung cancer cells

TRIM67 promotes NF‑κB pathway and cell apoptosis in GA‑13315‑treated lung cancer cells

Blockade of TRIM59 enhances esophageal cancer cell chemosensitivity to cisplatin by upregulating p53

The Tripartite Nexus: Autophagy, Cancer, and Tripartite Motif-Containing Protein Family Members

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