Trim44 facilitates the migration and invasion of human lung cancer cells via the NF-κB signaling pathway

Luo, Qingquan; Hao, Lin; Ye, Xiangyun; Huang, Jia; Lü, Shun; Xu, Lin

doi:10.1007/s10147-014-0752-9

Cited by 56 publications

(79 citation statements)

References 27 publications

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“…Existing studies reported that TRIMs play a critical role in the regulation of the NF-kB pathway 15–17 . TRIM20, known as MEFV (Mediterranean fever) protein, regulates the turnover of IκBα and interaction with NF-kB p65, and positively regulates the NF-kB pathway 18 .…”

Section: Discussionmentioning

confidence: 99%

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TRIM52 plays an oncogenic role in ovarian cancer associated with NF-kB pathway

Yang

Liu

et al. 2018

Cell Death Dis

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Emerging evidence suggests that the members of the tripartite motif (TRIM) family play a crucial role in cancer development and progression. The purpose of the study was to explore TRIM52's role in tumorigenesis and its potential molecular mechanism in ovarian cancer. The study demonstrated that knockdown of TRIM52 in SKOV3 and CAOV3 cells inhibited ovarian cancer cell invasion, migration, and proliferation, and induced cell apoptosis. On the contrary, overexpression of TRIM52 in HO8910 cells showed contrary results. Further, overexpression of TRIM52 enhanced the expression of phosphorylated IKKβ and IKBα proteins and nuclear protein P65, which implied the activation of NF-kB signal pathway. Knockdown of TRIM52 downregulated the mRNA and protein levels of NF-kB signal downstream effectors of the NF-kB pathway, including MMP9, Bcl2, IL8, and TNFα, but upregulated caspase-3 expression. These results suggested that activation of the NF-kB pathway is involved in TRIM52-mediated regulation in ovarian cancer. The nude mice study further confirmed that knockdown of TRIM52 blocked tumor growth, inhibited cell proliferation, and promoted cell apoptosis. Our data strongly suggested that TRIM52 plays an oncogenic role in ovarian cancer development associated with the NF-kB signal pathway and may be a potential target for cancer therapy.

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Section: Discussionmentioning

confidence: 99%

“…Documents have been reported that some members of the TRIM protein family are thought to be important regulators of carcinogenesis 10,17,23–27 . The famous promyelocytic leukemia (PML) gene, which encodes the protein TRIM19, is involved in the t(15;17) translocation that specifically occurs in acute promyelocytic leukemia (APL) 19 .…”

Section: Discussionmentioning

confidence: 99%

TRIM52 plays an oncogenic role in ovarian cancer associated with NF-kB pathway

Yang

Liu

et al. 2018

Cell Death Dis

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“…Recently, their biological functions in tumor biology have become an attractive research area. A number of TRIM proteins have been revealed to play a crucial role in proliferation, migration and invasion of lung cancer (19–22). However, no reports have evaluated the prognostic value of TRIM59 in lung cancer.…”

Section: Discussionmentioning

confidence: 99%

“…These proteins are involved in a plethora of cellular processes such as cell proliferation, migration, apoptosis, cell cycle regulation, differentiation and development (15–18). Recently, several groups reported that TRIM proteins including TRIM11, TRIM28, TRIM29, TRIM44 and others seemed to act as oncogenes in lung cancer (19–22), indicating significant roles of the TRIM family in lung tumorigenesis. TRIM59, a novel TRIM family member, is characterized by the presence of a RING finger domain, a B-box 2 domain, two coiled-coil domains and a transmenbrane domain in its structure (17), implicated in a wide range of biological processes in lung cancer and other multiple tumors.…”

Section: Introductionmentioning

confidence: 99%

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

Hao

2017

Oncology Letters

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Lung cancer is the leading cause of cancer-associated mortality worldwide and its prognosis is poor. Few effective biomarkers for non-small cell lung cancer (NSCLC) have been translated into the clinical practice aiming to assist in the treatment plan design and prognosis evaluation. The aim of the present study was to identify novel potential prognostic biomarkers for NSCLC. Tripartite motif 59 (TRIM59) was identified from a microarray dataset of matched-samples and was verified as an aberrantly upregulated gene in NSCLC tissue. The expression level of TRIM59 in NSCLC subtypes was observed to be significantly increased in large cell lung carcinoma and squamous cell carcinoma as compared with that in adenocarcinoma. Its expression correlated with several clinicopathological features, including gender, smoking habits, and unfavorable tumor node and pathological stages. Notably, TRIM59 demonstrated a negative correlation with survival time and its overexpression indicated a poor prognosis in NSCLC. Furthermore, univariate and multivariate Cox's regression analyses indicated that TRIM59 was an independent prognostic factor in tumor tissue as compared with age, gender, tumor stage, node stage, and metastasis. Gene set enrichment analysis and protein-protein interaction network construction revealed that TRIM59 was associated with oncogenic mammalian target of rapamycin (MTOR) and eukaryotic initiation factor 4E (EIF4E) signaling through ubiquitin C binding. In conclusion, it was revealed that TRIM59 is a novel prognostic biomarker modulating oncogenic MTOR and EIF4E signaling pathways in NSCLC. These findings provided a novel insight into the clinical application of TRIM59. Therefore, TRIM59 may serve as an independent predictor for prognosis and a potential therapeutic target for NSCLC.

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“…Accumulating data suggest that TRIM44 plays stimulatory and cancerogenic roles in multiple cancers. TRIM44 overexpression facilitates cell proliferation, migration, and invasion in gastric cancer, hepatocellular carcinoma, testicular germ cell tumors, and non‐small cell lung cancer (NSCLC) . In addition, knocking down endogenous TRIM44 expression inhibits proliferation and motility in cancer cells .…”

Section: Introductionmentioning

confidence: 99%

TRIM44 promotes human esophageal cancer progression via the AKT/mTOR pathway

Xiong

Chun

et al. 2018

Cancer Science

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Aberrant expression of TRIM‐containing protein 44 (TRIM44) acts as a promoter in multiple cancers. Here, we investigated the biological functions and clinical significance of TRIM44 in human esophageal cancer (HEC). TRIM44 expression was significantly higher in HEC tissues than corresponding normal tissues at both the mRNA (2.42 ± 0.52 vs 0.99 ± 0.25) and protein (1.01 ± 0.27 vs 0.30 ± 0.13) levels. Patients with high TRIM44 expression showed poor differentiation (P = 1.39 × 10−5), advanced TNM stage (P = 3.87 × 10−4) and, most importantly, significantly poorer prognosis (P = 2.80 × 10−5). TRIM44 played a crucial role in epithelial mesenchymal transition (EMT). A significant correlation was observed between TRIM44 and Ki67 expression. We demonstrated that TRIM44 markedly enhanced HEC cell proliferation, migration, and invasion. Additionally, TRIM44 was involved in the AKT/mTOR signaling pathway and its downstream targets, such as STAT3 phosphorylation. Thus, elevated TRIM44 expression promotes HEC development by EMT via the AKT/mTOR pathway, and TRIM44 may be a novel prognostic indicator for HEC patients after curative resection.

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Trim44 facilitates the migration and invasion of human lung cancer cells via the NF-κB signaling pathway

Abstract: Our data suggest that Trim44 promotes NSCLC development through activation of NF-κB signaling via upregulating CXCL16 and MMP9 expression.

Cited by 56 publications

References 27 publications

TRIM52 plays an oncogenic role in ovarian cancer associated with NF-kB pathway

TRIM52 plays an oncogenic role in ovarian cancer associated with NF-kB pathway

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

TRIM44 promotes human esophageal cancer progression via the AKT/mTOR pathway

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