Thyroid hormone receptor interactor 13 (TRIP13) overexpression associated with tumor progression and poor prognosis in lung adenocarcinoma

Li, Wěi; Zhang, Gengyan; Li, Xiaojun; Wang, Xiaojing; Li, Qing; Hong, Lei; Shen, Yuangbing; Zhao, Chenling; Gong, Xiaomeng; Chen, Yuqing; Zhou, Jihong

doi:10.1016/j.bbrc.2018.03.129

Cited by 37 publications

(34 citation statements)

References 17 publications

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“…TRIP13 has been suggested to be overexpressed in multiple human cancers and to function as an oncogene in regulating tumor cell proliferation, migration and invasion. 27 – 30 Therefore, we further confirmed the relationship of TINCR expression with TRIP13 mRNA and protein expressions in prostate cancer tissues, and found that TINCR expression was negatively correlated with TRIP13 mRNA and protein expressions. Moreover, upregulation of TINCR expression dramatically reduced TRIP13 mRNA and protein expressions, and downregulation of TINCR expression markedly increased TRIP13 mRNA and protein expressions in prostate cancer cell lines.…”

Section: Discussionsupporting

confidence: 55%

LncRNA TINCR is associated with clinical progression and serves as tumor suppressive role in prostate cancer

Dong¹,

Ding²,

Li³

et al. 2018

CMAR

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IntroductionTerminal differentiation-induced non-coding RNA (TINCR) has been suggested to have aberrant expression in multiple human cancers, and functions as tumor suppressor or promoter in various types of human tumors depending on the specific cancer types. The expression status and biological function of TINCR in prostate cancer is still unknown.Materials and methodsIn our study, we detected TINCR expression in prostate cancer tissue samples and cell lines, and analyzed the association between TINCR expression and clinical parameters in 160 prostate cancer patients. Moreover, we conducted gain-of-function and loss-of-function studies in prostate cancer cell to explore the biological function and molecular mechanism of TINCR.ResultsIn our results, low-expression TINCR was observed in prostate cancer, and correlated with advanced clinical T stage, lymph node involvement, distant metastasis, high Gleason score and poor prognosis in prostate cancer patients. Moreover, levels of TINCR expression were negatively associated with TRIP13 mRNA and protein expressions in prostate cancer tissues, and negatively regulated the TRIP13 mRNA and protein expressions in prostate cancer cell lines. TINCR inhibits prostate cancer cell proliferation, migration and invasion via suppressing TRIP13 expression.ConclusionTINCR plays a tumor suppressive role in regulating prostate cancer cell proliferation, migration and invasion through modulating TRIP13 expression.

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Section: Discussionsupporting

confidence: 55%

LncRNA TINCR is associated with clinical progression and serves as tumor suppressive role in prostate cancer

Dong¹,

Ding²,

Li³

et al. 2018

CMAR

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“…TRIP13 plays critical roles in cell cycle regulation and chromosome segregation ( Yost et al., 2017 ). Recent findings suggested that TRIP13 is overexpressed in and can promote tumorigenesis of several cancers, such as lung adenocarcinoma, chronic lymphocytic leukemia, head and neck cancer and colorectal cancer ( Banerjee et al., 2014 ; Li et al., 2018 ; Sheng et al., 2018 ; Zhou et al., 2017 ). TRIP13 can ‘turn off’ the division-inhibiting spindle assembly checkpoint (SAC) complex through transforming the ‘closed’, active structure of the SAC effector Mad2 to an ‘open’ and inactive form ( Alfieri, Chang & Barford, 2018 ; Ye et al., 2015 ).…”

Section: Discussionmentioning

confidence: 99%

Meta-analysis of microarray datasets identify several chromosome segregation-related cancer/testis genes potentially contributing to anaplastic thyroid carcinoma

Qiu

Jin

et al. 2018

PeerJ

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AimAnaplastic thyroid carcinoma (ATC) is the most lethal thyroid malignancy. Identification of novel drug targets is urgently needed.Materials & MethodsWe re-analyzed several GEO datasets by systematic retrieval and data merging. Differentially expressed genes (DEGs) were filtered out. We also performed pathway enrichment analysis to interpret the data. We predicted key genes based on protein–protein interaction networks, weighted gene co-expression network analysis and genes’ cancer/testis expression pattern. We also further characterized these genes using data from the Cancer Genome Atlas (TCGA) project and gene ontology annotation.ResultsCell cycle-related pathways were significantly enriched in upregulated genes in ATC. We identified TRIP13, DLGAP5, HJURP, CDKN3, NEK2, KIF15, TTK, KIF2C, AURKA and TPX2 as cell cycle-related key genes with cancer/testis expression pattern. We further uncovered that most of these putative key genes were critical components during chromosome segregation.ConclusionWe predicted several key genes harboring potential therapeutic value in ATC. Cell cycle-related processes, especially chromosome segregation, may be the key to tumorigenesis and treatment of ATC.

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“…Alternatively known as 16E1BP, TRIP13 is a protein encoded by the TRIP13 gene that interacts with thyroid hormone receptors. TRIP13 is also a member of the AAA + protein family, which can alter the conformation of terminal macromolecules, therefore affecting cell signaling pathways and participating in many cell activities [14–16]. TRIP13 plays an important role in meiosis and mitosis, especially it not only enables chromosome re-pairing and association, but also activates recombination detection points for double-stranded DNA breaks and affects the role of spindle assembly checkpoints [17–22].…”

Section: Introductionmentioning

confidence: 99%

Silencing TRIP13 inhibits cell growth and metastasis of hepatocellular carcinoma by activating of TGF-β1/smad3

Yao

Zhang

et al. 2018

Cancer Cell Int

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BackgroundTRIP13 is highly expressed in several cancers and is closely connected with cancer progression. However, its roles on the growth and metastasis of hepatocellular carcinoma (HCC), and the underlying mechanism are still unclear.MethodsCombining bioinformatics with previous studies, the correlation between TRIP13 and HCC was predicted. TRIP13 expressions from 52 HCC patients and several cell lines were determined. The effects of silencing TRIP13 on cell viability, apoptosis, migration and invasion were respectively detected using CCK-8, flow cytometry and Transwell. qRT-PCR and western blot were performed to reveal associated mechanism. A HCC model was established in BALB/c-nu mice by transplanting HepG2 cells. TRIP13 protein expression and apoptosis in mice tissues were accordingly detected by Immunohistochemistry and TUNEL.ResultsHigh expression of TRIP13 in HCC affected the survival rate and it was enriched in RNA degradation and fatty acid metabolism according to bioinformatics and prediction from previous literature. Increased expression of TRIP13 in HCC patient tissues was associated with the progression of HCC. Silencing TRIP13 inhibited cell viability, migration and invasion, and induced cell apoptosis. TRIP13 knockdown also suppressed the formation of tumor in vivo. Meanwhile, silencing TRIP13 decreased the expressions of Ki67 and MMP-2 and increased the expressions of TIMP-2, active-caspase-3 and TGF-β1/smad3 signaling- related genes.ConclusionsSilencing TRIP13 acts as a tumor suppresser of HCC to repress cell growth and metastasis in vitro and in vivo, and such a phenomenon possibly involved activation of TGF-β1/smad3 signaling.

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Thyroid hormone receptor interactor 13 (TRIP13) overexpression associated with tumor progression and poor prognosis in lung adenocarcinoma

Cited by 37 publications

References 17 publications

LncRNA TINCR is associated with clinical progression and serves as tumor suppressive role in prostate cancer

LncRNA TINCR is associated with clinical progression and serves as tumor suppressive role in prostate cancer

Meta-analysis of microarray datasets identify several chromosome segregation-related cancer/testis genes potentially contributing to anaplastic thyroid carcinoma

Silencing TRIP13 inhibits cell growth and metastasis of hepatocellular carcinoma by activating of TGF-β1/smad3

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