Evaluation of the TRIP13 level in breast cancer and insights into potential molecular pathways

Jin, Lan; Huang, Jingzhan; Tao, Xinyi; Gao, Yuan; Zhang, Longshan; Huang, Weiqiang; Luo, Junjie; Liu, Chuqin; Deng, Yuan-Run; Liu, Lixin; Liu, Xiaolong

doi:10.1111/jcmm.17278

Cited by 10 publications

(8 citation statements)

References 46 publications

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“…Therefore, targeting the PI3K/Akt/mTOR pathway holds promise as a therapeutic strategy in leukemia. Recently, some evidence suggested that TRIP13 can modulate the activity of the PI3K/Akt/mTOR signaling pathway so as to participate in cancer progression, such as in lung cancer, , breast cancer, and hepatocellular carcinoma . However, the relationship between TRIP13 and PI3K/Akt/mTOR in leukemia still needs to be fully understood.…”

Section: Resultsmentioning

confidence: 99%

TRIP13 Plays an Important Role in the Sensitivity of Leukemia Cell Response to Sulforaphane Therapy

Liu,

Liao,

Fan

et al. 2024

ACS Omega

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Sulforaphane is one of the most characterized isothiocyanate compounds in cruciferous vegetables and shows anticancer effects, especially antileukemia properties. However, the molecular mechanism of the growth inhibition effect of sulforaphane in acute myeloid leukemia (AML) has not been fully explored. In the present study, a proteomic analysis was performed on the AML cell line U937 responding to sulforaphane treatment to identify novel and efficient therapeutic targets of sulforaphane on AML cells. Key driver analysis was run on the leukemia network, and TRIP13 was identified as a key regulatory factor in sulforaphane-induced growth inhibition in U937 cells. Pretreatment with DCZ0415, an inhibitor of TRIP13, could significantly attenuate sulforaphane-induced cell apoptosis and cell cycle arrest in vitro through the PI3K/Akt/mTOR signaling pathway. In addition, the inhibitory effect of sulforaphane on the tumor volume could also be obviously attenuated by the pretreatment of DCZ0415 in vivo. These results indicate that TRIP13 plays an important role in the sensitivity of leukemia cell response to sulforaphane treatment, and these findings expand the understanding of the mechanism of the antileukemic effect of sulforaphane and provide a new target for the treatment of AML.

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Section: Resultsmentioning

confidence: 99%

TRIP13 Plays an Important Role in the Sensitivity of Leukemia Cell Response to Sulforaphane Therapy

Liu,

Liao,

Fan

et al. 2024

ACS Omega

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“…Based on these findings, we focused on TRIP13 , a member of the large superfamily of AAA+ ATPase proteins [ 45 ]. The AAA+ ATPase family is involved in a wide range of biological processes, including protein folding and DNA recombination, replication, and repair [ 46 , 47 ].…”

Section: Discussionmentioning

confidence: 99%

Oncogenic Targets Regulated by Tumor-Suppressive miR-30c-1-3p and miR-30c-2-3p: TRIP13 Facilitates Cancer Cell Aggressiveness in Breast Cancer

Mitsueda,

Toda,

Shinden

et al. 2023

Cancers

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Accumulating evidence suggests that the miR-30 family act as critical players (tumor-suppressor or oncogenic) in a wide range of human cancers. Analysis of microRNA (miRNA) expression signatures and The Cancer Genome Atlas (TCGA) database revealed that that two passenger strand miRNAs, miR-30c-1-3p and miR-30c-2-3p, were downregulated in cancer tissues, and their low expression was closely associated with worse prognosis in patients with BrCa. Functional assays showed that miR-30c-1-3p and miR-30c-2-3p overexpression significantly inhibited cancer cell aggressiveness, suggesting these two miRNAs acted as tumor-suppressors in BrCa cells. Notably, involvement of passenger strands of miRNAs is a new concept of cancer research. Further analyses showed that seven genes (TRIP13, CCNB1, RAD51, PSPH, CENPN, KPNA2, and MXRA5) were putative targets of miR-30c-1-3p and miR-30c-2-3p in BrCa cells. Expression of seven genes were upregulated in BrCa tissues and predicted a worse prognosis of the patients. Among these genes, we focused on TRIP13 and investigated the functional significance of this gene in BrCa cells. Luciferase reporter assays showed that TRIP13 was directly regulated by these two miRNAs. TRIP13 knockdown using siRNA attenuated BrCa cell aggressiveness. Inactivation of TRIP13 using a specific inhibitor prevented the malignant transformation of BrCa cells. Exploring the molecular networks controlled by miRNAs, including passenger strands, will facilitate the identification of diagnostic markers and therapeutic target molecules in BrCa.

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“…TRIP13 has been studied in various cancers, including colorectal, lung, breast, multiple myeloma, and ovarian cancers [14][15][16][17] . However, the role of TRIP13 in UCEC has not been elucidated to date.…”

Section: Discussionmentioning

confidence: 99%

Protein and transcript expression levels of TRIP13 signify worse prognosis in endometrioid carcinoma

Wu,

Wang,

et al. 2023

Preprint

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This study investigated the genes implicated in endometrioid adenocarcinoma development to provide insights into the molecular diagnosis, targeted therapy, and prognostic prediction of the disease. Two mRNA microarray datasets were obtained from the Gene Expression Omnibus. Differentially expressed genes were identified, and a protein–protein interaction network was constructed. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed on the genes within the network modules. Prognostic significance was determined through a survival analysis to identify the key genes. The UALCAN website was used to validate TRIP13 mRNA expression, and immunohistochemical staining was performed to evaluate TRIP13 protein expression in patient samples. Sixteen genes were significantly associated with patient prognosis. The results revealed significantly elevated TRIP13 transcription and protein expression levels in endometrial cancer tissues compared to those in normal tissues. High TRIP13 expression was significantly correlated with shorter survival and considered an independent risk factor for endometrioid adenocarcinoma. Further, a negative correlation between TRIP13 expression and infiltrating CD8 + T cell levels in uterine corpus endometrial carcinoma was observed. This study validated the correlation between TRIP13 expression and poor patient prognosis, suggesting that TRIP13 may be a biomarker for endometrioid adenocarcinoma prognosis predictions.

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Evaluation of the TRIP13 level in breast cancer and insights into potential molecular pathways

Cited by 10 publications

References 46 publications

TRIP13 Plays an Important Role in the Sensitivity of Leukemia Cell Response to Sulforaphane Therapy

TRIP13 Plays an Important Role in the Sensitivity of Leukemia Cell Response to Sulforaphane Therapy

Oncogenic Targets Regulated by Tumor-Suppressive miR-30c-1-3p and miR-30c-2-3p: TRIP13 Facilitates Cancer Cell Aggressiveness in Breast Cancer

Protein and transcript expression levels of TRIP13 signify worse prognosis in endometrioid carcinoma

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