Oncogenic gene TRIM10 confers resistance to cisplatin in osteosarcoma cells and activates the NF‐κB signaling pathway

Xi, Xinhua; Bao, Yongzheng; Zhou, Yangfan; Chen, Yu; Zhong, Xueren; Liao, Junjian; Zhou, Jun; Xu, Sitao; Cao, Ziye; Hu, Konghe; Hu, Yongyu; He, Xijing; Zhou, Longze; Lin, Hongsheng; Wu, Qiang

doi:10.1002/cbin.11468

Cited by 10 publications

(7 citation statements)

References 34 publications

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“…The regulation of the TRIMs for the NF-κB signaling pathway is diverse, and some members of the triple structural domain protein family are involved in the activation of the NF-κB signaling pathway, for example, TRIM1 is involved in the tumor necrosis factor (TNF) α/LPS-induced activation of the NF-κB signaling pathway (26), TRIM52 acts as a positive regulator to regulate the NF-κB signaling pathway (27), and TRIM22 also has an activating effect on the NF-κB signaling pathway (28). It has been reported that TRIM22/ activates NF-κB signaling in glioblastoma by accelerating the degradation of IκBα (29); TRIM47 activates NF-κB signaling via PKC-ε/PKD3 stabilization and contributes to endocrine therapy resistance in breast cancer (30), and TRIM10 activates the NF-κB signaling pathway in osteosarcoma (31). In contrast, some members of the triple structural domain protein family down-regulate the NF-κB signaling pathway in some tumors, namely, TRIM39 inhibits the NF-κB signaling pathway by stabilizing actin expression (32), and TRIM45 inhibits tumor cell proliferation by suppressing the NF-κB signaling pathway (33).…”

Section: Discussionmentioning

confidence: 99%

Tripartite motif 52 (TRIM52) promotes proliferation, migration, and regulation of colon cancer cells associated with the NF-κB signaling pathway

Guo¹,

Zhou²,

Gu³

et al. 2022

J Gastrointest Oncol

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Background: With the advancement of early detection and treatment, the incidence of colon cancer (CC) has declined steadily worldwide; however, the mortality remains unacceptably high. Tripartite motif 52 (TRIM52) is a member of the family of highly conserved RBCC (a RING-finger, two B-boxes, and a predicted alpha-helical Coiled-Coil domain were linked to the N-terminal region in sequence) proteins with more than 70 isoforms, which plays an important role in tumorigenesis through different signaling pathways.How it regulates the development of CC remains unknown.Methods: Western blot was used to reveal that TRIM52 protein expression is up-regulated in CC cells.The Analysis of The Cancer Genome Atlas (TCGA) database was used to find the different expressions of TRIM52 between colon cancer tissues and normal colonic epithelial tissues. Cell proliferation assays, migration and invasion assays, and apoptosis were used to verify the changes in cell function after knockdown or overexpression of TRIM52 in CC cells. After that, the key proteins of the nuclear factor (NF)-κB signaling pathway were validated by western blot to explore the role of TRIM52 in the NF-κB signaling pathway.Finally, in order to explore the potential sites of TRIM52, LPS and PDTC were employed to activate and block the NF-κB signaling pathway, and the key proteins of the NF-κB signaling pathway were validated by western blot.Results: TGCA database revealed that TRIM52 expression was elevated in CC tissues and correlated with prognosis. It was verified that TRIM52 promoted the proliferation, migration, and invasion of CC cells, and inhibited cell apoptosis. Most of the tripartite motif proteins (TRIMs) have ubiquitin ligase activity related to their highly conserved RING structure. Detection of the key proteins of the NF-κB signaling pathway in CC cells revealed that TRIM52 activated the NF-κB signaling pathway. Conclusions:We confirmed that TRIM52 promotes proliferation, migration, and invasion while inhibiting apoptosis of CC cells. The regulatory effect of TRIM52 on CC cells is related to the activation of the NF-κB signaling pathway. As TRIM52 acted as an upstream stimulator, stimulating the transfer of P65 into the nucleus to activate the NF-κB signaling pathway, it may provide a potential target for prognosis prediction and treatment of CC.

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Section: Discussionmentioning

confidence: 99%

Tripartite motif 52 (TRIM52) promotes proliferation, migration, and regulation of colon cancer cells associated with the NF-κB signaling pathway

Guo¹,

Zhou²,

Gu³

et al. 2022

J Gastrointest Oncol

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“…Deregulation of the IFN‐I signaling pathway has multiple implications in the treatment of endotoxic shock caused by Gram‐negative pathogens, as well as in autoimmune conditions such as rheumatoid arthritis and SLE. A recent study reported that TRIM10 is highly expressed in chemotherapy‐resistant osteosarcoma tissues and promotes cisplatin resistance in osteosarcoma cells, demonstrating that it may be involved in the development of osteosarcoma [41]. Indeed, TRIM family members, such as TRIM26 and TRIM36, have various functions in modulating cancer development and progression [42, 43].…”

Section: Discussionmentioning

confidence: 99%

TRIM10 binds to IFN‐α/β receptor 1 to negatively regulate type I IFN signal transduction

et al. 2021

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The type I interferon (IFN‐I) system is important for antiviral and anticancer immunity. Prolonged activation of IFN/JAK/STAT signaling is closely associated with autoimmune diseases. TRIM10 dysfunction may be associated closely with certain autoimmune disorders. Here, we observed that the serum TRIM10 protein level is lower in patients with systemic lupus erythematosus than in healthy control subjects. We speculated the possible involvement of TRIM10‐induced modulation of the IFN/JAK/STAT signaling pathway in systemic lupus erythematosus. In line with our hypothesis, TRIM10 inhibited the activation of JAK/STAT signaling pathway triggered by various stimuli. TRIM10 restricted the IFN‐I/JAK/STAT signaling pathway, which was independent of its E3 ligase activity. Mechanistically, TRIM10 interacted with the intracellular domain of IFNAR1 and blocked the association of IFNAR1 with TYK2. These data suggest the possible TRIM10 suppresses IFN/JAK/STAT signaling pathway through blocking the interaction between IFNAR1 and TYK2. Targeting TRIM10 is a potential strategy for treating autoimmune diseases.

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“…206 The oncogene TRIM10 upregulates nuclear levels of p65, thereby activating classical NF-κB signaling to promote cisplatin resistance in OS cells. 207 Contemporary research on NF-κB-associated mechanisms in OS is centered on the modulation of miRNAs and lncRNAs that are possible upstream modulators of NF-κB and could exert their oncogenic or their inhibitory properties on tumors by affecting the levels of STAT3 expressed in OS cells. 208,209 When the expression of lncRNA NKILA was detected in 60 cases of OS and adjacent tissues, lncRNA NKILA expression was found to be reduced in OS tissues, and the proliferation, invasive rate, and migration of OS cells were enhanced after transfection of NKILA-siRNA with cells, while the NF-κB inhibitor (JSH) could reverse the inhibitory impact of NKILA on cell migration and proliferation, implying that lncRNA NKILA is involved in OS development and acts through the NF-κB/NAIL signaling pathway.…”

Section: Nf-κb Signaling Pathway and Os Development And Progressionmentioning

confidence: 99%

“…Notably, alpha thalassemia and intellectual disability syndrome X‐linked (ATRX) deficiency promotes OS cell invasion by increasing NF‐κB signaling and integrin β3 binding 206 . The oncogene TRIM10 upregulates nuclear levels of p65, thereby activating classical NF‐κB signaling to promote cisplatin resistance in OS cells 207 …”

Section: Signaling Pathways In Osmentioning

confidence: 99%

Targeting signaling pathways in osteosarcoma: Mechanisms and clinical studies

Shen

Lan

et al. 2023

MedComm

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Osteosarcoma (OS) is a highly prevalent bone malignancy among adolescents, accounting for 40% of all primary malignant bone tumors. Neoadjuvant chemotherapy combined with limb‐preserving surgery has effectively reduced patient disability and mortality, but pulmonary metastases and OS cells' resistance to chemotherapeutic agents are pressing challenges in the clinical management of OS. There has been an urgent need to identify new biomarkers for OS to develop specific targeted therapies. Recently, the continued advancements in genomic analysis have contributed to the identification of clinically significant molecular biomarkers for diagnosing OS, acting as therapeutic targets, and predicting prognosis. Additionally, the contemporary molecular classifications have revealed that the signaling pathways, including Wnt/β‐catenin, PI3K/AKT/mTOR, JAK/STAT3, Hippo, Notch, PD‐1/PD‐L1, MAPK, and NF‐κB, have an integral role in OS onset, progression, metastasis, and treatment response. These molecular classifications and biological markers have created new avenues for more accurate OS diagnosis and relevant treatment. We herein present a review of the recent findings for the modulatory role of signaling pathways as possible biological markers and treatment targets for OS. This review also discusses current OS therapeutic approaches, including signaling pathway‐based therapies developed over the past decade. Additionally, the review covers the signaling targets involved in the curative effects of traditional Chinese medicines in the context of expression regulation of relevant genes and proteins through the signaling pathways to inhibit OS cell growth. These findings are expected to provide directions for integrating genomic, molecular, and clinical profiles to enhance OS diagnosis and treatment.

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Oncogenic gene TRIM10 confers resistance to cisplatin in osteosarcoma cells and activates the NF‐κB signaling pathway

Cited by 10 publications

References 34 publications

Tripartite motif 52 (TRIM52) promotes proliferation, migration, and regulation of colon cancer cells associated with the NF-κB signaling pathway

Tripartite motif 52 (TRIM52) promotes proliferation, migration, and regulation of colon cancer cells associated with the NF-κB signaling pathway

TRIM10 binds to IFN‐α/β receptor 1 to negatively regulate type I IFN signal transduction

Targeting signaling pathways in osteosarcoma: Mechanisms and clinical studies

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