TRIM31 is upregulated in hepatocellular carcinoma and promotes disease progression by inducing ubiquitination of TSC1–TSC2 complex

Guo, Pengbo; Ma, Xiaoxiao; Zhao, Wei; Huai, Wanwan; Li, T; Qiu, Yumin; Zhang, Y; Han, Lihui

doi:10.1038/onc.2017.349

Cited by 79 publications

(81 citation statements)

References 38 publications

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“…To further verify the role of NOD2 in HCC, xenograft tumor models were constructed as described before 14 . After visible tumors appeared, the formed tumors were transfected with specific small interference RNA (SiRNA) against NOD2 (Si-NOD2) to construct the loss-of-function model in vivo according to the protocol described before 15 . The mice were sacrificed on day 38 after the first transfection, and the formed tumors were statistically analyzed.…”

Section: Nod2 Suppressed Malignancy Of Hcc Cells In Vivo and In Vitromentioning

confidence: 99%

“…The immunofluorescence assay was performed as described before 15 . Antibody against NOD2 was purchased from Abcam (#ab31488, Cambridge, MA, USA), and the other antibodies were the same as used for western blot.…”

Section: Clinical Specimensmentioning

confidence: 99%

“…Antibody against NOD2 was purchased from Abcam (#ab31488, Cambridge, MA, USA), and the other antibodies were the same as used for western blot. The in vitro protein translation assay was performed by TNT Quick Coupled Transcription and Translation System (Promega, Madison, WI, USA) as previously described 15 .…”

Section: Clinical Specimensmentioning

confidence: 99%

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NOD2 inhibits tumorigenesis and increases chemosensitivity of hepatocellular carcinoma by targeting AMPK pathway

Qiu

Sun

et al. 2020

Cell Death Dis

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Nucleotide binding oligomerization domain 2 (NOD2) is a recognized innate immune sensor which can initiate potent immune response against pathogens. Many innate immune sensors have been reported to be of great importance in carcinogenesis. However, the role of NOD2 in cancer is not well understood. Here we investigated the role of NOD2 in the development of hepatocellular carcinoma (HCC). We demonstrated that NOD2 deficiency promoted hepatocarcinogenesis in N-nitrosodiethylamine (DEN)/carbon tetrachloride (CCl 4) induced HCC mice model and xenograft tumor model. In vitro investigation showed that NOD2 acted as a tumor suppressor and inhibited proliferation, colony formation and invasion of HCC cells. Clinical investigation showed that NOD2 expression was completely lost or significantly downregulated in clinical HCC tissues, and loss of NOD2 expression was significantly correlated with advanced disease stages. Further investigation showed that NOD2 exerted its anti-tumor effect through activating adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK) signaling pathway, and NOD2 significantly enhanced the sensitivity of HCC cells to sorafenib, lenvatinib and 5-FU treatment through activating AMPK pathway induced apoptosis. Moreover, we demonstrated that NOD2 activated AMPK pathway by directly binding with AMPKα-LKB1 complex, which led to autophagy-mediated apoptosis of HCC cells. Altogether, this study showed that NOD2 acted as a tumor suppressor as well as a chemotherapeutic regulator in HCC cells by directly activating AMPK pathway, which indicated a potential therapeutic strategy for HCC treatment by upregulating NOD2-AMPK signaling axis.

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Section: Nod2 Suppressed Malignancy Of Hcc Cells In Vivo and In Vitromentioning

confidence: 99%

Section: Clinical Specimensmentioning

confidence: 99%

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NOD2 inhibits tumorigenesis and increases chemosensitivity of hepatocellular carcinoma by targeting AMPK pathway

Qiu

Sun

et al. 2020

Cell Death Dis

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“…The IF assay was performed according to previously established protocols (23). Cells were seeded into 24-well plates and fixed with 4% paraformaldehyde after 48-h treatment of puerarin or control.…”

Section: Immunofluorescence (If) Assaymentioning

confidence: 99%

Puerarin inhibits hepatocellular carcinoma invasion and metastasis through miR-21-mediated PTEN/AKT signaling to suppress the epithelial-mesenchymal transition

Zhou

Xue

Wang

et al. 2020

Braz J Med Biol Res

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Erratum for: "Puerarin inhibits hepatocellular carcinoma invasion and metastasis through miR-21mediated PTEN/AKT signaling to suppress the epithelial-mesenchymal transition" [Braz J Med Biol Res (2020) 53(4): e8882] Yuan Zhou 0 0 0 0 -0 0 0 0 -0 0 0 0 -0 0 0 0The authors would like to correct the Corresponding authors' names and emails and the Acknowledgments section of the article "Puerarin inhibits hepatocellular carcinoma invasion and metastasis through miR-21-mediated PTEN/AKT signaling to suppress the epithelial-mesenchymal transition". The Editors highlight that the information presented in the original version was provided by the authors at submission and revision. In addition, the authors had the opportunity to correct the information during proofreading, before approving for publication.Correspondence: Haozhen Ren: orenhaozhen1984@163.com4 | Jinglin Wangocw20120817@163.com4 *These authors contributed equally to this study.Braz J Med Biol Res | AbstractHepatocellular carcinoma (HCC) is one of the most common primary malignant tumors of the liver worldwide. Liver resection and transplantation are currently the only effective treatments; however, recurrence and metastasis rates are still high. Previous studies have shown that the epithelial-mesenchymal transition (EMT) is a key step in HCC invasion and metastasis. Inhibition of EMT has become a new therapeutic strategy for tumors. Recently, puerarin, a well-characterized component of traditional Chinese medicine, has been isolated from Pueraria radix and exerts positive effects on many diseases, particularly cancers. In this study, CCK-8, EdU immunofluorescence, colony formation, wound healing, and migration assays were used to detect the effects of puerarin on HCC cells. We further analyzed the relationship between puerarin and miR-21/PTEN/EMT markers in HCC cell lines. Our results showed that HCC cell proliferation, migration, invasion, tumor formation, and metastasis were reduced by puerarin in vitro and in vivo. Additionally, puerarin inhibited the EMT process of HCC by affecting the expression of Slug and Snail. Moreover, oncogenic miR-21 was inhibited by puerarin, coupled with an increase in the tumor suppressor gene PTEN. Increasing miR-21 expression or decreasing PTEN expression reversed the inhibition effects of puerarin in HCC. These data confirmed that puerarin affects HCC through the miR-21/PTEN/EMT regulatory axis. Overall, puerarin may represent a chemopreventive and/or chemotherapeutic agent for HCC treatment.

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“…TRIM31 expression is significantly up-regulated in hepatocellular carcinoma (HCC) tissues and significantly correlated with advanced disease status. TRIM31 promotes the malignant behaviors of HCC cells through regulation of mammalian target of rapamycin complex1 (mTORC1) pathway [8]. In addition, TRIM31 has been proven to be associated with radiosensitivity and chemosensitivity in cancers.…”

Section: Introductionmentioning

confidence: 99%

TRIM31 promotes acute myeloid leukemia progression and sensitivity to daunorubicin through the Wnt/β-catenin signaling

Xiao

Deng

et al. 2020

Bioscience Reports

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Tripartite motif (TRIM) 31 is a member of TRIM family and exerts oncogenic role in the progression and drug resistance of several cancers. However, little is known about the relevance of TRIM31 in acute myeloid leukemia (AML). Herein, we investigated the role of TRIM31 in AML. We examined the expression levels of TRIM31 in the blood samples from 34 patients with AML and 34 healthy volunteers using qRT-PCR. The mRNA levels of TRIM31 in human bone marrow stromal cells (HS-5) and five AML cell lines were also detected. Loss/gain-of-function assays were performed to assess the role of TRIM31 in AML cells proliferation, apoptosis and sensitivity to daunorubicin. The expression levels of pro-caspase 3, cleaved caspase 3, Wnt3a, β-catenin, cyclin D1 and c-Myc were measured using Western blot. TRIM31 expression levels were significantly up-regulated in AML patients and cell lines. Knockdown of TRIM31 suppressed cell proliferation and promoted apoptosis in AML-5 and U937 cells. The IC50 of daunorubicin was significantly decreased in TRIM31 siRNA (si-TRIM31) transfected cells. Oppositely, induced cell proliferation and decreased cell apoptosis were observed in pcDNA-3.1-TRIM31 transfected cells. Furthermore, knockdown of TRIM31 suppressed the activation of Wnt/β-catenin pathway in AML cells. Activation of Wnt/β-catenin pathway by LiCl abolished the effects of si-TRIM31 on cell proliferation, apoptosis and sensitivity to daunorubicin in AML cells. In conclusion, the results indicated that TRIM31 promoted leukemogenesis and chemoresistance to daunorubicin in AML. The oncogenic role of TRIM31 in AML was mediated by the Wnt/β-catenin pathway. Thus, TRIM31 might serve as a therapeutic target for the AML treatment.

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TRIM31 is upregulated in hepatocellular carcinoma and promotes disease progression by inducing ubiquitination of TSC1–TSC2 complex

Cited by 79 publications

References 38 publications

NOD2 inhibits tumorigenesis and increases chemosensitivity of hepatocellular carcinoma by targeting AMPK pathway

NOD2 inhibits tumorigenesis and increases chemosensitivity of hepatocellular carcinoma by targeting AMPK pathway

Puerarin inhibits hepatocellular carcinoma invasion and metastasis through miR-21-mediated PTEN/AKT signaling to suppress the epithelial-mesenchymal transition

TRIM31 promotes acute myeloid leukemia progression and sensitivity to daunorubicin through the Wnt/β-catenin signaling

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