Knockdown of TRIM44 inhibits the proliferation and invasion in papillary thyroid cancer cells through suppressing the Wnt/β-catenin signaling pathway

Zhou, Zhenyu; Liu, Yang; Moody, M. Anthony; Chang, Liang

doi:10.1016/j.biopha.2017.09.132

Cited by 47 publications

(50 citation statements)

References 26 publications

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“…Xue et al24 showed that TRIM33 as a tumour suppressor that can abrogate tumour cell proliferation and tumorigenesis by degrading nuclear β‐catenin. Knockdown of TRIM28 or TRIM44 suppresses the tumorigenesis by down‐regulating the Wnt/β‐catenin signalling pathway 25, 26. β‐Catenin can also be triggered by TRIM65 via enhancement of the ubiquitination of Axin1 in the progression of hepatocellular carcinoma 27.…”

Section: Discussionmentioning

confidence: 99%

TRIM32 promotes cell proliferation and invasion by activating β‐catenin signalling in gastric cancer

Wang

et al. 2018

J Cellular Molecular Medi

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The tripartite motif (TRIM) family comprises more than 70 members involved in the regulation of many cellular pathways. TRIM32 acts as an E3 ubiquitin ligase and has been reported to participate in many human cancers. Here, we aimed to investigate the role of TRIM32 in gastric cancer (GC) and the clinical implications. High expression of TRIM32 was observed in GC tissues and cell lines, and was significantly associated with poor prognosis. Knockdown TRIM32 expression remarkably suppressed the proliferation, migration, and invasion of GC cells in vitro and tumour growth in vivo, whereas overexpression of TRIM32 yielded the opposite results. Western blotting and quantitative reverse‐transcription PCR (qRT‐PCR) analyses revealed that up‐regulation of TRIM32 significantly enhanced expression of β‐catenin protein and of its downstream targets TCF1, cyclin D1, Axin2 and MMP7 mRNAs. Moreover, we found that the mechanism behind the TRIM32‐promoted GC progression was related to the β‐catenin signalling pathway. Collectively, these data suggest that TRIM32 promotes GC cell proliferation, migration, and invasion by activating the β‐catenin signalling pathway.

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Section: Discussionmentioning

confidence: 99%

TRIM32 promotes cell proliferation and invasion by activating β‐catenin signalling in gastric cancer

Wang

et al. 2018

J Cellular Molecular Medi

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“…A previous study demonstrated that the silencing of TRIM44 may inhibit the proliferation, migration and invasion of human papillary thyroid cancer cells through suppression of the Wnt/β-catenin signaling pathway (10). Kawabata et al demonstrated that TRIM44 knockdown attenuated the tumor necrosis factor-α-dependent phosphorylation of the p65 subunit of nuclear factor (NF)-κB and inhibitor of NF-κBα in breast cancer cells (11).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of TRIM44 is an independent marker for predicting poor prognosis in epithelial ovarian cancer

Liu

Yin

et al. 2018

Exp Ther Med

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Tripartite motif-containing 44 (TRIM44) has been demonstrated to be important in tumor metastasis and progression. However, the expression pattern and prognostic value of the expression of TRIM44 in epithelial ovarian cancer (EOC) remain to be fully elucidated. In the present study, the aim was to investigate the expression and clinical role of TRIM44 in EOC. A total of 109 patients, who underwent primary surgery with the goal of maximal tumor resection followed by standard combination chemotherapy with carboplatin and paclitaxel, were analyzed in the present study. The expression level of TRIM44 was determined by western blot analysis and immunohistochemistry in 109 ECO tissues. It was found that the expression of TRIM44 was low in normal tissues and high in EOC tissues. Univariate survival analysis showed that the overexpression of TRIM44 was significantly associated with International Federation of Gynecology and Obstetrics stage and lymph node metastasis (P<0.05). Kaplan-Meier analysis suggested that there was a significant difference in overall survival and disease-free survival rates between patients with a high expression of TRIM44 and patients with a low expression of TRIM44. Patients with a high expression level of TRIM44 exhibited poorer overall survival and disease-free survival rates, compared with patients expressing a low level of TRIM44 (P<0.001). In addition, the results of the multivariate analysis revealed that the predictive value of the expression of TRIM44 was independent of other clinicopathological factors for predicting prognosis. These findings demonstrated that a high expression of TRIM44 was associated with the progression and prognosis of EOC.

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“…Accumulating studies have shown that TRIM family proteins may positively or negatively regulate carcinogenesis depending on the types of TRIM or the origin of cancer . Specifically, TRIM44 has been reported in a number of studies showing oncogenic effect in various cancers . Ong et al have reported that TRIM44 overexpression resulted from genomic amplification in 16.1% of all epithelial cancers.…”

Section: Discussionmentioning

confidence: 99%

“…In non–small cell lung cancer cells and breast cancers, TRIM44 promoted migration of cancer cells via the NF‐κβ signaling pathway . Zhou et al have revealed that TRIM44 knockdown inhibited cell proliferation, migration and the epithelial‐mesenchymal transition (EMT) process through suppression of Wnt/beta‐catenin pathway in papillary thyroid cancer cells. An in vitro study in cholangiocarcinoma has indicated that TRIM44 overexpression activated MAPK signaling and reversed cell EMT and apoptosis .…”

Section: Discussionmentioning

confidence: 99%

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TRIM44 promotes cell proliferation and migration by inhibiting FRK in renal cell carcinoma

et al. 2020

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TRIM44 has oncogenic roles in various cancers. However, TRIM44 expression and its function in renal cell carcinoma (RCC) are still unknown. Here in this study, we investigated the clinical significance of TRIM44 and its biological function in RCC. TRIM44 overexpression was significantly associated with clinical M stage, histologic type (clear cell) and presence of lymphatic invasion (P = .047, P = .005, and P = .028, respectively). Moreover, TRIM44 overexpression was significantly associated with poor prognosis in terms of cancer‐specific survival (P = .019). Gain‐of‐function and loss‐of‐function studies using TRIM44 and siTRIM44 transfection showed that TRIM44 promotes cell proliferation and cell migration in two RCC cell lines, Caki1 and 769P. To further investigate the role of TRIM44 in RCC, we performed integrated microarray analysis in Caki1 and 769P cells and explored the data in the Oncomine database. Interestingly, FRK was identified as a promising candidate target gene of TRIM44, which was downregulated in RCC compared with normal renal tissues. We found that cell proliferation was inhibited by TRIM44 knockdown and then recovered by siFRK treatment. Taken together, the present study revealed the association between high expression of TRIM44 and poor prognosis in RCC patients and that TRIM44 promotes cell proliferation by regulating FRK.

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Knockdown of TRIM44 inhibits the proliferation and invasion in papillary thyroid cancer cells through suppressing the Wnt/β-catenin signaling pathway

Cited by 47 publications

References 26 publications

TRIM32 promotes cell proliferation and invasion by activating β‐catenin signalling in gastric cancer

TRIM32 promotes cell proliferation and invasion by activating β‐catenin signalling in gastric cancer

Overexpression of TRIM44 is an independent marker for predicting poor prognosis in epithelial ovarian cancer

TRIM44 promotes cell proliferation and migration by inhibiting FRK in renal cell carcinoma

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