Proliferation and invasion of ovarian cancer cells are suppressed by knockdown of TRIM11

Chen, Yan; Sun, Jin; Ma, Junyan

doi:10.3892/ol.2017.6432

Cited by 34 publications

(25 citation statements)

References 25 publications

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“…It has been demonstrated that TRIM11 upregulation contributes to the growth and metastasis of hepatocellular cancer cells as well as ovarian cancer cells [21,22]. In the present analysis, TRIM11 silencing deeply suppressed the proliferation and improved the apoptosis of OS cells.…”

Section: Discussionsupporting

confidence: 49%

Tripartite Motif Containing 11 Interacts with DUSP6 to Promote the Growth of Human Osteosarcoma Cells through Regulating ERK1/2 Pathway

Wang¹,

Xu²,

Tang³

et al. 2019

BioMed Research International

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Tripartite Motif Containing 11 (TRIM11), an E3 ubiquitin ligase, is identified as a carcinogen causing certain human cancers. However, the specific role of TRIM11 is still uncovered in human osteosarcoma (OS) cells. To explore the role of TRIM11 in OS cells, TRIM11 was induced by silencing and overexpression in OS cells using RNA interference (RNAi) and lentiviral vector, respectively. qRT-PCR and western blot were used to examine the transcription and translation levels of the target gene. Cell count kit-8 (CCK-8) assays were established to analyze cell proliferation. Cell apoptosis ratio was determined via flow cytometry. In our analyses, TRIM11 was suggested to be upregulated, and it functioned as a pro-proliferation and antiapoptosis factor in OS cells. Moreover, the extracellular-signal-regulated kinase 1/2 (ERK1/2) inhibitor PD98059 was used to examine the relationship between TRIM11 and ERK1/2 in OS cells. Results demonstrated that the role of TRIM11 was significantly disrupted by the ERK1/ 2 inhibitor PD98059. Interestingly, we found TRIM11 overexpression did not affect dual-specificity phosphatase 6 (DUSP6) transcription, but improved its translation in OS cells. Co-immunoprecipitation (Co-IP) analyses revealed that TRIM11 interacted with DUSP6. Importantly, overexpression of TRIM11 enhanced DUSP6 ubiquitination in OS cells. erefore, TRIM11 might suppress the translation of DUSP6 via improving its ubiquitination. Additionally, TRIM11 silencing in OS cells significantly reduced its tumorigenicity in vivo. Overall, our findings firstly revealed that TRIM11 was an oncogene gene in the growth of OS cells and illustrated its potential function as a target in the treatment of OS.

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Section: Discussionsupporting

confidence: 49%

Tripartite Motif Containing 11 Interacts with DUSP6 to Promote the Growth of Human Osteosarcoma Cells through Regulating ERK1/2 Pathway

Wang¹,

Xu²,

Tang³

et al. 2019

BioMed Research International

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“…Tripartite motif-containing protein 11 (TRIM11), encoded by the TRIM11 gene, is an E3 ubiquitin ligase. Recent studies have demonstrated that the expression levels of TRIM11 are increased in gliomas [13], ovarian cancer [14], and lung cancers [8]. These studies have shown that TRIM11 has a role in regulating the development of human malignancies.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, TRIM11 expression was reported to be increased in high-grade gliomas and to have an oncogenic role and to be associated with the progression of glioma [13]. Chen et al showed that TRIM11 was upregulated in ovarian cancer tissue, and that knockdown of the TRIM11 gene suppressed proliferation and induced apoptosis of cancer cells [14]. Also, the overexpression of TRIM11 has been shown to promote cell proliferation, migration, and invasion of lung cancer cells [8].…”

Section: Introductionmentioning

confidence: 99%

Expression of Tripartite Motif-Containing Proteactiin 11 (TRIM11) is Associated with the Progression of Human Prostate Cancer and is Downregulated by MicroRNA-5193

et al. 2019

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BackgroundTripartite motif-containing protein 11 (TRIM11), encoded by the TRIM11 gene, has been studied in some human malignant tumors. MicroRNA-5193 (miRNA-5193) was predicted to target TRIM11, according to bioinformatics data from TargetScan. However, the roles of TRIM11 and miRNA-5193 in prostate cancer remain unknown. This study aimed to investigate the regulatory effects of miRNA-5193 on the expression of TRIM11 in prostate cancer tissues compared with adjacent normal prostate, and in human prostate cancer cell lines, PC3 and DU145 in vitro.Material/MethodsProstate tumor tissue and adjacent normal tissue from 137 patients with stage T1c (n=66), stage T2 (n=48), and stage T3 (n=23) prostate cancer were studied. Expression levels of the TRIM 11 protein and the TRIM11 gene in prostate cancer, normal prostate tissue, and human prostate cancer cell lines, PC3 and DU145, were measured by Western blot and quantitative real-time polymerase chain reaction (qRT-PCR), respectively. Transfection with TRIM11 small interfering RNA (siRNA) resulted in gene knockdown. Transfection with a miR-5193 mimic resulted in overexpression of miR-5193. Proliferation and invasion assays were performed for PC3 and DU145 cells in vitro.ResultsTRIM11 expression was upregulated in prostate cancer specimens compared with normal prostate tissue and was significantly correlated with reduced outcome. In human prostate cancer cell lines, PC3 and DU145, TRIM11 overexpression promoted cell proliferation. Upregulation of miR-5193 downregulated the expression of TRIM11.ConclusionsTRIM11 was upregulated in prostate cancer tissue and was associated with reduced prognosis. TRIM11 expression increased cell proliferation in vitro and was downregulated by miR-5193.

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“…Other TRIMs, although do not exert a specific role in the regulation of cell cycle phase transitions, are yet involved in controlling carcinogenesis and cancer progression (Table 1). Most of these TRIMs, like TRIM11 [70,71,72,73,74], TRIM23 [75], TRIM24 [76], TRIM25 [77,78,79], TRIM31 [80], TRIM37 [81], TRIM47 [82,83], TRIM65 [84], and TRIM71 [85] are up-regulated in cancer cells and tissues, playing an oncogenic role in different types of cancer. These TRIMs are often associated with unfavorable prognosis and promote cancer cells proliferation and migration, being often associated with proteins of central signaling pathways.…”

Section: Trims and Cell Cycle Progressionmentioning

confidence: 99%

E3 Ubiquitin Ligase TRIM Proteins, Cell Cycle and Mitosis

Venuto

Merla

2019

Cells

117

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The cell cycle is a series of events by which cellular components are accurately segregated into daughter cells, principally controlled by the oscillating activities of cyclin-dependent kinases (CDKs) and their co-activators. In eukaryotes, DNA replication is confined to a discrete synthesis phase while chromosome segregation occurs during mitosis. During mitosis, the chromosomes are pulled into each of the two daughter cells by the coordination of spindle microtubules, kinetochores, centromeres, and chromatin. These four functional units tie chromosomes to the microtubules, send signals to the cells when the attachment is completed and the division can proceed, and withstand the force generated by pulling the chromosomes to either daughter cell. Protein ubiquitination is a post-translational modification that plays a central role in cellular homeostasis. E3 ubiquitin ligases mediate the transfer of ubiquitin to substrate proteins determining their fate. One of the largest subfamilies of E3 ubiquitin ligases is the family of the tripartite motif (TRIM) proteins, whose dysregulation is associated with a variety of cellular processes and directly involved in human diseases and cancer. In this review we summarize the current knowledge and emerging concepts about TRIMs and their contribution to the correct regulation of cell cycle, describing how TRIMs control the cell cycle transition phases and their involvement in the different functional units of the mitotic process, along with implications in cancer progression.

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Proliferation and invasion of ovarian cancer cells are suppressed by knockdown of TRIM11

Cited by 34 publications

References 25 publications

Tripartite Motif Containing 11 Interacts with DUSP6 to Promote the Growth of Human Osteosarcoma Cells through Regulating ERK1/2 Pathway

Tripartite Motif Containing 11 Interacts with DUSP6 to Promote the Growth of Human Osteosarcoma Cells through Regulating ERK1/2 Pathway

Expression of Tripartite Motif-Containing Proteactiin 11 (TRIM11) is Associated with the Progression of Human Prostate Cancer and is Downregulated by MicroRNA-5193

E3 Ubiquitin Ligase TRIM Proteins, Cell Cycle and Mitosis

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