Negative correlation of ITCH E3 ubiquitin ligase and miRNA-106b dictates metastatic progression in pancreatic cancer

Luo, Zhu-Lin; Luo, Huijun; Chen, Fang; Cheng, Long; Huang, Zhu; Dai, Ruiwu; Li, Kun; Tian, Fanghua; Wang, Tao; Tang, Lijun

doi:10.18632/oncotarget.6395

Cited by 34 publications

(20 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The tumorigenesis ability of E3 ubiquitin ligase is also emerging with defined biological activities. Several E3 ubiquitin ligase, including NEDD4 5, 10, ITCH 11, WWP2 12, 13, and FBXO32 6 have been confirmed to be related with the tumorigenesis. In order to find the tongue cancer‐related E3 ligases, we screened the human E3 ubiquitin ligase library and found the candidate molecule, RNF126.…”

Section: Discussionmentioning

confidence: 97%

E3 Ubiquitin ligase RNF126 regulates the progression of tongue cancer

Wang

Zhao

et al. 2016

Cancer Medicine

View full text Add to dashboard Cite

This study aims to analyze the role of RNF126 in the oncogenesis of tongue cancer. The cell proliferation and viability of human tongue cancer cells, SCC25 and SCC9 cells, were determined by cell counting and MTT assay, respectively. The effect of RNF126 on regulating AKT signaling pathway was analyzed through western blotting. The transplantation tumor model of nude mice was used to evaluate the tumorigenecity of RNF126. Knockdown of RNF126 inhibited the proliferation and viability of SCC9 and SCC25 cells. Inhibition of RNF126 also decreased the activity of AKT1 as well as its downstream molecules. Furthermore, RNF126 regulated the tumor volume on mice model. These data suggested that RNF126 might be related to the progression of tongue cancer through regulating AKT signaling pathway.

show abstract

Section: Discussionmentioning

confidence: 97%

E3 Ubiquitin ligase RNF126 regulates the progression of tongue cancer

Wang

Zhao

et al. 2016

Cancer Medicine

View full text Add to dashboard Cite

show abstract

“…For example, lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) was highly expressed in OS tissues and cells and promoted OS cell growth and tumor progression by inhibiting miR-376a [45]. Besides, tumor-suppressor miR-141 overexpression suppressed osteoblastic cell proliferation by down-regulating lncRNA H19 in OS [12].…”

Section: Discussionmentioning

confidence: 99%

LncRNA SNHG15 contributes to proliferation, invasion and autophagy in osteosarcoma cells by sponging miR-141

et al. 2017

View full text Add to dashboard Cite

BackgroundLncRNA small nucleolar RNA host gene 15 (SNHG15) was reported to play an oncogenic role in tumors. However, the role of SNHG15 and its molecular mechanism in osteosarcoma (OS) cells are largely unknown.MethodsqRT-PCR was performed to evaluate the expression levels of SNHG15 and miR-141 in OS tissues and cells. Cell transfection with different siRNAs, miRNAs or pcDNAs into U2OS and MG63 cells were carried out by Lipofectamine 2000. The effects of SNHG15 and miR-141 on OS cell proliferation, invasion and the levels of autophagy-related proteins were analyzed by MTT assay, Transwell invasion/migration assay and western blot, respectively. Luciferase reporter assay was used to confirm whether SNHG15 could directly interact with miR-141.ResultsWe found that up-regulation of SNHG15 was inversely correlated with miR-141 expression in OS tissues. SNHG15 knockdown and miR-141 overexpression significantly suppressed cell proliferation, invasion, migration and autophagy while SNHG15 overexpression and miR-141 repression exhibited the opposite effects on OS cells. Besides, SNHG15 could directly interact with miR-141 and regulate its expression. Furthermore, miR-141 suppressing significantly overturned the inhibition on proliferation, invasion, migration and autophagy mediated by SNHG15 knockdown while miR-141 overexpression remarkably attenuated SNHG15 overexpression-induced proliferation, invasion, migration and autophagy in OS cells.ConclusionOur data showed that SNHG15 contributes to proliferation, invasion, migration and autophagy in OS by negatively regulating miR-141, providing a new potential target and prognostic biomarker for the treatment of OS.

show abstract

“…For instance, miR-106b targets ITCH mRNA, encoding an E3 ligase that promotes LATS1 degradation, and in this way positively modulates LATS1 protein levels. 114 Likewise, miR-9 and miR-137 suppress the translation of CUL4A, a negative regulator of LATS1. 115 Notably, miR-9-3p (processed from the complementary strand of miR-9) targets TAZ mRNA; 116 thus, both strands of miR-9 function to reinforce the tumor suppressive potential of the Hippo pathway and quench the output of its oncogenic effectors.…”

Section: Post-transcriptional Regulation Of Lats Mrnamentioning

confidence: 99%

The LATS1 and LATS2 tumor suppressors: beyond the Hippo pathway

2017

View full text Add to dashboard Cite

Proper cellular functionality and homeostasis are maintained by the convergent integration of various signaling cascades, which enable cells to respond to internal and external changes. The Dbf2-related kinases LATS1 and LATS2 (LATS) have emerged as central regulators of cell fate, by modulating the functions of numerous oncogenic or tumor suppressive effectors, including the canonical Hippo effectors YAP/TAZ, the Aurora mitotic kinase family, estrogen signaling and the tumor suppressive transcription factor p53. While the basic functions of the LATS kinase module are strongly conserved over evolution, the genomic duplication event leading to the emergence of two closely related kinases in higher organisms has increased the complexity of this signaling network. Here, we review the LATS1 and LATS2 intrinsic features as well as their reported cellular activities, emphasizing unique characteristics of each kinase. While differential activities between the two paralogous kinases have been reported, many converge to similar pathways and outcomes. Interestingly, the regulatory networks controlling the mRNA expression pattern of LATS1 and LATS2 differ strongly, and may contribute to the differences in protein binding partners of each kinase and in the subcellular locations in which each kinase exerts its functions.

show abstract

Negative correlation of ITCH E3 ubiquitin ligase and miRNA-106b dictates metastatic progression in pancreatic cancer

Cited by 34 publications

References 29 publications

E3 Ubiquitin ligase RNF126 regulates the progression of tongue cancer

E3 Ubiquitin ligase RNF126 regulates the progression of tongue cancer

LncRNA SNHG15 contributes to proliferation, invasion and autophagy in osteosarcoma cells by sponging miR-141

The LATS1 and LATS2 tumor suppressors: beyond the Hippo pathway

Contact Info

Product

Resources

About