Knockdown of circ_0084043 suppresses the development of human melanoma cells through miR-429/tribbles homolog 2 axis and Wnt/β-catenin pathway

Chen, Zhibing; Chen, Junjie; Wa, Qingde; He, Mei; Wang, Xiao; Zhou, Jianwen; Cen, Ying

doi:10.1016/j.lfs.2020.117323

Cited by 35 publications

(26 citation statements)

References 24 publications

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“…Apparently, circ_0084043 knockdown inhibited expression of β-catenin, c-Myc and cyclinD1 through downregulating TRIB2 via miR-429. Moreover, knockdown of circ_0084043 or TRIB2 suppressed melanoma development, indicating that they could be a potential therapeutic target [ 73 ].…”

Section: Trib2 In Cancermentioning

confidence: 99%

The Critical Role of TRIB2 in Cancer and Therapy Resistance

Mayoral-Varo

Jiménez

Link

2021

Cancers

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The Tribbles pseudokinases family consists of TRIB1, TRIB2, TRIB3 and STK40 and, although evolutionarily conserved, they have distinctive characteristics. Tribbles members are expressed in a context and cell compartment-dependent manner. For example, TRIB1 and TRIB2 have potent oncogenic activities in vertebrate cells. Since the identification of Tribbles proteins as modulators of multiple signalling pathways, recent studies have linked their expression with several pathologies, including cancer. Tribbles proteins act as protein adaptors involved in the ubiquitin-proteasome degradation system, as they bridge the gap between substrates and E3 ligases. Between TRIB family members, TRIB2 is the most ancestral member of the family. TRIB2 is involved in protein homeostasis regulation of C/EBPα, β-catenin and TCF4. On the other hand, TRIB2 interacts with MAPKK, AKT and NFkB proteins, involved in cell survival, proliferation and immune response. Here, we review the characteristic features of TRIB2 structure and signalling and its role in many cancer subtypes with an emphasis on TRIB2 function in therapy resistance in melanoma, leukemia and glioblastoma. The strong evidence between TRIB2 expression and chemoresistance provides an attractive opportunity for targeting TRIB2.

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Section: Trib2 In Cancermentioning

confidence: 99%

The Critical Role of TRIB2 in Cancer and Therapy Resistance

Mayoral-Varo

Jiménez

Link

2021

Cancers

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“…Given the evidence that miR-429-3p might be a significantly involved in the process of abdominal adipose deposition, we further investigated its role in this biological process. In the past decades, role of miR-429-3p has been extensively explored in tumorigenesis (Wu et al, 2018(Wu et al, , 2019Shen et al, 2019;Chen et al, 2020). However, little is known about its role in adipogenesis.…”

Section: Discussionmentioning

confidence: 99%

miR-429-3p/LPIN1 Axis Promotes Chicken Abdominal Fat Deposition via PPARγ Pathway

Chao¹,

Guo²,

Wang³

et al. 2020

Front. Cell Dev. Biol.

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To explore the regulatory mechanism of abdominal fat deposition in broilers, 100-day-old Sanhuang chickens (n = 12) were divided into high-fat and low-fat groups, according to the abdominal fat ratio size. Total RNA isolated from the 12 abdominal fat tissues was used for miRNA and mRNA sequencing. Results of miRNA and mRNA sequencing revealed that miR-429-3p was highly expressed in high-fat chicken whereas LPIN1 expression was downregulated. Further, we determined that miR-429-3p promoted preadipocyte proliferation and differentiation, whereas LPIN1 exerted an opposite effect. Notably, we found that the miR-429-3p/LPIN1 axis facilitated PPARγ pathway activation, which is closely associated with the progression of adipogenesis. In conclusion, our results provide evidence that a novel miR-429-3p/LPIN1 axis is involved in the regulation of adipogenesis, which may have a guiding role in the improvement of breeding for abdominal fat traits in broiler chickens.

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“…Notably, the down-regulation of TRIB2 following circ_0084043 knock-down not only reduced proliferation, migration and invasion of BRAF-mutant A375 and SK-MEL-28 cells, but also inhibited β-catenin, c-Myc and cyclin D1 expression. These results highlighted the ability of circ_0084043/miR-429/TRIB2 axis to control the Wnt/β-catenin signaling pathway [121], which is frequently activated in EMT and metastasis [102]…”

Section: Accepted Articlementioning

confidence: 90%