NUP62, nucleoporin 62, 23636

N. diseases: 273; N. variants: 6
Source: ALL
Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE Dynamic LC3B and p62 changes are suggested to be involved in gastric tumorigenesis and cancer progression. 31810936 2019
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 AlteredExpression phenotype BEFREE Our data indicate that accumulation of p62 by impaired autophagic flux is involved in the activation of NRF2 and contributes to skin tumorigenesis due to chronic arsenite exposure. 31781319 2019
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE Overall, our findings place Nrf2 and p62 as the key components of the mesenchymal subtype network, with implications to tumorigenesis and treatment resistance. 31444413 2019
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE Recent studies have demonstrated that p62 has a close relationship with tumorigenesis and progression, but the impact of p62 on patients' survival has not been comprehensively understood. 30410612 2018
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE Together, this work demonstrates that FliI functions as a checkpoint protein for selective autophagy in the crosstalk between FliI and p62-recruited cargoes, and its phosphorylation may serve as a prognostic marker for breast cancer.<b>Significance:</b> Flightless-I functions as a checkpoint protein for selective autophagy by interacting with p62 to block its recognition of LC3, leading to tumorigenesis in breast cancer.<i></i>. 29898994 2018
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE The concerted metabolic reprogramming across cancer and normal cellular compartments of the tumor microenvironment can favor tumorigenesis by increasing the survival and proliferating capacities of transformed cells. p62 has emerged as a critical signaling adaptor, beyond its role in autophagy, by playing an intricate context-dependent role in metabolic reprogramming of the cell types of the tumor and stroma, which shapes the tumor microenvironment to control tumor progression. 29702207 2018
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE The multidomain scaffold protein p62 (also called sequestosome-1) is involved in autophagy, antimicrobial immunity, and oncogenesis. 30514811 2018
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE Our findings have identified LIMD1 as a novel player in EBV latency and oncogenesis, and open a novel research avenue, in which LIMD1 and p62 play crucial roles in linking DNA damage response (DDR), apoptosis, and autophagy and their potential interplay during viral oncogenesis. 29464072 2018
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 AlteredExpression phenotype BEFREE Verteporfin inhibited tumorigenesis of both normal prostate epithelial cells with p62 expression and prostate cancer cells and decreased p62, constitutive Nrf2, and Bcl-xL in xenograft tumor tissues, indicating that p62 can be developed as a drug target against prostate cancer. 29368435 2018
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE Here we report that p62 is a critical mediator of TSC2-driven tumorigenesis, as Tsc2<sup>+/-</sup> and Tsc2f/f Ksp-CreERT2<sup>+</sup> mice crossed to p62<sup>-/-</sup> mice were protected from renal tumor development. 28512249 2017
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE Recently, tolerance to cisplatin has been attributed to other factors unrelated to DNA. p62 (also known as SQSTM1) functions as a multifunctional hub participating in tumorigenesis and may be a therapeutic target. 28498503 2017
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 AlteredExpression phenotype BEFREE Thus, p62 directly targets nuclear transcription factors to control metabolic reprogramming in the microenvironment and repress tumorigenesis, and identifies ATF4 as a synthetic vulnerability in p62-deficient tumor stroma. 28988820 2017
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE Suppression of autophagy causes p62 accumulation and thereby contributes to tumorigenesis. 24927592 2014
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 AlteredExpression phenotype BEFREE Here we show that p62 levels were reduced in the stroma of several tumors and that its loss in the tumor microenvironment or stromal fibroblasts resulted in increased tumorigenesis of epithelial prostate cancer cells. 25002027 2014
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE The ectopic overexpression of p62 and autophagy activation contributes to colorectal tumorigenesis. p62 and autophagy will be therapy targets for the treatment of colorectal cancer. 24065390 2014
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 PosttranslationalModification phenotype BEFREE The lack of cdk1-mediated phosphorylation of p62 leads to a faster exit from mitosis, which translates into enhanced cell proliferation and tumorigenesis in response to Ras-induced transformation. 20974803 2011
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 AlteredExpression phenotype BEFREE GTF2H1, the p62 subunit of the multiprotein complex transcription factor IIH (TFIIH), participates in both the nucleotide excision repair process and transcription control by specifically interacting with a variety of factors important in carcinogenesis. 18692935 2009