Genomic instability establishes dependencies on acquired gene regulatory networks: A novel role of p62 in myeloid malignancies with del(5q)

Fang, Jing; Starczynowski, Daniel T.

doi:10.1080/23723556.2015.1014219

Cited by 2 publications

(2 citation statements)

References 10 publications

(9 reference statements)

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“…Importantly, in the study, the lack of p62 had little effect on the lifespan and function of normal HSPCs. This suggested that disturbing p62/TRAF6 binding may hold promise for treating miR-146a-deficient leukemia 127 .…”

Section: Autophagy-related Proteins Affect Human Disease By Regulatin...mentioning

confidence: 99%

Autophagy-related Proteins in Genome Stability: Autophagy-Dependent and Independent Actions

Zhang¹,

Guo²,

Wang³

et al. 2022

Int. J. Biol. Sci.

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It is emerging that autophagy-related proteins regulate the adaptive response to DNA damage in maintaining genome stability at multiple pathways. Here, we discuss recent insights into how autophagy-related proteins participate in DNA damage repair processes, influence chromosomal instability, and regulate the cell cycle through autophagy-dependent and independent actions. There is increasing awareness of the importance of these pathways mediated by autophagy-related proteins to DNA damage response (DDR), and disturbances in these regulatory connections may be linked to genomic instability participated in various human diseases, such as cancer and aging.

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Section: Autophagy-related Proteins Affect Human Disease By Regulatin...mentioning

confidence: 99%

Autophagy-related Proteins in Genome Stability: Autophagy-Dependent and Independent Actions

Zhang¹,

Guo²,

Wang³

et al. 2022

Int. J. Biol. Sci.

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“…In multiple myeloma cells treated with TNF-α, high-risk myelodysplastic syndromes/acute myeloid leukemia (AML) del(5q) cells and hematopoietic stem cells/progenitor cells with miR-146a deletion, the sustained expression of SQSTM1/p62 has an oncogenic effect that leads to the marked activation of NF-κB or p38 MAPK cascades through the following mechanisms: i) Direct binding to and ubiquitination of TRAF-6 through its TRAF-binding domain to activate the NF-κB signaling pathway (63)(64)(65); ii) direct binding with receptor-interacting protein 1 through its C-terminal region ZZ domain, as well as with atypical PKCs through its N-terminal PB1 domain to activate the NF-κB signaling pathway (66,67); and iii) direct binding to p38 MAPK through its p38 domain to activate the p38 MAPK signaling pathway (68). Activated NF-κB can further enhance SQSTM1/p62 gene expression, ultimately generating predominately positive feedback loops to continuously amplify its deleterious effect in exacerbating unrestrained growth, proliferation and malignant transformation, and inhibiting osteoblast activation to hamper bone formation (66,69).…”

Section: Hematological Malignancymentioning

confidence: 99%

Sequestosome 1/p62: A multitasker in the regulation of malignant tumor aggression (Review)

Tang

Xia

et al. 2021

Int J Oncol

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Sequestosome 1 (SQSTM1)/p62 is an adapter protein mainly involved in the transportation, degradation and destruction of various proteins that cooperates with components of autophagy and the ubiquitin-proteasome degradation pathway. Numerous studies have shown that SQSTM1/p62 functions at multiple levels, including involvement in genetic stability or modification, post-transcriptional regulation and protein function. As a result, SQSTM1/p62 is a versatile protein that is a critical core regulator of tumor cell genetic stability, autophagy, apoptosis and other forms of cell death, malignant growth, proliferation, migration, invasion, metastasis and chemoradiotherapeutic response, and an indicator of patient prognosis. SQSTM1/p62 regulates these processes via its distinct molecular structure, through which it participates in a variety of activating or inactivating tumor-related and tumor microenvironment-related signaling pathways, particularly positive feedback loops and epithelial-mesenchymal transition-related pathways. Therefore, functioning as a proto-oncogene or tumor suppressor gene in various types of cancer and tumor-associated microenvironments, SQSTM1/p62 is capable of promoting or retarding malignant tumor aggression, giving rise to immeasurable effects on tumor occurrence and development, and on patient treatment and prognosis.

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Genomic instability establishes dependencies on acquired gene regulatory networks: A novel role of p62 in myeloid malignancies with del(5q)

Cited by 2 publications

References 10 publications

Autophagy-related Proteins in Genome Stability: Autophagy-Dependent and Independent Actions

Autophagy-related Proteins in Genome Stability: Autophagy-Dependent and Independent Actions

Sequestosome 1/p62: A multitasker in the regulation of malignant tumor aggression (Review)

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