Open AccessSequestosome 1/p62: A multitasker in the regulation of malignant tumor aggression (Review)
Author(s) -
Jinlong Tang,
Yuan Li,
Shuli Xia,
Jinfan Li,
Qi Yang,
Kefeng Ding,
Honghe Zhang
Publication year - 2021
Publication title -
international journal of oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.405
H-Index - 122
ISSN - 1019-6439
DOI - 10.3892/ijo.2021.5257
Subject(s) - sequestosome 1 , oncogene , biology , cancer research , epithelial–mesenchymal transition , cell cycle , autophagy , tumor microenvironment , cancer , tumor progression , signal transducing adaptor protein , deubiquitinating enzyme , apoptosis , regulator , signal transduction , microbiology and biotechnology , metastasis , ubiquitin , gene , genetics , tumor cells
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.