Abstract
Autophagy is a widely conserved process in eukaryotes that is involved in a series of physiological and pathological events, including development, immunity, neurodegenerative disease, and tumorigenesis. It is regulated by nutrient deprivation, energy stress, and other unfavorable conditions through multiple pathways. In general, autophagy is synergistically governed at the RNA and protein levels. The upstream transcription factors trigger or inhibit the expression of autophagy- or lysosome-related genes to facilitate or reduce autophagy. Moreover, a significant number of non-coding RNAs (microRNA, circRNA, and lncRNA) are reported to participate in autophagy regulation. Finally, post-transcriptional modifications, such as RNA methylation, play a key role in controlling autophagy occurrence. In this review, we summarize the progress on autophagy research regarding transcriptional regulation, which will provide the foundations and directions for future studies on this self-eating process.
Highlights
Macroautophagy, hereafter referred to as autophagy, is the main type of autophagy, which is characterized by the formation of autophagosomes
LncRNA HOX transcript antisense RNA (HOTAIR) downregulates the expression of LC3B, BECLIN1, ATG3, and ATG7 to inhibit autophagy, which suppresses the invasion of oral squamous cell carcinoma cells [57]
Many studies have unveiled that several transcription factors, including MIT/TFE, PPARα, ATF4, E2F1, C/EBPβ, FOXO, NF-κB, E93, Signal transducer and activator of transcription (STAT), and p53, are critical for autophagy induction in response to various upstream signal cascades [13,16,23,33,70]
Summary
Macroautophagy, hereafter referred to as autophagy, is the main type of autophagy, which is characterized by the formation of autophagosomes. Small heterodimer partner (SHP), which is an orphan nuclear receptor responsible for maintaining the homeostasis of bile acids, is required for hFGF19 (bile acid-induced fibroblast growth factor-19, mFGF15)mediated inhibition of hepatic autophagy, and plays a negative role in autophagy induction through FGF19-SHP-LSD1 axis by repressing the expression of most autophagy-associated genes, including Atg, Atg, Atg, Atg, WIPI1, Uvrag, and Tfeb. In preadipocyte 3T3-L1 cells, adipogenic transcription factors C/EBPβ (CCAAT/enhancer binding protein beta) and PPARγ (peroxisome proliferator-activated receptor gamma) directly bind to the promoter region of autophagy genes, leading to the expression of LC3, Beclin, and Atg4b, to facilitate autophagy. The overexpression of TGA9 upregulates the mRNA levels of Atg genes and induces autophagy [31] Knockdown of E93 reduces the expression of several Atg genes in B. mori [40]. 20E-EcR-USP upregulates the transcription of Atg genes to induce autophagy [11]
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