An Rb family–independent E2F3 transcription factor variant impairs STAT5 signaling and mammary gland remodeling during pregnancy in mice

Liao, Yang; Du, Wei

doi:10.1074/jbc.ra117.000583

Cited by 8 publications

(7 citation statements)

References 57 publications

(63 reference statements)

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“…The E2F transcription factor is essential to cell proliferation. Complexes formed by E2F and Rb inhibit the expression of the E2F target genes, and Rb phosphorylation causes Rb to separate from E2F (Liao & Du, ). E2F1 is a member of the E2F transcription factor family and plays a vital role in regulating DNA synthesis, G1/S transition, and apoptosis (DeGregori, Leone, Miron, Jakoi, & Nevins, ; Wu et al, ).…”

Section: Resultsmentioning

confidence: 99%

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Kp‐10 promotes bovine mammary epithelial cell proliferation by activating GPR54 and its downstream signaling pathways

Cao

Wang

et al. 2019

Journal Cellular Physiology

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It has been reported that the proliferation and apoptosis of mammary epithelial cells affect milk production. Therefore, ensuring adequate mammary epithelial cells is expected to enhance milk production. This study is devoted to studying the effects of kisspeptin-10 (Kp-10), a peptide hormone composed of 10 amino acids, on bovine mammary epithelial cell (bMEC) proliferation and exploring the underlying mechanism of its action. bMECs were treated with various concentrations of Kp-10 (1, 10, 100, and 1,000 nM), and 100 nM Kp-10 promoted the proliferation of the bMECs. Kp-10 promoted the cell cycle transition from G1 to the S and G2 phases, increased the protein levels of Cyclin D1 and Cyclin D3, and reduced the expression levels of the p21 gene. This study also showed that inhibition of G protein-coupled receptor 54 (GPR54), AKT, mTOR, and ERK1/2 reduced the proliferation of the bMECs that had been induced by Kp-10. In addition, Kp-10 decreased the complexes formed by Rb and E2F1 and increased the expression levels of the E2F1 target genes. These results indicate that Kp-10 promotes bMEC proliferation by activating GPR54 and its downstream signaling pathways. K E Y W O R D S4EBP1, bMEC, Kp-10, proliferation, Rb/E2F1

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Section: Resultsmentioning

confidence: 99%

Section: Mtor Inhibitor Attenuates Kp-10-induced Proliferation Of Bmentioning

confidence: 99%

Kp‐10 promotes bovine mammary epithelial cell proliferation by activating GPR54 and its downstream signaling pathways

Cao

Wang

et al. 2019

Journal Cellular Physiology

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“…cDNA was synthesized using M-MLV reverse transcriptase from Promega. Quantitative real-time PCR was carried out as described 35 . Primer pairs used for reverse-transcription PCR (RT-PCR) are: human Sesn2, 5′-CTCCTG GCGCCACTACATTG-3′ (sense) and 5′-ACTCAGGGTCACCACCAGT-3′ (antisense); human CHOP, 5′-TGGAAGCCTGGTATGAGGAC-3′ (sense) and 5′-TGTGACCTCTGCTGGTTCTG-3′ (antisense); human ATF3, 5′-GCAGAGCTAAGCAGT CGTGG -3′ (sense) and 5′-CGCCT TGATGGTTCTCTGCT-3′ (antisense); human GAPDH, 5′-CTCTGACTTCAACAGCGACAC-3′ (sense) and 5′-CATACCAGGAAATGAGCTTGACAA-3′ (antisense); mouse Sesn2, 5′-GCACCTTCGCCTCCCAGTGA-3′ (sense) and 5′-GCAGGCTCTCCTGAAGCTGC-3′ (antisense); mouse GAPDH, 5′-GCACAGTCAAGGCCGAGAAT-3′ (sense) and 5′-GCCTTCTCCATGGTGGTGAA-3′ (antisense).…”

Section: Methodsmentioning

confidence: 99%

Ginseng metabolite Protopanaxadiol induces Sestrin2 expression and AMPK activation through GCN2 and PERK

Jin

Wang

et al. 2019

Cell Death Dis

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Ginseng is one of the most commonly used herbs that is believed to have a variety of biological activities, including reducing blood sugar and cholesterol levels, anti-cancer, and anti-diabetes activities. However, little is known about the molecular mechanisms involved. In this study, we showed that protopanaxadiol (PPD), a metabolite of the protopanaxadiol group ginsenosides that are the major pharmacological constituents of ginsengs, significantly altered the expression of genes involved in metabolism, elevated Sestrin2 (Sesn2) expression, activated AMPK, and induced autophagy. Using CRISPR/CAS9-mediated gene editing and shRNA-mediated gene silencing, we demonstrated that Sesn2 is required for PPD-induced AMPK activation and autophagy. Interestingly, we showed that PPD-induced Sesn2 expression is mediated redundantly by the GCN2/ATF4 amino acid-sensing pathway and the PERK/ATF4 endoplasmic reticulum (ER) stress pathway. Our results suggest that ginseng metabolite PPD modulates the metabolism of amino acids and lipids, leading to the activation of the stress-sensing kinases GCN2 and PERK to induce Sesn2 expression, which promotes AMPK activation, autophagy, and metabolic health.

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“…Total RNA was extracted using TRI reagent (Invitrogen) from about 30 eye/antenna discs dissected from 3rd instar larvae cultured at 25˚C with expression of RNAi constructs driven by eyFLP, Act>CD2>Gal4. cDNA synthesis and qRT-PCR reactions were performed as previously described [66]. Ribosomal protein gene rp49 was used as an internal control in qPCR analysis.…”

Section: Rna Isolation and Quantitative Real-time Pcrmentioning

confidence: 99%

NatB regulates Rb mutant cell death and tumor growth by modulating EGFR/MAPK signaling through the N-end rule pathways

Sheng

2020

PLoS Genet

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Inactivation of the Rb tumor suppressor causes context-dependent increases in cell proliferation or cell death. In a genetic screen for factors that promoted Rb mutant cell death in Drosophila, we identified Psid, a regulatory subunit of N-terminal acetyltransferase B (NatB). We showed that NatB subunits were required for elevated EGFR/MAPK signaling and Rb mutant cell survival. We showed that NatB regulates the posttranscriptional levels of the highly conserved pathway components Grb2/Drk, MAPK, and PP2AC but not that of the less conserved Sprouty. Interestingly, NatB increased the levels of positive pathway components Grb2/Drk and MAPK while decreased the levels of negative pathway component PP2AC, which were mediated by the distinct N-end rule branch E3 ubiquitin ligases Ubr4 and Cnot4, respectively. These results suggest a novel mechanism by which NatB and Nend rule pathways modulate EGFR/MAPK signaling by inversely regulating the levels of multiple conserved positive and negative pathway components. As inactivation of Psid blocked EGFR signaling-dependent tumor growth, this study raises the possibility that NatB is potentially a novel therapeutic target for cancers dependent on deregulated EGFR/Ras signaling.

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An Rb family–independent E2F3 transcription factor variant impairs STAT5 signaling and mammary gland remodeling during pregnancy in mice

Cited by 8 publications

References 57 publications

Kp‐10 promotes bovine mammary epithelial cell proliferation by activating GPR54 and its downstream signaling pathways

Kp‐10 promotes bovine mammary epithelial cell proliferation by activating GPR54 and its downstream signaling pathways

Ginseng metabolite Protopanaxadiol induces Sestrin2 expression and AMPK activation through GCN2 and PERK

NatB regulates Rb mutant cell death and tumor growth by modulating EGFR/MAPK signaling through the N-end rule pathways

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