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Last update 08 May 2025

BTG2

Last update 08 May 2025

Basic Info

Synonyms

APRO1, BTG anti-proliferation factor 2, BTG family member 2

+ [7]

Introduction

Anti-proliferative protein; the function is mediated by association with deadenylase subunits of the CCR4-NOT complex. Activates mRNA deadenylation in a CNOT6 and CNOT7-dependent manner. In vitro can inhibit deadenylase activity of CNOT7 and CNOT8. Involved in cell cycle regulation. Could be involved in the growth arrest and differentiation of the neuronal precursors (By similarity). Modulates transcription regulation mediated by ESR1. Involved in mitochondrial depolarization and neurite outgrowth.

Drugs associated with BTG2

HG-1339

Target

BTG2 x BTG3

Mechanism

BTG2 gene modulators [+1]

Active Org.-

Originator Org.

Human Genome Sciences, Inc.

Active Indication-

Inactive Indication

Neoplasms

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with BTG2

100 Translational Medicine associated with BTG2

0 Patents (Medical) associated with BTG2

625

Literatures (Medical) associated with BTG2

01 May 2025·Behavioural Brain Research

MiR-29a-3p ameliorate behavioral deficiency in hypoxia-ischemia brain damage in neonatal mice by inhibiting BTG2

Article

Author: Hu, Quan ; Xiao, Yilei ; Xing, Xiaohui ; Song, Yan ; Wang, Zhen ; Liu, Weiyang ; Luo, Qian ; Gu, Bing

It has been reported that miR-29a-3p played a part in series neurological disorders. However, it remains unclear whether miR-29a-3p participate in the pathological mechanism in hypoxia-ischemia (HI) brain injury. In this study, we detected the change of miR-29a-3p level in the ipsilateral cortex following HI brain injury and found that miR-29a-3p was significantly increased at 3 days in the ipsilateral cortex following HI insult in neonatal mice. Therefore, we further explored the role of miR-29a-3p in HI brain injury and its molecular mechanism. The results showed that miR-29a-3p mimics attenuated and miR-29a-3p antagomir aggravated brain infarction volume at 3 days following HI insult. We further found that overexpression of miR-29a-3p also suppressed apoptosis and neuroinflammation, reduced synaptic loss and prevent HI-induced microglial morphological changes 3 days following HI insult. Neurobehavioral tests revealed that overexpression of miR-29a-3p could improve both short-term and long-term behavioral defects after HI injury. Furthermore, we proved that miR-29a-3p targets B-cell translocation gene 2 (BTG2) and further inhibits the expression of Bax by luciferase reporter assay and qRT-PCR. Moreover, overexpression of miR-29a-3p, by applying liposomes through intranasal route, could also achieve the same therapeutic effect in HI injury. Our data showed that by inhibiting BTG2/Bax, increasing level of miR-29a-3p might serve as a strategy to prevent brain damage and behavioral deficiency in HI.

01 Apr 2025·Phytomedicine

Linggui Zhugan decoction ameliorating mitochondrial damage of doxorubicin-induced cardiotoxicity by modulating the AMPK-FOXO3a pathway targeting BTG2

Article

Author: Wang, Jia-Hua ; Li, Xue-Tao ; Cao, Hui-Min ; Kong, Liang ; Wang, Ya-Zhu ; Guo, Rui-Bo ; Jia, Lian-Qun ; Yu, Yang ; Lv, Mei-Jun ; Zang, Juan ; Zhang, Lu ; Liu, Yang ; Sun, Wan-Ping

BACKGROUNDDoxorubicin (DOX), a widely used anthracycline chemotherapy agent, is effective against various malignant tumors. However, its clinical application is significantly limited due to dose-dependent cardiotoxicity. Linggui Zhugan Decoction (LGZGD), a traditional Chinese medicine formulation, has demonstrated notable cardioprotective effects. However, its potential to mitigate DOX-induced cardiotoxicity (DIC) remains unexplored.OBJECTIVEThis study investigated the protective effects of LGZGD against DIC and explores its ability to enhance mitochondrial function by modulating the AMPK-FOXO3a pathway via targeting BTG2.METHODSA zebrafish DIC model was established to evaluate the cardioprotective effects of LGZGD on embryos and adults. Further investigations included in vitro studies with H9c2 cells and in vivo experiments using mouse models to assess LGZGD's pharmacological actions and their impact on mitochondrial function. Network pharmacology and transcriptomic analyses were performed to predict the potential mechanism of LGZGD in regulating the AMPK-FOXO3a pathway via BTG2. Verification was conducted through molecular docking, molecular dynamics (MD) simulations, and immunofluorescence co-localization.RESULTSLGZGD enhanced survival rates and alleviated heart tissue damage in zebrafish. In vitro, LGZGD reduced DOX-induced reactive oxygen species (ROS) production in H9c2 cells, decreased apoptosis, improved mitochondrial membrane potential, and preserved mitochondrial function. In vivo, LGZGD improved cardiac function and prevented myocardial structural damage in mice. Additionally, it mitigated oxidative stress, inflammation, and apoptosis while reversing DOX-induced mitochondrial structural damage. Network pharmacology and transcriptomic analyses suggested that LGZGD regulates the BTG2 gene and AMPK-FOXO3a pathway activity. Molecular docking, MDs, and immunofluorescence co-localization supported the hypothesis that LGZGD modulates the AMPK-FOXO3a pathway by targeting BTG2.CONCLUSIONLGZGD exerts significant cardioprotective effects against DIC by reducing oxidative stress, inflammation, and apoptosis preserving while mitochondrial structure and function. These findings offer a novel insight into LGZGD's clinical relevance in DIC management. Targeting BTG2 to regulate the AMPK-FOXO3a pathway highlights LGZGD as a promising therapeutic strategy for preventing and treating DIC.

01 Mar 2025·Journal of Assisted Reproduction and Genetics

B cell translocation gene 2 expression levels in human granulosa cells is negatively associated with in vitro fertilization/intracytoplasmic sperm injection outcomes: a pilot study

Article

Author: Zhao, Shuhua ; Rao, Meng ; Song, Mengjie ; Zhou, Ling ; Cheng, Yulin ; Wang, Huawei ; Luo, Jiahuan ; Wang, Longda ; Wang, Jinyuan ; Tang, Li

PURPOSEThis study aimed to monitor the expression of B-cell translocation gene 2 (BTG2) in granulosa cells of patients undergoing IVF/ICSI with respect blastocyst quality outcomes.METHODSWe recruited 181 women undergoing IVF/ICSI cycles for infertility. Granulosa cells were extracted from follicular fluid. BTG2 expression level of granulosa cells were stratified into tertiles (low, middle, and high), and the patients of each tertile were compared for outcome indicators by Kruskal-Wallis analysis. Spearman's correlation analyses were used to evaluate the correlation between BTG2 mRNA levels and outcome indicators. Generalized linear models and generalized additive models with smoothing splines were used to adjust for potential confounders.RESULTSPatients in the low BTG2 tertile had higher oocyte retrieval, fertilization, blastocyst formation, and high-quality blastocyst rates than those in the high BTG2 tertile. Patients in the high BTG2 tertile exhibited a downward trend in implantation and clinical pregnancy rates compared to those in the low or middle BTG2 tertiles, whereas the early pregnancy loss rate showed an upward trend, although the difference was not significant. After adjusting for confounding factors, the expression level of BTG2 was negatively correlated with oocyte retrieval, blastocyst formation, and high-quality blastocyst rates. Stratified analysis of AMH > 4 ng/ml showed elevated BTG2 expression was associated with reduced oocyte retrieval, fertilization, cleavage, blastocyst formation, and high-quality blastocyst rates. No differences in these outcomes were observed in patients with AMH ≤ 4 ng/ml.CONCLUSIONIn women with high AMH levels (> 4 ng/ml) elevated BTG2 expression in granulosa cells was associated with poor quality blastocyst outcomes.

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BTG2

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