Ask about this productRelated genes to: ADRA2C antibody
- Gene:
- ADRA2C NIH gene
- Name:
- adrenoceptor alpha 2C
- Previous symbol:
- ADRA2L2, ADRA2RL2
- Synonyms:
- ADRARL2
- Chromosome:
- 4p16.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2014-11-19
Related products to: ADRA2C antibody
Related articles to: ADRA2C antibody
- The antitumoral activity of monoamine receptor ligands appears to be important as a potential approach to cancer medication. In the present study, we evaluated the effects of trace amine compounds, including octopamine, tyramine, 3-methoxytyramine, and synephrine, on SH-SY5Y neuroblastoma cells. Previously, these compounds exhibited TAAR1-specific activity at nanomolar concentrations. However, in SH-SY5Y neuroblastoma cells, the effect of octopamine and 3-methoxytyramine was identified in concentrations of 1000 µM or above and is apparently non-specific. Neither public transcriptomic datasets nor qPCR analysis detected significant expression in SH-SY5Y cells, suggesting that the observed effects may be mediated by adrenoceptors. Among these, was the most highly expressed in SH-SY5Y cells. Analysis of transcriptomic data from the GEO database revealed that adrenoceptors are widely expressed in neuroblastomas. The expression profiles of adrenoceptors in tumors are polymorphic and more complex than in SH-SY5Y cells. Thus, the effects of trace amines on other neuroblastoma cell lines and in vivo tumors warrant further investigation, and the involvement of adrenoceptors in this process may be speculated. Our findings suggest the non-specific activity of trace amines against tumor cells, with a paradoxical stimulatory effect in differentiated neuroblastoma cells, which highlights the need for caution in studies involving TAAR1-specific compounds. - Source: PubMed
Publication date: 2026/06/02
Lopachev Aleksandr VKazanskaya Rogneda BGainetdinov Raul RKanov Evgeny VVaganova Anastasia N - Lidocaine, a widely used local anesthetic, has been reported to exert anti-cancer activity against hepatocellular carcinoma (HCC). However, its molecular mechanisms remain incompletely understood. This study sought to elucidate the mechanisms underlying lidocaine’s effects on HCC. Potential lidocaine targets in HepG2 cells were identified using network pharmacology and transcriptomic profiling. The prognostic and clinical relevance of candidate genes were assessed through bioinformatics analyses. Key targets were validated by RT–qPCR. The functional role of SLC6A3 in regulating HepG2 cell proliferation, apoptosis, migration, and invasion was examined through in vitro assays. Network pharmacology predicted 433 lidocaine targets, while transcriptomic profiling revealed 442 differentially expressed genes. Nine overlapping targets (SLC6A3, CHRNB2, GRIN1, ADRA2C, LIPE, SLC18A2, KCNQ2, TERT, and ALOX12) were enriched in pathways associated with neuronal signaling, synaptic transmission, and drug addiction. Among these, SLC6A3 and TERT were significantly associated with poor prognosis and increased tumor immune infiltration. Both genes demonstrated predictive value for 1- to 2-year survival, with SLC6A3 showing the stronger prognostic relevance. Molecular docking revealed hydrophobic interactions between lidocaine and SLC6A3 (binding energy: −5.6 kcal/mol). Silencing of SLC6A3 markedly promoted apoptosis and suppressed proliferation, migration, and invasion of HepG2 cells. Collectively, these findings suggest that lidocaine inhibits HCC progression by targeting and downregulating SLC6A3. Lidocaine exerts anti-HCC effects by directly targeting and downregulating SLC6A3, thereby inducing apoptosis and suppressing tumor progression. - Source: PubMed
Publication date: 2026/04/07
Li PeiyangTong WulanHe HongLiu HaoYang Xi - Drug-induced amnesia is underrecognized due to absence of label indications. This study utilized the FAERS database to identify drugs associated with amnesia and investigated causal relationships through Mendelian randomization (MR) analysis. - Source: PubMed
Publication date: 2026/03/17
Li ChenChen YanYao YinhuiShang Yazhen - This study aimed to integrate bioinformatics, network pharmacology, and single-cell sequencing to explore the potential neuro-immune mechanisms by which the traditional Chinese medicine formula Xiao-Yao-San (XYS) ameliorates chronic stress-induced colorectal cancer (CRC) progression. - Source: PubMed
Publication date: 2026/03/03
Li YingYang ShengyaLi HaoranLi HuachaoSun YunchuanHe XinyingZhang YingruWang Yan - Diethyl phthalate (DEP) is a ubiquitous environmental endocrine-disrupting chemical (EDC). Epidemiological studies have suggested a potential association between DEP exposure and an increased risk of endometrial cancer (EC); however, its underlying molecular mechanisms remain largely unclear. Four GEO datasets were integrated, and differential expression analysis combined with weighted gene co-expression network analysis (WGCNA) was performed to identify candidate genes potentially linking DEP exposure to EC. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted to explore relevant signaling pathways. Machine learning models, coupled with Shapley Additive Explanations (SHAP), were employed to prioritize key genes. Molecular docking and molecular dynamics (MD) simulations were used to assess the binding affinity between DEP and the identified targets. A series of in vitro experiments in EC cell lines were subsequently conducted to validate the biological effects of DEP. Nineteen overlapping DEP-EC genes were identified, predominantly enriched in the MAPK, cAMP, and cGMP-PKG signaling pathways. Among them, FOS, NR4A1, ADRA2C, JUN, and SLC6A2 were prioritized as core genes through machine learning and SHAP analysis. Molecular simulations confirmed stable binding between DEP and these targets. In vitro assays demonstrated that DEP exposure induces oxidative stress, significantly enhances ERK1/2 and AKT phosphorylation, upregulates Cyclin D1/CDK4 expression, promotes G1/S phase transition, and facilitates EC cell proliferation. These findings suggest that DEP may promote endometrial carcinogenesis by triggering oxidative stress-mediated signaling crosstalk and accelerating cell cycle progression. This study establishes a multi-layered methodological framework-from computational screening and machine learning to experimental validation-offering novel mechanistic insights into the carcinogenic potential of environmental endocrine disruptors such as DEP. - Source: PubMed
Publication date: 2026/02/10
Chen XiWang ZijingWang FengfengWu YuexiaoHu DanCheng YuemeiXing YijuanDu JunhongJiang TaoYang YongxiuLiang XiaoleiBi Xuehan