Ask about this productRelated genes to: ARNTL2 antibody
- Gene:
- ARNTL2 NIH gene
- Name:
- aryl hydrocarbon receptor nuclear translocator like 2
- Previous symbol:
- -
- Synonyms:
- BMAL2, MOP9, CLIF, PASD9, bHLHe6
- Chromosome:
- 12p11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2003-08-21
- Date modifiied:
- 2016-10-05
Related products to: ARNTL2 antibody
Related articles to: ARNTL2 antibody
- Nonsmall cell lung cancer (NSCLC) is the predominant form of lung cancer. Ferroptosis is a novel therapeutic target against treatment resistance in NSCLC. However, its regulation by m6A RNA modification remains incompletely elucidated. m6A RNA modification mediates mRNA stability, translation, and splicing to target transcripts. Methyltransferase like 7B (METTL7B) has been implicated in tumor progression, but its role in NSCLC ferroptosis m6A modification has not been reported. We aimed to investigate the mechanism of METTL7B-mediated m6A modification in NSCLC cell ferroptosis. NSCLC cells (SK-MES-1/PC9/H1975/A549) and normal cells (BEAS-2B) were cultured. The expression of METTL7B, long non-coding RNA 02159 (LINC02159), and aryl hydrocarbon receptor nuclear translocator-like 2 (ARNTL2) was determined. After METTL7B knockdown, cell viability was measured by MTT assay; ferroptosis-related factors were analyzed. m6A quantification was performed. m6A enrichment on LINC02159 was analyzed. The interaction between LINC02159 and KAT2A was verified. KAT2A and H3K27ac enrichment on the ARNTL2 promoter was detected. The roles of LINC02159 and ARNTL2 were validated. METTL7B, LINC02159, and ARNTL2 were upregulated in NSCLC cells compared to BEAS-2B cells. METTL7B knockdown increased iron ions, reactive oxygen species, and malondialdehyde levels and decreased cell viability, superoxide dismutase, and glutathione levels. METTL7B potentially upregulated LINC02159 expression through m6A modification. LINC02159 may recruit KAT2A to enhance H3K27ac enrichment on the ARNTL2 promoter, thereby promoting ARNTL2 expression. Overexpression of LINC02159 or ARNTL2 partially reversed the pro-ferroptotic effects of METTL7B knockdown on NSCLC cells. In conclusion, METTL7B inhibits ferroptosis in NSCLC cells the LINC02159/KAT2A/ARNTL2 axis in an m6A-dependent manner. - Source: PubMed
Publication date: 2026/03/12
Tao RancenLiu ZuoZhang ZhenningZhang Zhenfa - Although the liver exhibits remarkable regenerative capacity, expanding hepatocytes in large quantities in vitro without compromising their function remains challenging, presumably due to the absence of key environmental signals. Identifying factors that enable long-term in vitro expansion of hepatocytes is essential for advancing liver research. - Source: PubMed
Publication date: 2026/02/03
Li BingGuo RenWang ShitongZhang JingweiWang ShunYuan QiantingZheng HuixiangWang YaxuanSun BinTang ErjiangXie Xin - To analyze the expression of Aryl Hydrocarbon Receptor Nuclear Translocator-Like 2 (ARNTL2) and miR-204-5p in non-small cell lung cancer (NSCLC) patients and their correlation with clinicopathological characteristics. - Source: PubMed
Publication date: 2025/12/15
You ShuyingLi NaZeng XiangboWang Lile - Aryl hydrocarbon receptor nuclear transporter-like 2 (ARNTL2) can bind to clock circadian regulator (CLOCK) to regulate gene expression and is abnormally expressed in various cancers. Nevertheless, its effects on esophageal cancer (ESCC) are unclear. This work can uncover the intriguing mechanism of ARNTL2 in ESCC. - Source: PubMed
Publication date: 2025/11/16
Qin YanziCi HongfeiWang ZhaoyiZhang YandieXu XifengWu Qiang - : The circadian rhythm regulates important functions in the body, such as metabolism, the cell cycle, DNA repair, and immune balance. Disruption of this rhythm can contribute to the development of cancer. Circadian rhythm genes (CRGs) are attracting attention for their connection to various cancers. However, their roles in LUAD are not yet well understood. Additionally, our knowledge of how they function at both the bulk tissue and single-cell levels is limited. This gap hinders a complete understanding of how CRGs impact the development and outcomes of LUAD. : We selected 554 CRGs from public databases. We then obtained transcriptome data from TCGA and GEO. A total of 101 machine learning algorithm combinations were tested using 10 algorithms and 10-fold cross-validation. The best-performing model was based on Stepwise Cox regression and SuperPC. This model was validated with additional datasets. We also examined the relationships between CRGs, immune features, tumor mutation burden (TMB), and the response to immunotherapy. Drug sensitivity was also assessed. Single-cell data identified the cell types with active CRGs. Next, we performed qRT-PCR and other basic experiments to validate the expression of ARNTL2 in LUAD tissues and cell lines. The results indicated that ARNTL2 may play a key role in lung adenocarcinoma. : The CRG-based model clearly distinguished LUAD patients based on their risk. High-risk patients exhibited low immune activity, high TMB, and poor predicted responses to immunotherapy. Single-cell data revealed strong CRG signals in epithelial and fibroblast cells. These cell groups also displayed different communication patterns. Laboratory experiments showed that ARNTL2 was highly expressed in LUAD. It promoted cell growth, movement, and invasion. This suggests that ARNTL2 may play a role in promoting cancer. : This study developed a machine learning model based on CRGs. It can predict survival and immune status in LUAD patients. The research also identified ARNTL2 as a key gene that may contribute to cancer progression. These findings highlight the significance of the circadian rhythm in LUAD and provide new perspectives for diagnosis and treatment. - Source: PubMed
Publication date: 2025/09/05
Mu QiuqiaoZhang HanWang KaiTan LinLi XinSun Daqiang