ARNTL2 _ BMAL2
- Known as:
- ARNTL2 _ BMAL2
- Catalog number:
- ARP39398_P050
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- ARNTL2 _ BMAL2
Related genes to: ARNTL2 _ BMAL2
- 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 _ BMAL2
Related articles to: ARNTL2 _ BMAL2
- This study investigated the prognostic value and molecular mechanisms of miR-517c-3p in lung cancer. miR-517c-3p in 112 lung cancer tissues was detected using qRT-PCR. Kaplan-Meier survival analysis and Cox regression were used to assess its prognostic significance. Functional experiments, including cell proliferation, migration, and invasion, were conducted in lung cancer cell lines (H1229, A549) after miR-517c-3p overexpression. Target gene prediction and validation were performed using bioinformatics tools and dual-luciferase reporter assays. The regulatory effects of miR-517c-3p on ARNTL2 were further explored through gene overexpression and rescue experiments. miR-517c-3p was significantly downregulated in lung cancer tissues (p < 0.001) and correlated with advanced TNM stage, lymph node metastasis, and larger tumor size. Patients with low miR-517c-3p expression exhibited poorer overall survival (p < 0.001), and Cox regression identified miR-517c-3p as an independent prognostic factor (HR = 0.110, 95% CI = 0.047-0.256). Functional assays demonstrated that miR-517c-3p overexpression inhibited lung cancer cell proliferation, migration, and invasion. Dual-luciferase reporter assays confirmed ARNTL2 as a direct target of miR-517c-3p, and ARNTL2 restoration reversed the suppressive effects of miR-517c-3p on tumor progression. miR-517c-3p is significantly downregulated in lung cancer and associated with poor patient prognosis. Furthermore, miR-517c-3p suppresses tumor progression by directly targeting ARNTL2. - Source: PubMed
Chen JiaRen QiuSun BowenSun YongJiang HongjieWang Junwen - 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