Aurora kinase A, as a pro-carcinogenic in gastric cancer and glioma kinase, is enhanced in several human tumors. However, it's regulatory mechanism in esophageal squamous cell carcinoma (ESCC) remains unclear. Thus, this study aimed to investigate the expression status, functional roles, and molecular mechanisms of AURKA in ESCC development. AURKA expression was analyzed by the screening of the GEO database and detected using an immunohistochemical method. The biological function of AURKA on ESCC was evaluated in vitro and in vivo. Western blot assay, malondialdehyde (MDA), iron, and glutathione (GSH) kits were utilized to assess changes in ferroptosis. Database analysis results showed that AURKA was a differential gene in ESCC and was highly expressed in human ESCC tissues. Functionally, AURKA knockdown decreased ESCC cell proliferation, invasion, and metastasis both in vitro and in vivo. Moreover, when AURKA was knockdown, cells were more correctly blocked in the G2/M phase, and the ferroptosis-related MDA and Fe increased, whereas the GSH reduced. Consistently, Glutathione peroxidase 4 (GPX4) and solute carrier family 7a member 11 (SLC7A11) expression were downregulated by AURKA knockdown. However, ferroptosis inhibitor partially restore ESCC cell proliferation, invasion, and metastasis caused by AURKA knockdown. AURKA knockdown enhances ferroptosis and acts against cancer progression in ESCC. AURKA acts as a tumor-promoting gene and may serve as potential target for ESCC treatment.

The present study aimed to explore the central relationship between cardiovascular conditions and aging. D-galactose (D-gal) was utilized to induce an accelerated aging model and to evaluate the effects of hydrogen sulfide (H₂S) on aging-related cardiovascular risk factors and mechanisms. Eight-week-old Sprague Dawley rats were given an intraperitoneal injection of 250 mg/kg D-gal every day with or without H₂S (56 μmol/kg) for 12 weeks. We found that D-gal treatment induced a noticeably aging-related increase in p16, p53 and p21 protein levels and senescence-associated beta-galactosidase staining. In addition, the level of noradrenalin was increased, accompanied by enhanced blood pressure and renal sympathetic nerve activity in aged rats. The greater sympathetic responses were related with the increased level of inflammation. The decreased level of klotho in the paraventricular nucleus neuron also contributed to sympathetic activation in D-gal-induced aged rats. However, the exogenous administration of H₂S attenuated the sympathetic activity in aged rats, as evidenced by the decreased blood pressure, renal sympathetic nerve activity and noradrenalin level. The ameliorated cellular senescence, inflammation and heightened klotho in the paraventricular nucleus were attributed to the protective effects of H₂S. The present study provides further evidence for the drug development of H₂S for the prevention or treatment of the aging-associated cardiovascular diseases.

通过细胞实验和动物实验结果，探讨miR-2110对肺腺癌（lung adenocarcinoma, LUAD）细胞增殖、凋亡及转移等生物学行为的影响。 通过生物信息学网站（ENCORI、TargetScan、miRTarBase和Tarbase）分析在LUAD组织中miR-2110的表达变化并进行miR-2110靶基因的预测。收集LUAD组织样本及肺腺癌细胞通过PCR技术验证miR-2110的表达变化。采用CCK-8、克隆形成实验、Transwell和流式细胞术分析LUAD细胞的功能变化。将10只6～8周龄BALB/c雌性裸鼠随机分为2组，通过体内实验验证miR-2110对LUAD的影响。 miR-2110在LUAD组织及细胞中相比于正常肺组织显著降低，其过表达可抑制LUAD细胞的增殖、转移并促进了肿瘤细胞的凋亡（P<0.05）。通过生物信息学预测和双荧光素酶报告基因测定，验证了miR-2110可靶向结合CDT1，并通过过表达CDT1基因发现相比于过表达miR-2110组，逆转了其增殖、转移和凋亡的作用（P<0.05）。裸鼠体内实验发现相比于对照组，过表达miR-2110可以明显降低肿瘤的增殖指标Ki67和转移指标vimentin、MMP9的表达。 miR-2110可以通过靶向CDT1抑制LUAD的增殖、转移，为LUAD的治疗提供新的依据。