Despite the widespread theranostic utilization of cyanine dyes (Cy7), their synthetic method is still limited with pyridine or cyclohexanone derivatives as starting materials. Herein, we report the synthesis of Cy7 from furfural derivatives. First, a one-pot reaction strategy is developed to solve the unstable problem of the Stenhouse salts. Second, a stepwise condensation strategy is exploited to regioselectively synthesize asymmetrical Cy7. The methodology possesses advantages, such as easy handling, high yield, wide substrate scopes, and good functional group tolerance.

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Peroxynitrite (ONOO−) is a crucial reactive oxygen species that plays a vital role in cellular signal transduction and homeostatic regulation. Determining and visualizing peroxynitrite accurately in biological systems is important for understanding its roles in physiological and pathological activity. Among the various detection methods, fluorescent probe-based spectroscopic detection offers real-time and minimally invasive detection, high sensitivity and selectivity, and easy structural and property modification. This review categorizes fluorescent probes by their fluorophore structures, highlighting their chemical structures, recognition mechanisms, and response behaviors in detail. We hope that this review could help trigger novel ideas for potential medical diagnostic applications of peroxynitrite-related molecular diseases.

Background: Synthetic lethality is a new strategy of cancer therapy. Epigenetic based synthetic lethality may provide more opportunities for cancer prevention and treatment. TMEM176A is frequently methylated in esophageal, hepatic and colorectal cancer. The role of TMEM176A methylation in lung cancer and its therapeutic application remains unclear.Methods: Nine lung cancer cell lines and 123 cases of cancer tissue samples were employed. Methylation specific PCR, MTT assay, flow cytometry, and xenograft mouse models were applied.Results: The expression of TMEM176A was found to be regulated by promoter region methylation in lung cancer cells. TMEM176A was methylated in 53.66% (66/123) of primary lung cancer. Reduced expression of TMEM176A was associated with promoter region methylation in 40 cases of matched lung cancer and adjacent tissue samples (P<0.05). No association was found between TMEM176A methylation and age, gender, alcohol abuse, smoking, tumor size, lymph node metastasis, differentiation and TNM stage (all P >0.05). Restoration of TMEM176A expression induced cell apoptosis and G2/M phase arrest and inhibited colony formation, cell proliferation, migration and invasion in H1299 and H23 cells. TMEM176A suppressed H1299 cell xenograft growth in mice. Methylation of TMEM176A activated ERK1/2 signaling, and sensitized H1299 and H23 cells to AZD0156, an ATM inhibitor.Conclusion: TMEM176A is frequently methylated in human lung cancer, and the expression of TMEM176A is regulated by promoter region methylation. TMEM176A suppresses lung cancer growth by inhibiting ERK1/2 signaling. Methylation of TMEM176A is a potential lung cancer diagnostic marker and a novel synthetic lethal therapeutic marker for AZD0156, an ATM inhibitor.