A lysosome-targetable fluorescent probe for the ratiometric detection of formaldehyde in living cells and in vivo.

Inspired by the synthetic method of benzoxazine derivatives and our previous research, a fluorescent probe (SWJT-6) was designed for formaldehyde (FA) detection based on the cyclization reaction. The synthetic SWJT-6 showed excellent colorimetric and ratiometric response to formaldehyde, and could be perfectly used as test strips to detect formaldehyde. It also showed a fast detection time (3 min), low detection limit (5.65 µM) and high selectivity for formaldehyde within various interfering analytes. In addition, SWJT-6 has been successfully applied in bioimaging of intracellular and lysosomal formaldehyde in both HeLa cells and zebrafish.

Down-regulation expression of TGFB2-AS1 inhibits the proliferation, migration, invasion and induces apoptosis in HepG2 cells.

BACKGROUND: Hepatocellular carcinoma (HCC) is the leading cause of cancer mortality and without effective prognosis. Previous study has been confirmed that the abnormal expression of long non-coding RNAs (lncRNAs) TGFB2-AS1 was involved in tumorigenesis. However, the biological functions of TGFB2-AS1 in hepatocellular carcinoma (HCC) remain largely unclear. OBJECTIVE: We comprehensively assess the clinical significance of TGFB2-AS1 and investigate the biological functions of TGFB2-AS1 on HCC HepG2 cells. METHODS: We firstly confirmed the expression of TGFB2-AS1 between tumor and normal tissues using public available transcriptome data. We analyzed the clinical significance of TGFB2-AS1 using the TCGA HCC datasets. The biological functions of TGFB2-AS1 on HCC HepG2 cells were explored by multiple in vitro assays. RESULTS: We found that TGFB2-AS1 was remarkably increased in HCC tissues (P = 0.00148) and exhibited a potential predictive marker for HCC, with an area under curve (AUC) of 0.708 (P = 0.0034) using the fifty pairs of matched HCC tissues of TCGA. Besides, higher expression of TGFB2-AS1 in HCC tissues was identified as being positively associated with advanced tumor (P = 0.012) and disease stage (P = 0.009) in 355 HCC cases using independent sample nonparametric test. Downregulation of TGFB2-AS1 expression significantly restrained proliferation (P < 0.01) and impaired colony formation (P < 0.05). Furthermore, TGFB2-AS1 depletion remarkably promoted the apoptosis of HepG2 cells (P < 0.05) and inhibited migration and invasion (P < 0.01). CONCLUSION: Taken together, these findings suggested that TGFB2-AS1 might serve as a potential therapeutic target for HCC.