Fluorescent nanoprobes show similar fluorescence properties to traditional organic dyes, but the addition of nanotechnology accurately controls the size, shape, chemical composition, and surface chemistry of the nanoprobes with unique characteristics and properties, such as bright luminescence, high photostability, and strong biocompatibility. For example, modifying aptamers or antibodies on a fluorescent nanoprobe provides high selectivity and specificity for different objects to be tested. Fluorescence intensity, life, and other parameters of targets can be changed by different sensing mechanisms based on the unique structural and optical characteristics of fluorescent nanoprobes. What’s more, the detection of fluorescent nanoprobes is cost-saving, simple, and offers great advantages in rapid food detection. Sensing mechanisms of fluorescent nanoprobes were introduced in this paper, focusing on the application progress in pesticide residues, veterinary drug residues, heavy metals, microbes, mycotoxins, and other substances in food safety detection in recent years. A brief outlook for future development was provided as well.

Purpose: Regulator of G-protein signaling (RGS) proteins are GTPase-activating proteins that target the α-subunit of heterotrimeric G proteins. Many studies have shown that RGS proteins contribute to tumorigenesis and metastasis. However, the mechanism in which RGS proteins, especially RGS4, affect the development of non-small cell lung cancer (NSCLC) remains unclear. The aim of this study was to characterize the role of RGS4 in NSCLC. Methods: RGS4 expression in NSCLC tissues was assessed using an immunohistochemistry tissue microarray. Additionally, RGS4 was knocked down using short-hairpin RNA to assess the regulatory function of RGS4 in the biological behaviors of human NSCLC cell lines. A xenograft lung cancer model in nude BALB/c mice was established to study whether RGS4 knockdown inhibits cancer cell proliferation in vivo. Results: We observed an increase in RGS4 protein levels in NSCLC samples. RGS4 knockdown inhibited cell proliferation and induced apoptosis in H1299 and PC9 cell lines, but did not affect cell migration. Moreover, we found that RGS4 negatively regulated the expression of microRNA-16 (miR-16), a tumor suppressor. The inhibition of miR-16 resulted in upregulated RGS4 expression. We also found that RGS4 regulated the expression of brain-derived neurotrophic factor (BDNF) and activated the BDNF-tropomyosin receptor kinase B signaling pathway. Conclusion: This study revealed that RGS4 overexpression positively correlated with the development of NSCLC. TDownstream RGS4 targets (eg, miR-16 and BDNF) might be involved in the development of NSCLC and may serve as potential therapeutic targets for its treatment.

Background: The aberrant expression of microRNA-454 (miR-454) has been confirmed to be involved in the development of cancers. However, the functional role of miR-454 in the progression of ovarian cancer remains unclear. Methods: The expression of miR-454 in ovarian cancer cells and serum of ovarian cancer patients was detected by RT-PCR. CCK8, colony formation, transwell, and flow cytometry assays were conducted to assess the effects of miR-454 on ovarian cancer cell proliferation, migration, invasion, and apoptosis, respectively. Dual-luciferase reporter assay was used to confirm the targeting relationship between miR-454 and E2F6. The expression pattern of E2F6 in ovarian cancer tissues was detected using immunohistochemistry (IHC) assay. The relative expression of related proteins was examined using western blot analysis. Results: miR-454 was markedly down-regulated by hypoxia in ovarian cancer cells. Compared with normal samples, the expression of miR-454 was up-regulated in the serum of ovarian cancer patients, and correlated with the clinicopathological stages of ovarian cancer. Next, we found that miR-454 overexpression inhibited the proliferation, migration and invasion of OVCAR3 and SKOV3 cells, as well as promoted apoptosis. In addition, the Akt/mTOR and Wnt/β-catenin signaling pathway were inhibited by miR-454 in ovarian cancer cells. Mechanically, bioinformatic analysis and dual-luciferase reporter assay confirmed that E2F6 was a direct target of miR-454 and negatively regulated by miR-454 in ovarian cancer cells. Moreover, IHC analysis showed that E2F6 was highly expressed in ovarian cancer tissues. Finally, we found that the increasing cell proliferation and migration triggered by E2F6 overexpression were abolished by miR-454 overexpression. Conclusion: Taken together, these results highlight the role of miR-454 as a tumor suppressor in ovarian cancer cells by targeting E2F6, indicating that miR-454 may be a potential diagnostic biomarker and therapeutic target for ovarian cancer.

Hepatocellular carcinoma (HCC) is a common and highly malignancy tumor. Pyrroline-5-carpoxylate reductase-1 (PYCR1) is an active enzyme involved in cell metabolism. In this study, we explored the role of PYCR1 in the HCC cell lines, Hep3B and HepG2. The expression of PYCR1 was up-regulated in liver hepatocellular carcinoma (LIHC) tissue by GEPIA. Meanwhile the overall survival rate (OS) showed that patients with high PYCR1 expression had a worse prognosis compared with patients with low PYCR1 level. In addition, knockdown of PYCR1 suppressed the proliferation, invasion and migration of Hep3B and HepG2 cells and promoted the apoptosis and G1 arrest. Knockdown of PYCR1 reduced the expression of the anti-apoptotic protein Bcl-2 and increased the expression of pro-apoptotic protein Bax and Caspase3. Furthermore, knockdown of PYCR1 changed the expression of p-AKT and its target gene Cyclin D1. In conclusion, knockdown of PYCR1 inhibited the malignant phenotype of human HCC cells by regulating the AKT pathway activation, which provides a potential strategy for the human HCC therapy.

Protein arginine methyltransferase 5 (PRMT5) complexes with methylosome protein 50 (MEP50) play crucial roles in tumor progress. However, the regulatory mechanism of governing the PRMT5-MEP50 hetero-octameric complex remains unclear. Here, we demonstrate that C6orf223, to our knowledge an uncharacterized protein, facilitates PRMT5-MEP50 multiprotein complex assembling, thereby promoting colorectal cancer (CRC) growth and metastasis. C6orf223 forms dimers through disulfide bonds, with its N-terminal arginine-enriched region binding to the C-terminal negatively charged groove of PRMT5, thus stabilizing PRMT5-MEP50 multiprotein and enhancing PRMT5 methyltransferase activity. Consequently, PRMT5-mediated H4R3me2s substantially decreases the expression of the tumor suppressor GATA5, leading to the upregulation of multiple oncogenic target genes including WWTR1, FGFR1, and CLU. Targeting C6orf223 using siRNAs encapsulated in ferritin protein shells effectively suppresses CRC tumor growth and metastasis. Collectively, our findings characterize the role of C6orf223 in facilitating PRMT5-MEP50 hetero-octameric complex assembling and suggest that C6orf223 could serve as a potential therapeutic target for CRC.