One of the main clinical treatment for advanced nasopharyngeal carcinoma is chemotherapy, but systemic administration can cause serious adverse reactions. New type of nanomaterial which can actively targeting, imaging and treating nasopharyngeal carcinoma at the same time to enhance the effect of chemotherapy, meanwhile monitoring the intracellular drug release process at the level of single cancer cell was urgently needed. GE11, an EGFR antagonist peptide, was used to target nasopharyngeal carcinoma which has positive expression of EGFR on its nucleus. GE11 modified graphene quantum dots (GQDs@GE11) were used as drug carrier for clinical chemotherapeutics cisplatin (CDDP) and doxorubicin (DOX). The emission spectrum of GQDs (460 nm) and the excitation spectrum of DOX (470 nm) have a good overlap, thus the transfer and release process of DOX can be sensitively detected by the fluorescence resonance energy transfer (FRET). CDDP was used to enhance the chemotherapy effect of nanoprobe, and the loading amount of DOX and CDDP on GQDs@GE11 nanoprobe were up to 67 mg/g and 50 mg/g respectively. In vivo experiments have confirmed that GQDs@GE11/CDDP/DOX nanoprobe can be enriched to tumor site through specific targeting effect, and significantly inhibit tumor cell proliferation. This new type of targeted therapy fluorescent probe provides new ideas for the study of drug release process and the treatment of nasopharyngeal carcinoma.

Laryngeal squamous cell carcinoma (LSCC) is one of the most common head and neck squamous cell carcinomas (HNSCC). Rho-associated kinase1 (ROCK1) is considered to promote progression of numerous cancers, however, its role in LSCC is still unknown. Here, the expression level of ROCK1 is higher in LSCC tissues than non-tumor tissues, and the expression level of ROCK1 is positively correlated with advanced stage and poor survival prognosis. ROCK1 knockdown in TU686 and TU212 cells dramatically inhibits cellular proliferation, migration and invasion. Whereas the overexpression of ROCK1 reversed these changes. FAK signaling pathway plays an essential role in promoting LSCC progression. Inhibiting FAK activity with TAE226 observably impairs the tumor-promoting effects. In conclusion, ROCK1 promotes LSCC tumorigenesis and progression via the FAK signaling pathway, targeting the ROCK1 molecule may represent potential targets for clinical LSCC treatment.

We previously found that the Rho-associated kinase 1 (ROCK1) activated Cancer-associated fibroblasts (CAFs) to promote LSCC metastasis. Accumulating evidence indicates that pyridine nucleotide-disulfide oxidoreductase domain 1 (PYROXD1) is an oncogene; however, the crosstalk between ROCK1 and PYROXD1 in LSCC metastasis remains largely unknown. Here, we found that ROCK1 could target PYROXD1. The knockdown of ROCK1 expression reduces the expression of PYROXD1, while the knockdown of PYROXD1 expression did not alter the expression of ROCK1 indicating that ROCK1 is upstream of PYROXD1. Further, LSCC cells cocultured with PYROXD1 knocked-down CAFs exhibited lower proliferation, migration, invasion and metastasis abilities. Conversely, LSCC cells cocultured with PYROXD1-overexpressing CAFs showed opposite results. In conclusion, the crosstalk between ROCK1 and PYROXD1 regulated CAFs activation and promoted LSCC metastasis.

We previously found the protein kinase ROCK1 actives CAFs to promote LSCC metastasis. Accumulating evidence indicates that the oxidoreductase PYROXD1 is an oncogene; however, the crosstalk between ROCK1 and PYROXD1 in LSCC metastasis is largely unknown. Here, we found that ROCK1 can target PYROXD1 and that knockdown of ROCK1 expression reduces the expression of PYROXD1, while knockdown of PYROXD1 expression cannot alter the expression of ROCK1; these results indicate that ROCK1 is upstream of PYROXD1. Furthermore, LSCC cells cocultured with PYROXD1-knockdown CAFs exhibit lower proliferation, migration, invasion and metastasis. Conversely, LSCC cells cocultured with PYROXD1-overexpressing CAFs show the opposite results. In conclusion, the crosstalk between ROCK1 and PYROXD1 regulates CAFs activation and promotes LSCC metastasis.