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Dysregulation of the cell cycle and the resulting aberrant cellular proliferation has been highlighted as a hallmark of cancer. Certain traditional Chinese medicines can inhibit cancer growth by inducing cell cycle arrest. In this study we explore the effect of Hedyotis diffusae Herba-Andrographis Herba on the cell cycle of nasopharyngeal carcinoma (NPC). Hedyotis diffusae Herba-Andrographis Herba-containing serum was prepared and then added to the cell culture medium. BrdU, comet, and FUCCI assays, western blot analysis and flow cytometry analysis revealed that Hedyotis diffusae Herba-Andrographis Herba treatment significantly alters cell proliferation, DNA damage, and cell cycle distribution. Xenograft mouse model experiments were performed, confirming these in vitro findings in vivo. Treatment with Hedyotis diffusae Herba-Andrographis Herba inhibited cell proliferation, promoted DNA damage, and arrested NPC cells progression from G1 to S phase. Further examination of the underlying molecular mechanisms revealed that treatment with Hedyotis diffusae Herba-Andrographis Herba increased the expression of p53 and p21, while reducing that of CCND1, Phospho-Rb, E2F1, γH2AX, and Ki-67 both in vivo and in vitro. Conversely, the inhibition of p53 and p21 could abolish the promoting effect of Hedyotis diffusae Herba-Andrographis Herba on the NPC cell cycle arrest at the G1 phase, contributing to the proliferation of NPC cells. Hedyotis diffusae Herba-Andrographis Herba suppressed the tumor growth in vivo. Overall, these findings suggest that Hedyotis Diffusae Herba-Andrographis prevent the progression of NPC by inducing NPC cell cycle arrest at the G1 phase through a p53/p21-dependent mechanism, providing a novel potential therapeutic treatment against NPC., (© 2021. The Author(s), under exclusive licence to Springer Nature America, Inc.)

Objective: Nasopharyngeal carcinoma (NPC) is a common malignant tumour in Southeast Asia, especially in southern China. ABO blood groups have been proven to play an important role in many cancers. However, it is still controversial whether the ABO blood group has a definite relationship to susceptibility to NPC and the prognosis of NPC patients. This meta-analysis was performed to elucidate the correlation between ABO blood group and NPC to provide more data for clinical practice. Methods: A systematic search was performed of the Chinese National Knowledge Infrastructure (CNKI), Wanfang, Web of Science, EMBASE, and PubMed databases up to December 31, 2020. Stata 11.0 statistical software was used for this meta-analysis. Results: According to the inclusion and exclusion criteria, a total of 6 studies including 6938 patients with NPC were selected. Blood group O was relevant to Chinese NPC patients, and patients with blood group O had a significantly lower incidence of NPC, while blood group A had no correlation with susceptibility to NPC. There was no difference in the 3-year overall survival (OS), locoregional relapse-free survival (LRRFS) or distant metastasis-free survival (DMFS) rates between patients with blood group O and those with non-O blood groups; worse 5-year OS, LRRFS and DMFS rates were found in patients with blood group O, whereas blood group A was not related to prognosis. Conclusion: Blood group O in Chinese patients with NPC seems to be a protective factor for morbidity. However, once patients with blood group O are diagnosed with NPC, this blood group often indicates unfavourable OS, LRRFS and DMFS rates. It is recommended that more attention should be paid to the influence of blood group factor on patients in the treatment of NPC. [ABSTRACT FROM AUTHOR]

Nasopharyngeal carcinoma (NPC) is one of the most common malignant head and neck cancers in southern China. Although the local and regional control of NPC has been considerably improved, patients with advanced disease still suffer from poor prognosis. Statins inhibit the mevalonate pathway and play antiproliferative and proapoptotic roles in a number of cancer cells. However, the effects and molecular mechanism of statins in NPC treatment remain unclear. In this study, the cell viability of NPC cell line, C666-1, after simvastatin exposure was determined using the alamarBlue Cell Viability Assay. Cell apoptosis in C666-1 treated with simvastatin was assessed by flow cytometry and TUNEL assay. The expression levels of cell cycle regulatory proteins were determined using western blotting. Simvastatin markedly decreased cell viability in a concentration-dependent manner, increased caspase 3 activity and induced apoptosis in C666-1 cells. Simvastatin induced Bim expression by regulating phosphorylation of transcriptional factor c-Jun. Simvastatin treatment induced cell cycle arrest in the G1 phase in C666-1 cells by inhibiting the expression of cyclin D1 and cyclin-dependent kinase 4, and enhancing p27 expression. Simvastatin treatment inhibited protein kinase B and extracellular signal regulated kinase 1/2 activation. In conclusion, the results of the present study reveal the possible molecular mechanism of simvastatin-induced anti-tumor effects in C666-1 and suggest that simvastatin is a potential chemotherapy agent in NPC treatment. [ABSTRACT FROM AUTHOR]

Viral, dietary and genetic factors have been implicated in nasopharyngeal carcinoma (NPC), however, the molecular mechanism underlying its pathogenesis remains to be fully elucidated. MicroRNAs (miRNAs) have been reported to be important in NPC tumorigenesis, with a previous miRNA microarray study showing the downregulation of miRNA (miR)-429 in NPC cells. However, the possible mechanisms of action of miR-429 have not been examined. In the present study, the expression profiles of miR-429 were detected using reverse transcription-quantitative polymerase chain reaction analysis in CNE-1 and CNE-2 cells, which are two generally used NPC cells with different degrees of differentiation. Subsequently, cell proliferation, invasion and migration were analyzed in miR-429-overexpressing CNE-2 cells, and the modulatory function of miR-429 was also investigated using two target genes, zinc finger E-Box-binding homeobox 1 (ZEB1) and CRK-like (CRKL), by transfection with miR-429 mimic or anti-miR-429. Significant changes in the expression of miR-429 were detected, particularly in low-differentiated CNE-2 cells, with higher levels of epidemicity and malignancy. Additional results revealed that miR-429 inhibited the invasion and migration of the CNE-2 cells, whereas no significant effect on cell growth was observed. In addition, the mRNA and protein expression levels of the two target genes, ZEB1 and CRKL, were negatively regulated by miR-429, demonstrated through gain-of-function and loss-of-function investigations, indicating that these two functional downstream targets may be involved in the inhibitory effects of miR-429 on NPC migration and invasion. miR-429 may act as a negative regulatory factor of NPC tumorigenesis, involving the functions of its downstream targets, ZEB1 and CRKL. The results suggested miR-429 as a potential candidate for miRNA-based prognosis or therapy against NPC. [ABSTRACT FROM AUTHOR]