Marine resources have tremendous potential for developing high-value biomaterials. The last decade has seen an increasing number of biomaterials that originate from marine organisms. This field is rapidly evolving. Marine biomaterials experience several periods of discovery and development ranging from coralline bone graft to polysaccharide-based biomaterials. The latter are represented by chitin and chitosan, marine-derived collagen, and composites of different organisms of marine origin. The diversity of marine natural products, their properties and applications are discussed thoroughly in the present review. These materials are easily available and possess excellent biocompatibility, biodegradability and potent bioactive characteristics. Important applications of marine biomaterials include medical applications, antimicrobial agents, drug delivery agents, anticoagulants, rehabilitation of diseases such as cardiovascular diseases, bone diseases and diabetes, as well as comestible, cosmetic and industrial applications.

Phosphoglycerate kinase 1 (PGK1), a critical component of the glycolytic pathway, relates to the development of various cancers. However, the mechanisms of PGK1 inhibition and physiological significance of PGK1 inhibitors in cancer cells are unclear. Long non-coding RNAs (lncRNA) play a vital role in tumor growth and progression. Here, we identified a lncRNA LINC00926 negatively correlated with PGK1 and predicting good clinical outcome of breast cancer. LINC00926 downregulates PGK1 expression by enhancing the ubiquitination of PGK1 mediated by E3 ligase STUB1. Moreover, hypoxia inhibits LINC00926 expression and activates PGK1 expression largely through FOXO3A. FOXO3A/LINC00926/PGK1 axis regulates breast cancer glycolysis, tumor growth and lung metastasis both in vitro and in vivo. In breast cancer patients, LINC00926 expression is negatively correlated with PGK1 and positively correlated with FOXO3A expression. Our work established FOXO3A/LINC00926/PGK1 as a critical axis to regulate BC growth and progression. Targeting PGK1 or supplement of LINC00926 or FOXO3A could be potential therapeutic strategies in breast cancer.

Lung adenocarcinoma (LUAD) is a common type of lung cancer with high frequent metastasis and a high death rate. However, genes responsible for LUAD metastasis are still largely unknown. Here, we identify an important role of ras homolog family member V (RHOV) in LUAD metastasis using a combination of bioinformatic analysis and functional experiments. Bioinformatic analysis shows five hub LUAD metastasis driver genes (RHOV, ZIC5, CYP4B1, GPR18 and TCP10L2), among which RHOV is the most significant gene associated with LUAD metastasis. High RHOV expression predicted shorter overall survival in LUAD patients. RHOV overexpression promotes proliferation, migration, and invasion of LUAD cells, whereas RHOV knockdown inhibits these biological behaviors. Moreover, knockdown of RHOV suppresses LUAD tumor growth and metastasis in nude mice. Mechanistically, RHOV activates Jun N-terminal Kinase (JNK)/c-Jun signalling pathway, an important pathway in lung cancer development and progression, and regulates the expression of markers of epithelial-to-mesenchymal transition, a process involved in cancer cell migration, invasion and metastasis. RHOV-induced malignant biological behaviors are inhibited by pyrazolanthrone, a JNK inhibitor. Our findings indicate a critical role of RHOV in LUAD metastasis and may provide a biomarker for prognostic prediction and a target for LUAD therapy.

Tick-borne rickettsioses are considered important emerging zoonoses worldwide, but their etiological agents, rickettsiae, remain poorly characterized in northeastern China, where many human cases have been reported during the past several years. Here, we determined the characteristics of Rickettsia spp. infections in ticks in this area. Ticks were collected by flagging vegetation from Jilin and Heilongjiang provinces of northeastern China followed by morphological identification. The presence of Rickettsia spp. in ticks was detected by PCR targeting the 23S-5S ribosomal RNA intergenic spacer, citrate synthase (gltA) gene, and 190-kDa outer membrane protein gene (ompA). The newly-generated sequences were subjected to phylogenetic analysis using the software MEGA 6.0. The overall infection rate of Rickettsia spp. was 6.12 %. Phylogenetic analyses based on the partial gltA and ompA genes demonstrated that rickettsiae detected in the ticks belong to four species, including “Candidatus Rickettsia tarasevichiae”, Rickettsia heilongjiangensis, Rickettsia raoultii, and a potential new species isolate. The associated tick species were also identified, i.e. Dermacentor nuttalli and Dermacentor silvarum for R. raoultii, Haemaphysalis concinna and Haemaphysalis longicornis for R. heilongjiangensis, and Ixodes persulcatus for “Ca. R. tarasevichiae”. All Rickettsia spp. showed significantly high infection rates in ticks from Heilongjiang when compared to Jilin Province. Rickettsia heilongjiangensis, R. raoultii and “Ca. R. tarasevichiae” are widely present in the associated ticks in northeastern China, but more prevalent in Heilongjiang Province. The data of this study increase the information on the distribution of Rickettsia spp. in northeastern China, which have important public health implications in consideration of their recent association with human diseases.

Oral and pharyngeal cancer is the most common malignant human cancers. Chemotherapy is an effective approach for anti-oral cancer therapy, while the drug tolerance and resistance remain a problem for oral cancer patients. Aloe-emodin, rhein and physcion are classified as anthraquinones, which are the main pharmacodynamic ingredients of Rheum undulatum L.. This study was undertaken to investigate whether aloe-emodin, rhein and physcion show inhibiting growth and inducing apoptosis in oral squamous cell carcinoma SCC15 cells. We found that aloe-emodin show inhibiting growth and inducing apoptosis in oral squamous cell carcinoma SCC15 cells, we also investigated the underlying mechanisms of apoptosis induced by aloe-emodin. Thiazolyl blue tetrazolium bromide (MTT) test was used to detect cell proliferation. Cell apoptosis was detected by flow cytometry. We also used western blot analysis to detect the potential mechanisms of apoptosis. Aloe-emodin, rhein and physcion inhibit the proliferation of SCC15 cells and the order of inhibition level are aloe-emodin > Rhein > Physcion, the half maximal inhibitory concentrations (IC50) value of aloe-emodin was 60.90 μM at 48 h of treatment. Aloe-emodin treatment resulted in a time- and dose-dependent decrease in cell viability and increased the apoptotic cell ratio. The results of western blotting showed the expression levels of caspase-9 and caspase-3 proteins increased following aloe-emodin treatment. Our results revealed that aloe-emodin treatment could inhibit cell viability of SCC15 cells and the potential mechanism of inhibition might be through the induction of apoptosis by regulation of the expression levels of caspase-9 and caspase-3. This indicates that aloe-emodin may be a good agent for anti-oral cancer drug exploring.