Blastocytis sp. is the most common enteric protozoan in human, but its pathogenesis is still unclear. To study the infectious effects of Blastocytis sp. on tissue damage, we orally challenged the Sprague Dawley (SD) rats with different doses of Blastocytis subtype1 (ST1) and examined the histological changes. We found that there was no difference of disease incidence among the Blastocytis ST1-infected groups challenged with different doses of the protozoan. Histological results showed that the lamina propria was infected by Blastocytis ST1 in the vacuolar form, along with the mucus membrane slough and inflammatory cell infiltration into the lamina propria. Compared to the uninfected group, the histological scores were significantly higher in the infected groups. However, groups infected with various doses of Blastocystis ST1 showed no difference in terms of histological scores. In conclusion, this study indicates that the SD rats can be easily infected with Blastocytis ST1 even with low dose of cysts, and the histopathological effects of the infection in the intestine of the infected rats show individual differences.
Highlights Osteosarcoma (OS) chemoresistance and distant metastasis are directly associated with OS recurrence and dismal patient prognosis, which are serious concerns for the medical community. However, current knowledge on OS pathogenesis and treatment remains limited. We found that kinesin superfamily protein 4A (KIF4A) acts as a potential OS biomarker. KIF4A promoted OS cell proliferation and anti-apoptotic in vitro and enhanced tumor growth in vivo. Our results indicate that miR-195 inhibits the expression of KIF4A by directly targeting its 3’-untranslated region Hence, targeting KIF4A could be a novel therapeutic strategy for OS and miR-195 may be a potential KIF4A-targeting drug. Furthermore, this study demonstrates that normal human chondrocytes can be used to produce miR-195-carrying exosomes to successfully deliver miR-195 into OS cells. Thus, our results suggest that chondrocyte-derived exosomal miR-195 may be developed into a potential adjuvant chemotherapeutic drug.
Background: Osteosarcoma is a common bone tumor with extremely high malignancy, occurring mostly in children and adolescents. At present, the survival rate of osteosarcomas has made progress in some aspects; however, this can only be regarded as a partial success because substantial progress has not been made in the last few decades. Object: The kinesin superfamily is a group of proteins that play regulatory roles in various metabolic processes and are closely related to tumor metastasis. Increasing evidence shows that kinesins play key roles in the occurrence and development of human cancer. Purpose: This review summarizes the roles of the kinesin superfamily proteins in osteosarcoma and related functions.Abbreviations: ATPase, adenosine triphosphatase; KIFs, kinesin superfamily protein.
Background: Osteosarcoma (OS) is the most common primary bone cancer in children and adolescents.In clinical treatments, the insensitivity of OS to conventional radiotherapy regimens signi cantly contributes to poor patient prognosis and survival. EXO1 is responsible for DNA repair pathways and telomere maintenance. Meanwhile, ATM and ATR are considered switches as they can regulate the expression of EXO1. However, their expression and interaction in OS cells under irradiation (IR) remains unclear. This study aimed to investigate the roles of FBXO32, ATM, ATR and EXO1 in OS radiotherapy insensitivity and poor patient prognosis and explore potential pathogenic mechanisms. Methods: Bioinformaticsmethods were employed to analyze differential gene expression and the correlations with prognosis in OS. Cell counting kit 8 assays, clone formation assays, and ow cytometry were used to evaluate cell survivaland apopotosisunder IR. Co-IP assays detected protein-protein interactions. Results: Bioinformatics analysis revealed that EXO1 is closely related to the survival, apoptosis and poorer prognosis in OS. The silencingof EXO1 suppressed cell proliferation and increased the sensitivity of OS cells. Molecular biological experiments showed that the ATMand ATR acted as the switch to regulate EXO1 expression under IR. Conclusion: Higher expression of EXO1, which was closely correlated with IR insensitivity and poorer prognosis, might be used as a prognostic indicator for OS. Phosphorylated-ATM enhanced the expression of EXO1, and phosphorylated-ATR induced the degradation of EXO1. More importantly, FBXO32 degraded ATR via ubiquitination in time dependent. Our data may provide a reference for future research on mechanisms, clinical diagnosis, and treatment of OS.
Background: Osteosarcoma (OS) is the most common primary bone cancer in children and adolescents. In clinical treatments, the insensitivity of OS to conventional radiotherapy regimens significantly contributes to poor patient prognosis and survival. EXO1 is responsible for DNA repair pathways and telomere maintenance. Meanwhile, ATM and ATR are considered switches as they can regulate the expression of EXO1. However, their expression and interaction in OS cells under irradiation (IR) remains unclear. This study aimed to investigate the roles of FBXO32, ATM, ATR and EXO1 in OS radiotherapy insensitivity and poor patient prognosis and explore potential pathogenic mechanisms. Methods: Bioinformatics methods were employed to analyze differential gene expression and the correlations with prognosis in OS. Cell counting kit 8 assays, clone formation assays, and flow cytometry were used to evaluate cell survival and apopotosis under IR. Co-IP assays detected protein-protein interactions. Results: Bioinformatics analysis revealed that EXO1 is closely related to the survival, apoptosis and poorer prognosis in OS. The silencing of EXO1 suppressed cell proliferation and increased the sensitivity of OS cells. Molecular biological experiments showed that the ATM and ATR acted as the switch to regulate EXO1 expression under IR. Conclusion: Higher expression of EXO1, which was closely correlated with IR insensitivity and poorer prognosis, might be used as a prognostic indicator for OS. Phosphorylated-ATM enhanced the expression of EXO1, and phosphorylated-ATR induced the degradation of EXO1. More importantly, FBXO32 degraded ATR via ubiquitination in time dependent. Our data may provide a reference for future research on mechanisms, clinical diagnosis, and treatment of OS.
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