Chun Zhang

In our investigation, we probed the ramifications of low selenium diets and HT-2 mycotoxin exposure on spinal development and structural fidelity in murine models. A cohort of 48 male mice was segregated into six groups: a control set, a singular low selenium diet group, two cohorts exposed to distinct concentrations of HT-2 toxin (1.6 and 3.2 mg/kg·bw·d), and two assemblies subjected to a confluence of low selenium intake and each designated HT-2 dosage. Across an 8-week investigative period, parameters such as body mass, markers of bone metabolism, and cellular vigor were assiduously monitored. Analytical techniques encompassed biomechanical assessments, X-ray scrutiny, and micro-computed tomography (micro-CT) evaluations. Our results unveiled a dose-dependent diminution in the body mass of mice exclusively exposed to HT-2 toxin, whereas concurrent exposure to both low selenium and HT-2 toxins elicited a synergistic effect. Pertinent shifts were observed in calcium, phosphorus, and vitamin D concentrations, as well as in the operational dynamics of osteoblasts and osteoclasts, aligning with toxin dosage and combined exposure. Variations in biomechanical attributes were also discerned, mirroring the levels of toxin exposure. Micro-CT and X-ray examinations further corroborated the extensive detrimental impact on the cortical and trabecular architecture of the mice’s spinal columns. This inquiry elucidates the complex synergistic interactions between low selenium and HT-2 mycotoxin on murine spinal development and integrity under co-exposure conditions. These findings accentuate the exigency of comprehensively understanding the solitary and joint effects of these toxins on osseous health, providing pivotal insights for future toxicological research and public health strategies.

Elevated expression of survivin is observed in a number of cancer types, including human osteosarcoma. Few studies have demonstrated that survivin expression levels can be considered an independent predictor of survival for human osteosarcoma patients. However, the underlying molecular mechanisms of survivin in the process of human osteosarcoma carcinogenesis remain unclear. In the current study, we evaluated the biological effects of survivin knockdown on osteosarcoma cell proliferation, colony formation rate, and sensitivity to the chemotherapeutic agent cisplatin. We found that two different osteosarcoma cell lines, U2OS and Saos-2, have relatively higher expression levels of survivin, and specific knockdown of survivin resulted in a number of effects, such as inhibition of cell proliferation, decreased colony formation rate, cell cycle arrest at G2/M phase, induction of apoptosis, and increased sensitivity to cisplatin. In addition, we identified two microRNAs, miR-34a and miR-203, that are aberrantly expressed in human osteosarcoma cells and specifically target survivin by inhibiting its expression, therefore repressing osteosarcoma cell maintenance and proliferation.

Aim: To investigate whether the aberrant expression of microRNA (miR)-196a and miR-196b can be used as potential prognostic markers of human osteosarcoma. Methods: Quantitative real-time reverse transcriptase-polymerase chain reaction (qRT-PCR) analysis was performed to detect the expression levels of miR-196a and miR-196b in osteosarcoma tissues and patients’ sera. Results: Expression levels of miR-196a and miR-196b in osteosarcoma tissues were both significantly higher than those in noncancerous bone tissues (both p < 0.001), in line with which, the serum levels of the two miRNAs were also markedly upregulated in patients with osteosarcomas compared with healthy controls (both p < 0.001). Then, the elevation of serum miR-196a and miR-196b levels both more frequently occurred in osteosarcoma patients with high tumor grade (p = 0.008 and 0.01, respectively), positive metastasis (p = 0.001 and 0.006, respectively) and recurrence (p = 0.001 and 0.006, respectively). Moreover, high serum miR-196a, high serum miR-196b and conjoined expression of miR-196a/miR-196b were all independent prognostic factors for OS (overall survival) and DFS (disease-free survival) of osteosarcoma patients. Conclusion: Our present data indicate the involvement of miR-196a and miR-196b upregulation in the pathogenesis of osteosarcoma. More importantly, the altered levels of circulating miR-196a and miR-196b might have great potential to serve as novel and non-invasive prognostic factors for this malignancy.