MicroRNA-1202 plays a vital role in osteoarthritis via KCNQ1OT1 has-miR-1202-ETS1 regulatory pathway.

BACKGROUND: This study aimed to explore the molecular mechanism of osteoarthritis (OA) and provide information about new genes as potential targets for OA treatment. METHODS: Gene expression profile of GSE105027, including 12 OA serum samples (OA group) and 12 healthy serum samples (ctrl group), was downloaded. The differentially expressed miRNAs (DEMs) as well as miRNA-mRNAs interactions were investigated, followed by function and pathway investigation. Then the protein-protein interaction (PPI) network was performed. Furthermore, the long non-coding RNA (lncRNA)-miRNA-mRNA interactions (competing endogenous RNAs, ceRNAs) were investigated. RESULTS: A total of 17 downregulated miRNAs were revealed between OA and ctrl groups. These DEMs such as has-miR-1202 were mainly enriched in GO functions like histone acetyltransferase binding and KEGG pathways like cellular senescence. The integrated PPI network analysis showed that has-miR-1202, has-miR-33b-3p, has-miR-940, has-miR-4284, and has-miR-4281 were 5 downregulated miRNAs in this network. Furthermore, the lncRNA-miRNA-mRNA interactions such as KCNQ1OT1-has-miR-1202-ETS1 were revealed in the present ceRNA network. CONCLUSION: Key DEMs such as miR-33b-3p, miR-940, and miR-1202 may be involved in OA. miR-1202 may regulate OA development via histone acetyltransferase pathway binding function and cellular senescence pathway. Furthermore, KCNQ1OT1-has-miR-1202-ETS1 might be vital for the process of OA.

[Establishment of animal model of breast cancer dormancy].

OBJECTIVE: Tumor dormancy has been defined clinically as a condition in which tumor cells are present but do not grow for a long period of time. Breast cancer is noted for its long periods of tumor dormancy and metastases can occur many years after treatment. METHOD: Simulating the characteristics of breast cancer patients after treatment, we established the animal model of breast cancer dormancy by inoculating 500 Ca761-03 cells into the limb muscle of 615 mice and then selecting animals with tumor dormancy 2 months post inoculation (corresponding to 5 years for humans). RESULTS: Two months after inoculation of Ca761-03 cells into the muscle of 615 mice, tumor occurred in 30% of the mice. The remaining 70% of mice did not show tumor growth. After repeated traumatic stimulation, 90% of the mice developed tumors after 5 months, therefore representing tumor dormancy. CONCLUSIONS: These results demonstrate that breast cancer cells can remain in a dormant state for long periods of time in vivo. Trauma can stimulate the dormant tumor cells to proliferate again, and causes tumor relapse. This murine model system promises a sound animal model for the study of solid tumor dormancy.

[Establishment and characterization of a rabbit tumor cell line VX2].

OBJECTIVE: To establish a rabbit tumor cell line and to characterize its biological parameters. METHODS: VX2 tumor tissue was used for the primary culture in vitro. After 40 passages, the cell morphology, CK expression (immunohistochemical staining), cell cycle, karyotype and tumorigenecity in rabbits and nude mice were investigated. RESULTS: The newly established cell line VX2 was maintained in continuous culture for over 70 passages in 10 months. Morphologically, VX2 cells were polygonal to short spindled. Tonal fibril and tight junction were found under the electron microscope. CK was positive. The cell cycle analysis showed 69.3% in G1 phase, 5.6% in G2 phase and 25.1% in S phase. The population doubling time was 34.5 hours. The chromosomal analysis showed a hypotriploidy with a median chromosome number of 58 approximately 62. The tumorigenecity in rabbits and nude mice were both 100%. CONCLUSION: The established VX2 cell line derived from rabbit squamous carcinoma could serve as a model system for experimental oncology in the rabbit.