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Circular RNAs (circRNAs) appear to be significant modulators in various physiological processes. Recently, it is found that circRNA_101996 exerts important roles in various cancers. Our previous studies showed that circRNA_101996 promoted cervical cancer growth and metastasis by regulating miR‐8075/TPX2. However, the potential regulatory role of circRNA_101996 in cervical cancer still needs further investigation. Our results in this study suggested that circRNA_101996 was over‐expressed in cervical cancer patients. circRNA_101996 up‐regulation remarkably assisted cell proliferation, cell cycle progression, and cell migration in cervical cancer, while circRNA_101996 knockdown exerted the inverse effects. The molecular investigations indicated that circRNA_101996 could increase the expression level of miR‐1236‐3p, tripartite motif‐containing 37 (TRIM37), through binding to miR‐1236‐3p and reducing its expression. Moreover, in vivo results demonstrated that circRNA_101996 shRNA can function as a tumor suppressor through down‐regulating TRIM37 in cervical cancer. In conclusion, our data indicated that circRNA_101996/miR‐1236‐3p/TRIM37 axis accelerated cervical cancer development, providing novel insights into cervical cancer diagnosis and treatment. [ABSTRACT FROM AUTHOR]

Objective: To explore the effect of MicroRNA-146b-5p (miR-146b-5p) on the mouse bone essence derived MSC adipogenic differentiation., Methods: MSC were isolated from bone essence of C57BL/6 mice. The expression level of miR-146b-5p in the process of adipogenic differentiation of MSC was detected by q-PCR; the role of miR-146b-5p mimics or inhibitors in the process of mouse bone essence derived MSC adipogenic differentiation was analyzed through oil red staining the expression of C/EBPα and PPARγ after cultured for 14 days was detected by q-PCR; the protein level of PPARγ after miR-146b-5p transfection was detected by Western blot., Results: The MSC were successfully isolated from bone essence of mice, the q-PCR results showed an increasing expression level of miR-146-5p in the process of MSC adipogenic differentiation. Compared with the control group, MSC transfected with miR-146b-5p mimic could up-regulate the expression of miR-146b-5p (P<0.001), while miR-146b-5p inhibitor transfection could down-regulate the endogenous miR-146b-5p expression (P<0.01). After culture for 14 d, the result of Oil red staining showed that the miR-146b-5p inhibitor could inhibit adipogenic differentiation, while the miR-146b-5p mimic could promote the adipogenic differentiation of MSC. After induction for 14 d, compared with control, the PPARγ and C/EBPα in mimic group were higher expressed PPARγ and C/EBPα (P<0.01). Compared with induced group, the PPAPγ and C/EBPα were lower expressed in inhibitor group (P<0.05). The results of Western blot showed that the expression level of PPARγ was high in minic group, and it was low in inhibitor group., Conclusion: miR-146b-5p is up-regulated in the process of MSC adipogenic differentiation, and it promotes the adipogenesis of MSC originated from mouse bone essence.

Objective: To study the effects of virtual reality (VR) training on the gross motor function of the lower limb and the fine motor function of the upper limb in children with spastic diplegia cerebral palsy., Methods: Thirty-five children with spastic diplegia cerebral palsy were randomly assigned to VR training group (n=19) and conventional training group (n=16). The conventional training group received conventional physical therapy and occupational therapy for three months. The VR training group received VR training and occupational therapy for three months. Grip and visual-motor integration subtests in Peabody Developmental Motor Scales-2 were used to evaluate the fine movement in patients before and after treatment. The D and E domains of the 88-item version of the Gross Motor Function Measure (GMFM-88), Modified Ashworth Scale (MAS), and Berg Balance Scale (BBS) were used to evaluate the gross movement in patients before and after treatment., Results: Before treatment, there were no significant differences in grip, visual-motor integration, fine motor development quotient, scores of D and E domains of GMFM-88, MAS score, or BBS score between the two groups (P>0.05). After treatment, all the indices were significantly improved in the VR training group compared with the conventional training group (P<0.05)., Conclusions: VR training can effectively improve the gross motor function of the lower limb and the fine motor function of the upper limb in children with spastic diplegia cerebral palsy.

Objective: To establish the stably lower expression of vascular cell adhesion molecule-1 (VCAM-1) in MSC cell line (C3H10T1/2) by siRNA technology, and explore the effect of knockdown of VCAM-1 on the immunologic regulation capacity of murine MSC., Methods: The mouse GV118-VCAM-1-RNAi retrovirus vector was constructed by gene recombination technology. The recombinant plasmid was identified by restriction analysis and sequencing, and then the recombinant plasmid GV118-VCAM-1-RNAi was transfected into 293 cells by Lipofectamine, and the supernatant was collected to transfect C3H10T1/2. Moreover, the VCAM-1 lower expression on MSC was evaluated by flow cytometry and fluorescent microscopy. The knockdown VCAM-1 MSC was sorted by flow cytometry. Furthermore, the inhibitory effect of the knockdown VCAM-1 MSC on lymphocyte proliferation was tested by lymphoblast transformation assay (LTT) and mixed lymphocyte reaction assay(MLR)., Results: The recombinant retroviral vector of knockdown VCAM-1 (GV118-VCAM-1-RNAi) was successfully constructed and transfected into mouse MSC cell line C3H10T1/2. The knockdown VCAM-1/MSC was obtained by flow cytometric sorting. The LTT and MLR assay showed that the immunosuppressive effect of MSC lower-expressing VCAM-1 dramatically decreased (P<0.05)., Conclusion: Knockdown VCAM-1 in MSC can significantly down-regulate the inhibitory capability of MSC on the proliferation of T-cells. The data of this study laid an experimental foundation for studying effect of VCAM-1 transfecting into MSC on immune function.

Objective: To investigate the effect of vascular cell adhesion molecule-1 (VCAM-1) gene overexpression on adipogenic differentiation of mouse mesenchymal stem cells(MSC) and explore its molecular mechanism., Methods: VCAM-1 overexpression MSC (MIGR1-VCAM-1/MSC) and the empty plasmid transfection MSC (MIGR1/MSC) were induced to adipogenic differentiation, oil-red-O staining and real-time PCR were used to detect the adipogenic differentiation ability and the mRNA expression level of key transcription factors C/EBP α and PPAR γ. The activation of P38, ERK and JNK pathways were analyzed by Western blot. Furthermore, the specific chemical inhibitors of MAPK pathway (SB203580, PD98059 and JNK inhibitor II) were added to the induced culture system and the alteration of the MSC adipogenic differentiation ability were evaluated., Results: no matter in self or induced differentiation groups, the lipid droplets in MIGR1-VCAM-1/MSC became larger, the amount of adipocyte increased than that in MIGR1/MSC (P<0.01), the mRNA expression level of C/EBPα and PPARγ were upregulated, and JNK pathway were down-regulated while the P38 and ERK pathway were significantly up-regulated. The inhibition of JNK pathway of MIGR1-VCAM-1/MSC could lead to increased mRNA expression level of C/EBP α and PPAR γ, the amount of adipocytes increased (P<0.01), however, the inhibition of the P38 and ERK pathway of MIGR1-VCAM-1/MSC could lead to decreased mRNA expression level of C/EBP α and PPAR γ, and the lipid droplets and the number of adipocytes became smaller and less., Conclusion: The overexpression of VCAM-1 may promote MSC to differentiate into adipocytes through inhibiting JNK signaling pathway, activating P38 and ERK pathways.