Introduction: Long non-coding RNAs (LncRNAs) have been demonstrated to play a vital role in human carcinogenesis. HOXA cluster antisense RNA 2 (HOXA-AS2), a 1048-bp lncRNA located between the HOXA3 and HOXA4 genes, is identified as an oncogene in several malignancies, including glioma. However, the biological functions of HOXA-AS2 and its underlying molecular mechanisms in glioma progression remain to be investigated. Method: The expression of HOXA-AS2 and RND3 mRNA was determined using qRT-PCR analysis. The protein level of RND3 and EZH2 was measured by Western blot analysis. The biological function of HOXA-AS2 or RND3 in glioma was detected by CCK-8 assay, colony formation assays, transwell assay, and flow cytometry. Dual-luciferase reporter, RIP, RNAprotein pull down and ChIP assays were performed to explore the molecular mechanism of HOXA-AS2 in glioma. The effect of HOXA-AS2 in vivo was examined using xenograft tumor assay. Results: HOXA-AS2 expression was increased in glioma tissues and cells. High HOXA-AS2 expression was associated with larger tumor size and advanced pathological stage. Functionally, knockdown of HOXA-AS2 suppressed cell proliferation and invasion, and promoted apoptosis. Mechanically, HOXA-AS2 epigenetically inhibited RND3 transcription by binding to EZH2. Moreover, overexpression of RND3 exerted similar tumor-suppressive effects to the depletion of HOXA-AS2. Furthermore, the anti-cancer effects induced by si-HOXA-AS2 were greatly reversed by silencing of RND3. Finally, knockdown of HOXA-AS2 impaired tumor growth in vivo possibly via increasing RND3 expression. Conclusion: Taken together, HOXA-AS2 recruits EZH2 to the promoter region of RND3 and inhibits its expression, thereby facilitating glioma progression. Our findings provide a prospective therapeutic strategy for glioma intervention.
Background This study was designed to explore the combined effects of repetitive transcranial magnetic stimulation (rTMS) and human umbilical cord blood mesenchymal stem cells (hUCB-MSCs) transplantation on neural stem cell proliferation in rats with spinal cord injury (SCI). Material/Methods SCI was induced in 90 rats by laminectomy at T10. Fifteen rats each were treated with 0.5 Hz rTMS or 10 Hz rTMS or underwent hUCB-MSC transplantation; 15 each were treated with 0.5 Hz rTMS+hUCB-MSCs or 10 Hz rTMS+hUCB-MSCs; and 15 were untreated (control group). The Basso, Beattie, and Bresnahan (BBB) scores and motor evoked potentials (MEPs) were measured, and all rats underwent biotin dextran-amine (BDA) tracing of the corticospinal tract (CST). The levels of expression of neural stem cell proliferation related proteins, including BrdU, nestin, Tuj1, Ng2+ and GFAP, were measured, and the levels of bFGF and EGF determined by Western blotting. Results BBB scores and MEPs were increased after rTMS and hUCB-MSC transplantation, while histologically determined SCI–induced neuron apoptosis was attenuated. The numbers of BDA-positive fibers and Brdu-, nestin- and Tuj1-positive cells were markedly increased and the numbers of Ng2+- and GFAP-positive cells were markedly decreased following treatment with rTMS alone or rTMS plus hUCB-MSC transplantation. The levels of expression of bFGF and EGF were significantly upregulated following rTMS treatment and hUCB-MSC transplantation. Higher performance was observed after combined treatment with rTMS and hUCB-MSC transplantation than after either alone. Conclusions The combination of rTMS treatment and hUCB-MSC transplantation could attenuate SCI-induced neural stem cell apoptosis and motor dysfunction in rats.
Neuroblastoma (NB) is a huge threat to children's health. Adipose-derived stem cellsderived extracellular vesicles (ADSC-Evs) can regulate tumor progression. This study aimed to identify the role of ADSC-Evs in NB. Following ADSC-Ev isolation and identification, PKH26-labeled ADSC-Evs were cocultured with NB cells to observe the internalization of ADSC-Evs. ADSC-Ev effects on NB cell proliferation, invasion, and migration were assessed. The regulatory molecules related to NB development were predicted. The expressions of and relations among LINC00622, transcriptional factor androgen receptor (AR), and gamma-aminobutyric acid B-type receptor 1 (GABRR1) were detected and verified. LINC00622 was inhibited in ADSCs to evaluate ADSC-Ev effects on NB cells. Xenograft tumor experiment in nude mice was further performed to evaluate the effects of ADSC-Evs-carried LINC00622 on NB in vivo. ADSC-Evs inhibited NB cell proliferation, invasion, and migration. ADSC-Evs increased GABBR1 expression in NB cells. ADSC-Evs-carried LINC00622 mediated AR to promote GABBR1 expression. Silencing LINC00622 in ADSCs weakened the inhibition of ADSC-Evs on NB cell malignant behaviors. ADSC-Evs reduced tumor growth in nude mice, which was restored after inhibiting LINC00622 expression in ADSCs. We highlighted that ADSC-Evs carried LINC00622 into NB cells to inhibit transcription factor AR and promote GABBR1 expression, thus inhibiting NB cell growth.
BackgroundPAS domain containing repressor 1 (PASD1), the cancer-testis antigen (CTA), has been reported to be aberrantly expressed in various cancer tissues and cancer cell lines; however, normal PASD1 expression can be detected in normal tissue, excluding testicular tissue. Moreover, PASD1 is reported to be abnormally expressed in various malignant tumors. However, it remains unclear whether PASD1 participates in tumorigenesis of glioma.Material/MethodsPASD1 expression was detected by immunohistochemistry in 155 glioma tissue specimens in this study. Furthermore, the relationship of PASD1 expression with clinicopathological features in glioma cases was statistically analyzed. In addition, PASD1 was knocked down by small interference RNA (shRNA) in glioma cell line (LN229), so as to assess the potential to use it as the target for treating glioma.ResultsOur findings suggested that PASD1 expression in glioma patients was extremely upregulated compared with that in normal tissue samples and cell lines. Moreover, PASD1 expression was found to be markedly correlated with gender, The World Health Organization grade and p53 expression; in addition, high PASD1 expression indicated poor prognosis for glioma patients. Additionally, downregulation of PASD1 inhibited the proliferation ability of cells and resulted in cell arrest at the G2/M phase, which was achieved through accelerating apoptosis. Furthermore, our results indicated that PASD1 downregulation could upregulate some apoptosis-modulating proteins at the same time it downregulated some cycle-regulating proteins.ConclusionsTaken together, our findings demonstrated that PASD1, an oncogene, can potentially serve as an independent prognostic factor for glioma patients.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.