Dataset Information

Microarray profiling analysis of lncRNAs expression in glioma cells

ABSTRACT: Tremendous studies have found that the abnormality of long noncoding RNA (lncRNA) contributed to cancer initiation, progression, and recurrence via multiple signaling cascades. Nevertheless, the possible underlying mechanisms of lncRNA in temozolomide (TMZ)-resistant glioma were not well understood, hindering the improvement of TMZ-based therapies against glioma. The present study illustrated that the lncRNA KCNQ1OT1 increased in TMZ-resistant gliomas cells compared to the parental cells. Introduction of KCNQ1OT1 boosted glioma cell viability, clonogenicity and rhodamine 123 efflux while hampered apoptosis post-exposure to TMZ. Consistent with bioinformatic prediction, KCNQ1OT1 directly sponged miR-761, which was downregulated in TMZ-resistant glioma cell lines. Overexpression of miR-761 attenuated glioma cell viability and clonogenicity while triggered apoptosis and rhodamine 123 cellular accumulation post-exposure to TMZ, leading to rehabilitated glioma TMZ-sensitivity, which was against the function of KCNQ1OT1. miR-761 bound to 3’-untranslated region of PIM1, a proto-oncogene with constitutive serine/threonine kinase activity, attenuated PIM1-mediated signaling cascades. Furthermore, stable knockdown of KCNQ1OT1 by small hairpin RNA amplified the TMZ-induced tumor regression in TMZ-resistant U251 mouse models. Briefly, the present study evaluated KCNQ1OT1 conferred TMZ resistance by sponging miR-761 and releasing PIM1 expression, resulting in activation of PIM-mediated MDR1/c-Myc/Survivin signaling pathways. The findings mentioned above extended the knowledge of lnRNA KCNQ1OT1 in the regulation of chemoresistance in glioma and provided a promising therapeutic target for TMZ-resistant glioma patients. Long noncoding RNA profiling by array

ORGANISM(S): Homo sapiens

PROVIDER: GSE144784 | GEO | 2020/10/13

REPOSITORIES: GEO

ACCESS DATA

Similar Datasets

Project description:One of the major challenges for chemotherapy is appearance of resistance to compounds. Despite several singling pathways have been implicated in development of Adriamycin (ADM) resistance, mechanisms involved in ADM-resistant osteosarcoma progression remain largely unknown. The present study attempts to illustrate the role of long noncoding RNA ARSR in development of ADM-resistance. We found lncRNA ARSR overexpressed in the Adriamycin resistant cell lines U2OS/ADM and MG63/ADM, accompanied with acquired multidrug resistance against to paclitaxel and cisplatin. Overexpression of lncRNA ARSR triggered rhodamine 123 efflux and survival, as well as migration of ADM resistant cells. Conversely, depletion of ARSR promoted rhodamine 123 retention and apoptosis while reduced motility of ADM resistant cells. Further investigation revealed that upregulation of ARSR enhanced Akt phosphorylation on Ser473 and increment of multidrug resistance-associated protein-1, apoptosis inhibitor Survivin and matrix metalloproteinase-2. Reduction of ARSR overcame the resistance to ADM and magnified the suppression of Akt-mediated signaling pathways by MK-2206. The current study gained novel evidence for understanding the mechanisms underlying adaptive ADM resistance, and provided rational to improve Akt-targeted therapy towards refractory osteosarcoma. Methods: The expression of lncRNA was analyzed by RT2 lncRNA PCR Arrays. The differential expressed lncRNAs were further verified by qRT-PCR. The relationship between lncRNA expression and clinical features was evaluated with Spearman correlation test. Cell proliferation was measured by MTT assay. Cell apoptosis percentage was detected by ANNEXIN V-PI analysis. The promoter activity was illustrated by Luciferase assay, and the change of microRNA and protein was detected by qRT-PCR and western blot, separately. Results: The expression of HAND2-AS1 declined in bladder cancer and correlated with depth of invasion and grades negatively. Restoration of HAND2-AS1 hampered cell growth by provoking cell apoptosis. Furthermore, one of the HAND2-AS1 sponge, miR-146, was found overexpression in bladder cancer tissue and cell lines. Expression of miR-146 related to HAND2-AS1 expression negatively. One of the targeted genes of miR-146, retinoic acid receptor beta (RARB) was downregulated in bladder cancer. In addition, the expression of RARB related to miR-146 negatively. Lost-of-function and gain-of-function experiments were used to identify the mechanisms underlying association of lncRNA HAND2-AS1: miR-146: RARB. miR-146 targeted RARB directly and hindered RARB-mediate apoptosis. However, the hindrance was impaired by HAND2-AS1 notably. Conclusion: HAND2-AS1 diminished miR-146 expression, thereby releasing the suppression of miR-146 on RARB-mediated apoptosis, promoting bladder cancer regression. Long noncoding RNA profiling by array

Dataset Information

Microarray profiling analysis of lncRNAs expression in glioma cells

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure