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Research Paper Volume 11, Issue 22 pp 10266-10283
Silencing lncRNA FOXD2-AS1 inhibits proliferation, migration, invasion and drug resistance of drug-resistant glioma cells and promotes their apoptosis via microRNA-98-5p/CPEB4 axis
Relevance score: 6.414828Naibing Gu, Xinlai Wang, Zhengli Di, Jing Xiong, Yue Ma, Yu’e Yan, Yihua Qian, Quanzeng Zhang, Jia Yu
Keywords: lncRNA FOXD2-AS1, microRNA-98-5p, CPEB4, glioma, temozolomide, drug resistance
Published in Aging on November 26, 2019
Highly expressed FOXD2-AS1 is found in glioma. (A) The expression level of FOXD2-AS1 in glioma tumor tissues and corresponding para normal tissues was detected by RT-qPCR (N = 68); (B) RT-qPCR was used to detect the expression of FOXD2-AS1 in human normal glial brain cell line HEB and 4 human glioma cell lines. * P < 0.05 vs human normal glial brain cell line HEB. The data were all measurement data, represented by mean ± standard deviation. The comparison between the two groups was statistically analyzed by independent sample t test, and one-way ANOVA was used in comparisons among multiple groups, and Tukey’s post-hoc test was performed after ANOVA. The experiment was repeated three times.
Silencing of FOXD2-AS1 results in inhibition of the proliferation, migration, invasion and EMT of glioma U87 cells and promotion of their apoptosis (Data of U251 cells were shown in Supplementary Figure 1). (A) The expression of FOXD2-AS1 in U87 cells were detected by RT-qPCR. (B) EdU assay was used to detect proliferation of U87 cells. (C) The ability of cell colony formation of U87 was detected by colony formation assay; (D) Flow cytometry was used to detect cell apoptosis of U87 cells in each group. (E) Cell migration ability of U87 cells was tested by scratch test; (F) Transwell assay was used to detect cell invasion of U87 cells in each group. (G) Western blot analysis was conducted to detect the expression of factors related to EMT in U87 cells. * P < 0.05 vs the sh-NC group; The data were all measurement data, represented by mean ± standard deviation. The comparison between the two groups was statistically analyzed by independent sample t test, and the experiment was repeated for three times.
TMZ resistant cell lines U87TR and U251TR show higher chemotherapeutic resistance than that of the parent cell lines U87 and U251. (A) Morphological changes of drug-resistant cell lines U87TR and U251TR and parent cell lines U87 and U251 were observed by an optical microscope (× 200); (B) MTT assay was used to determine the cell proliferation capacity at the concentration of TMZ at 50 μg/mL; (C) Changes of parental cells and drug-resistant cells on IC50 of TMZ; (D) The expression of drug-resistant genes detected by western blot analysis; * P < 0.05 vs U87 cells or U251 cells; The data were all measurement data, represented by mean ± standard deviation. The comparison between the two groups was statistically analyzed by independent sample t test, and the experiment was repeated for three times.
Silencing of FOXD2-AS1 contributes to inhibition of proliferation and drug resistance of drug-resistant glioma cells and promotion of their apoptosis. (A) The expression differences of FOXD2-AS1 in drug-resistant cell lines (U87TR, U251TR) and parental cell lines (U87, U251) were detected by RT-qPCR. (B) EdU assay was used to detect cell proliferation activity. (C) Changes of IC50 in drug-resistant cell lines after silencing FOXD2-AS1; (D) Cell apoptosis was detected by flow cytometry; (E) Tumor growth in nude mice was detected by tumor formation experiment; * P < 0.05 vs the sh-NC group; The data were all measurement data, represented by mean ± standard deviation. The comparison between the two groups was statistically analyzed by independent sample t test, and the experiment was repeated for three times.
Overexpression of FOXD2-AS1 accelerates the proliferation and drug resistance of drug-resistant cells in glioma and inhibits their apoptosis. (A) The expression of FOXD2-AS1 in U87TR cell line was detected by RT-qPCR; (B) The expression of FOXD2-AS1 in U251TR cell line was examined by RT-qPCR; (C) The cell proliferation activity tested via EdU assay; (D) The changes of IC50 in drug-resistant cell lines after overexpression of FOXD2-AS1; (E) The apoptosis in U87TR and U251TR cell lines tested via flow cytometry; (F) The tumor growth tested via tumor xenograft in nude mice. * P < 0.05 vs the oe-NC group; The data in the figure were all measurement data, represented by mean ± standard deviation. The comparison between the two groups was statistically analyzed by independent sample t test, and the experiment was repeated for three times.
LncRNA FOXD2-AS1 is regarded as a sponge of miR-98-5p. (A) The subcellular localization of FOXD2-AS1 was verified by FISH assay. (B) The binding site of FOXD2-AS1 and miR-98-5p were predicted in the RNA22 website. (C) The binding of FOXD2-AS1 to miR-98-5p was verified by dual luciferase reporter gene assay, miR-98-5p-MUT was MUT plasmid of FOXD2-AS1 and miR-98-5p 3′UTR, and miR-98-5p-WT was WT plasmid of FOXD2-AS1 and miR-98-5p 3′UTR; (D) The binding of FOXD2-AS1 to Ago2 was detected by RIP assay. (E) RNA pull-down assay was used to detect the enrichment of FOXD2-AS1 by miR-98-5p. (F) Expression of miR-98-5p in glioma tumor tissues was detected by RT-qPCR, N = 86; * P < 0.05 vs the oe-NC group, IgG group, Bio-probe NC group or para normal tissues; The data were all measurement data, represented by mean ± standard deviations. The comparison between the two groups was statistically analyzed by independent sample t test, and one-way ANOVA was used in comparisons among multiple groups, and Tukey’s post-hoc test was performed after ANOVA. The experiment was repeated for three times.
FOXD2-AS1 acts as a ceRNA to adsorb miR-98-5p, thereby decreasing the expression of CPEB4. (A) The target relationship between miR-98-5p and CPEB4 was predicted by Targetscan website. (B) The targeting relationship between miR-98-5p and CPEB4 was verified through dual luciferase reporter gene assay, CPEB4-MUT was MUT plasmid of miR-98-5p and CPEB4 3′UTR, and CPEB4-WT was WT plasmid of miR-98-5p and CPEB4 3′UTR; (C) CPEB4 expression in glioma tumor tissues was detected by RT-qPCR, N = 86; (D) The expression levels of FOXD2-AS1, miR-98-5p and CPEB4 in cells after transfection were detected by RT-qPCR. * P < 0.05 vs the mimic-NC group, para normal tissues, the oe-FOXD2-AS1 + mimic NC group, the sh-FOXD2-AS1 + inhibitor NC group or the miR-98-5p inhibitor + sh-NC group; The data were all measurement data, represented by mean ± standard deviation. The comparison between the two groups was statistically analyzed by independent sample t test, and the experiment was repeated for three times.