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The Inhibition of microRNA-128 on IGF-1-Activating mTOR Signaling Involves in Temozolomide-Induced Glioma Cell Apoptotic Death

Chen, Peng-Hsu, Cheng, Chia-Hsiung, Shih, Chwen-Ming, Ho, Kuo-Hao, Lin, Cheng-Wei, Lee, Chin-Cheng, Liu, Ann-Jeng, Chang, Cheng-Kuei, Chen, Ku-Chung·2016·PLOS ONE
DOI 10.1371/journal.pone.0167096PMC PMC5125683
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Fig 1 Investigation of TMZ-mediated microRNA profiles. Volcano plot (A) and heatmap of hierarchical gene clustering (B) demonstrating TMZ-regulated microRNA signatures. After U87MG cells were treated with 400 μM TMZ for 24 h, total RNAs were extracted for the microarray. For all array analyses, a p value of less than 0.05 and a log2 (ratio) of more than or equal to 0.58 or less than or equal to −0.51-multiple of change cutoff were applied. Volcano plots exhibit multiples of change (log2 ratio) and probabilities (-log10 p values) of individual microRNAs from the microarray assay. Significantly upregulated and downregulated mRNAs are indicated by black dots. The red dot indicates miR-128. The heatmap depicts the 248 differentially expressed microRNAs between TMZ subsets. A color was assigned to each microRNA based on its relative expression across samples. (C) Detection of endogenous miR-128 levels in normal human astrocytes and three different glioma cell lines including HS683, M059K, and U87MG cells. Relative expression levels of miR-128 were measured through real-time PCR. The U6B level was used as an internal control. Data are the mean ± SD of three experiments.
Fig 1 Investigation of TMZ-mediated microRNA profiles. Volcano plot (A) and heatmap of hierarchical gene clustering (B) demonstrating TMZ-regulated microRNA signatures. After U87MG cells were treated with 400 μM TMZ for 24 h, total RNAs were extracted for the microarray. For all array analyses, a p value of less than 0.05 and a log2 (ratio) of more than or equal to 0.58 or less than or equal to −0.51-multiple of change cutoff were applied. Volcano plots exhibit multiples of change (log2 ratio) and probabilities (-log10 p values) of individual microRNAs from the microarray assay. Significantly upregulated and downregulated mRNAs are indicated by black dots. The red dot indicates miR-128. The heatmap depicts the 248 differentially expressed microRNAs between TMZ subsets. A color was assigned to each microRNA based on its relative expression across samples. (C) Detection of endogenous miR-128 levels in normal human astrocytes and three different glioma cell lines including HS683, M059K, and U87MG cells. Relative expression levels of miR-128 were measured through real-time PCR. The U6B level was used as an internal control. Data are the mean ± SD of three experiments.CC BY · PubMed Central
Fig 2 Lower miR-128 levels are significantly associated with a high-risk group and poor survival in patients with GBM and low-grade glioma. Correlation between miR-128-1/miR-128-2 levels and survival rates in patients with GBM (A and B) and low-grade glioma (C and D). The left panel shows relative miR-128-1/miR-128-2 expression levels according to the patient risk group based on GBM and low-grade glioma profiling from the TCGA database. High-risk individuals had lower miR-128-1/miR-128-2 expression levels, which are denoted by red symbols. By contrast, higher miR-128-1/miR-128-2 expression levels were associated with higher survival and are shown in green. The right panel shows results of the Kaplan–Meier analysis of survival data of patients with GBM and low-grade glioma profiles from the TCGA database. X axis values indicate the number of patients per group. Red curves indicate patients at a high risk. Green curves indicate patients at a low risk. The plus sign (+) indicates censored observations. p values were calculated using the log-rank test.
Fig 2 Lower miR-128 levels are significantly associated with a high-risk group and poor survival in patients with GBM and low-grade glioma. Correlation between miR-128-1/miR-128-2 levels and survival rates in patients with GBM (A and B) and low-grade glioma (C and D). The left panel shows relative miR-128-1/miR-128-2 expression levels according to the patient risk group based on GBM and low-grade glioma profiling from the TCGA database. High-risk individuals had lower miR-128-1/miR-128-2 expression levels, which are denoted by red symbols. By contrast, higher miR-128-1/miR-128-2 expression levels were associated with higher survival and are shown in green. The right panel shows results of the Kaplan–Meier analysis of survival data of patients with GBM and low-grade glioma profiles from the TCGA database. X axis values indicate the number of patients per group. Red curves indicate patients at a high risk. Green curves indicate patients at a low risk. The plus sign (+) indicates censored observations. p values were calculated using the log-rank test.CC BY · PubMed Central
Fig 3 TMZ upregulates miR-128-1 but not miR-128-2 activation. (A) Dose-dependent effects of TMZ on mature (A) and primary (B) miR-128 expression levels. After cells were treated with the indicated doses of TMZ for 24 h, endogenous miR-128, primary (pri)-miR-128-1, and pri-miR-128-2 levels were respectively measured through real-time PCR. U6B and 18S rRNA levels were used as internal controls for the mature and primary miR-128 genes, respectively. (C) TMZ dose-dependent activated miR-128-1 but not miR-128-2 promoter activity. (D) Identification of the core region in the miR-128-1 promoter. After cells were transfected with 500 ng pGL3-Basic, pGL3-miR-128-1-prom2500, or pGL3-128-1 variants for 24 h, luciferase activity was measured with TMZ treatment for another 24 h. pNL1.1.TK[Nluc/TK] plasmids at 5 ng were also cotransfected into cells, and the NanoLucR luciferase value was used as an internal control. Data are the mean ± SD of three experiments. * p < 0.05.
Fig 3 TMZ upregulates miR-128-1 but not miR-128-2 activation. (A) Dose-dependent effects of TMZ on mature (A) and primary (B) miR-128 expression levels. After cells were treated with the indicated doses of TMZ for 24 h, endogenous miR-128, primary (pri)-miR-128-1, and pri-miR-128-2 levels were respectively measured through real-time PCR. U6B and 18S rRNA levels were used as internal controls for the mature and primary miR-128 genes, respectively. (C) TMZ dose-dependent activated miR-128-1 but not miR-128-2 promoter activity. (D) Identification of the core region in the miR-128-1 promoter. After cells were transfected with 500 ng pGL3-Basic, pGL3-miR-128-1-prom2500, or pGL3-128-1 variants for 24 h, luciferase activity was measured with TMZ treatment for another 24 h. pNL1.1.TK[Nluc/TK] plasmids at 5 ng were also cotransfected into cells, and the NanoLucR luciferase value was used as an internal control. Data are the mean ± SD of three experiments. * p < 0.05.CC BY · PubMed Central
Fig 4 The JNK2/c-Jun signaling pathway is involved in temozolomide (TMZ)-upregulated miR-128 expression. (A) Effects of mitogen-activated protein kinase (MAPK) inhibitors including U0126 (an ERK inhibitor), SB203580 (a p38 inhibitor), and SP600125 (a JNK inhibitor) on endogenous miR-128 levels. (B) Inhibition of JNK2 and c-Jun expressions inhibited TMZ-upregulated miR-128 levels. After cells were respectively pretreated with 10 μM U0126, 5 μM SB203580, and 10 μM SP600125 for 1 h or respectively transfected with 1 μg of shRNAs for 24 h, 400 μM TMZ was added for another 24 h. miR-128 levels were measured through real-time PCR. Data are the mean ± SD of three experiments. * p < 0.05. (C) Time-dependent effects of TMZ on JNK and c-Jun activation. After cells were treated with 400 μM TMZ for the indicated time, phosphorylated and total forms of JNK and c-Jun were detected using immunoblotting assays. (D) SP600125 treatment, mutation of the activator protein (AP)-1-binding site, and inhibition of JNK2 or c-JUN attenuated TMZ-activated miR-128 promoter activity. After cells were transfected with 500 ng pGL3-miR-128-1-prom2500 or a pGL3-miR-128-1-prom2500 mutant for 24 h, luciferase activity was measured with SP600125 pretreatment for 1 h or cotransfected with 1 μg of shRNAs for 24 h followed by TMZ treatment for another 24 h. pNL1.1.TK[Nluc/TK] plasmids at 5 ng were also cotransfected into cells, and the NanoLucR luciferase value was used as an internal control. (E) The ChIP analysis showed that TMZ enhanced c-Jun binding to the miR-128 promoter. Procedures of the ChIP assay are described in “Materials and methods”. As positive or negative controls, protein–DNA complexes were incubated with anti-RNA polymerase or control mouse IgG antibodies. The input DNA represented one-fifth of the starting material. The right panel figure shows quantitative results from the left panel by densitometry. Overexpression and knockdown effects of miR-128 on TMZ-inhibited cell viability (F) and apoptosis-related protein expressions (G). After cells were respectively transfected with 750 ng of miR-128-overexpressing plasmids and 100 nM miR-128 inhibitor followed by TMZ treatment for another 24 h, cell viability and apoptosis-related protein expressions were measured using MTT and immunoblot assays. Data are the mean ± SD of three experiments. * p < 0.05.
Fig 4 The JNK2/c-Jun signaling pathway is involved in temozolomide (TMZ)-upregulated miR-128 expression. (A) Effects of mitogen-activated protein kinase (MAPK) inhibitors including U0126 (an ERK inhibitor), SB203580 (a p38 inhibitor), and SP600125 (a JNK inhibitor) on endogenous miR-128 levels. (B) Inhibition of JNK2 and c-Jun expressions inhibited TMZ-upregulated miR-128 levels. After cells were respectively pretreated with 10 μM U0126, 5 μM SB203580, and 10 μM SP600125 for 1 h or respectively transfected with 1 μg of shRNAs for 24 h, 400 μM TMZ was added for another 24 h. miR-128 levels were measured through real-time PCR. Data are the mean ± SD of three experiments. * p < 0.05. (C) Time-dependent effects of TMZ on JNK and c-Jun activation. After cells were treated with 400 μM TMZ for the indicated time, phosphorylated and total forms of JNK and c-Jun were detected using immunoblotting assays. (D) SP600125 treatment, mutation of the activator protein (AP)-1-binding site, and inhibition of JNK2 or c-JUN attenuated TMZ-activated miR-128 promoter activity. After cells were transfected with 500 ng pGL3-miR-128-1-prom2500 or a pGL3-miR-128-1-prom2500 mutant for 24 h, luciferase activity was measured with SP600125 pretreatment for 1 h or cotransfected with 1 μg of shRNAs for 24 h followed by TMZ treatment for another 24 h. pNL1.1.TK[Nluc/TK] plasmids at 5 ng were also cotransfected into cells, and the NanoLucR luciferase value was used as an internal control. (E) The ChIP analysis showed that TMZ enhanced c-Jun binding to the miR-128 promoter. Procedures of the ChIP assay are described in “Materials and methods”. As positive or negative controls, protein–DNA complexes were incubated with anti-RNA polymerase or control mouse IgG antibodies. The input DNA represented one-fifth of the starting material. The right panel figure shows quantitative results from the left panel by densitometry. Overexpression and knockdown effects of miR-128 on TMZ-inhibited cell viability (F) and apoptosis-related protein expressions (G). After cells were respectively transfected with 750 ng of miR-128-overexpressing plasmids and 100 nM miR-128 inhibitor followed by TMZ treatment for another 24 h, cell viability and apoptosis-related protein expressions were measured using MTT and immunoblot assays. Data are the mean ± SD of three experiments. * p < 0.05.CC BY · PubMed Central
Fig 5 Identification of roles of miR-128 in mediating glioma cell death. Effects of miR-128 overexpression on cell viability (A), apoptosis ratio (B), apoptosis-related proteins levels (C), reactive oxygen species (ROS) generation (D), loss of the mitochondrial membrane potential (MMP) (E), and autophagy formation (F). After cells were transfected with the indicated dose of miR-128-expressing plasmids for 24 h, cell viability, caspase-3 activation, poly(ADP ribose) polymerase (PARP) degradation, LC3-I/II levels, apoptosis, ROS generation, loss of the MMP, and autophagy were measured using MTT assay, immunoblot assays, flow cytometry with annexin V/propidium iodide double-staining, H2DCFDA staining, rhodamine 123, and acridine orange staining, respectively. The right panel shows quantitative results from the left panel. Data are the mean ± SD of three independent experiments. * p < 0.05. (G) Effects of 3-MA on miR-128-induced autophagy. After cells were transfected with the indicated dose of miR-128-expressing plasmids for 4 h followed by 1 mM 3-MA treatment for another 24 h, cell viability was measured using the MTT assay. Data are the mean ± SD of three independent experiments. * p < 0.05.
Fig 5 Identification of roles of miR-128 in mediating glioma cell death. Effects of miR-128 overexpression on cell viability (A), apoptosis ratio (B), apoptosis-related proteins levels (C), reactive oxygen species (ROS) generation (D), loss of the mitochondrial membrane potential (MMP) (E), and autophagy formation (F). After cells were transfected with the indicated dose of miR-128-expressing plasmids for 24 h, cell viability, caspase-3 activation, poly(ADP ribose) polymerase (PARP) degradation, LC3-I/II levels, apoptosis, ROS generation, loss of the MMP, and autophagy were measured using MTT assay, immunoblot assays, flow cytometry with annexin V/propidium iodide double-staining, H2DCFDA staining, rhodamine 123, and acridine orange staining, respectively. The right panel shows quantitative results from the left panel. Data are the mean ± SD of three independent experiments. * p < 0.05. (G) Effects of 3-MA on miR-128-induced autophagy. After cells were transfected with the indicated dose of miR-128-expressing plasmids for 4 h followed by 1 mM 3-MA treatment for another 24 h, cell viability was measured using the MTT assay. Data are the mean ± SD of three independent experiments. * p < 0.05.CC BY · PubMed Central
Fig 6 TMZ inhibited mammalian target of rapamycin (mTOR) pathways through miR-128 targeting. (A) Schematic diagram of potential miR-128-targeted sites in the 3’-untranslated region (UTR) of mTOR, RICTOR, IGF1, and PIK3R1 genes. (B) Effects of miR-128 on 3’-UTR luciferase activity of mTOR, RICTOR, IGF1, and PIK3R1 genes. To examine the effect of miR-128, different doses of miR-128-expressing plasmids were cotransfected with 500 ng pmiRGlo-3’-UTR or mutant 3’-UTR of mTOR, RICTOR, IGF1, and PIK3R1 genes. Luciferase activity was measured in these cells 24 h after transfection. Effects of miR-128 overexpression on mRNA (C) and protein (D) expressions of mTOR, RICTOR, IGF1, and PIK3R1 genes. After cells were respectively transfected with the indicated dose of miR-128-expressing plasmids for 24 h, relative mRNA and protein levels of the mTOR, RICTOR, IGF1, and PIK3R1 genes were analyzed through real-time PCR and immunoblotting assays. Data are the mean ± SD of three experiments. * p < 0.05. (E) miR-128 is involved in TMZ-reduced mTOR signaling. (F) The effects of IGF-1 stimulation on miR-128-targeted genes expression levels. (G) IGF-1 stimulation attenuated miR-128-induced cytotoxicity. After cells were transfected with 750 ng of miR-128-expressing plasmids or 100 nM of a miR-128 inhibitor, 400 μM of TMZ was added for another 24 h. For IGF-1 stimulation assays, cells were treated with 200ng/mL of IGF-1 recombinant proteins for 24 h or transfected with 500 ng of miR-128-expressing plasmids combined with 200ng/mL of IGF-1 treatment for 24 h. Protein levels of mTOR, RICTOR, IGF1, and PIK3R1 were analyzed using immunoblotting assays. Cell viability was measured using the MTT assay. Data are the mean ± SD of three experiments. * p < 0.05.
Fig 6 TMZ inhibited mammalian target of rapamycin (mTOR) pathways through miR-128 targeting. (A) Schematic diagram of potential miR-128-targeted sites in the 3’-untranslated region (UTR) of mTOR, RICTOR, IGF1, and PIK3R1 genes. (B) Effects of miR-128 on 3’-UTR luciferase activity of mTOR, RICTOR, IGF1, and PIK3R1 genes. To examine the effect of miR-128, different doses of miR-128-expressing plasmids were cotransfected with 500 ng pmiRGlo-3’-UTR or mutant 3’-UTR of mTOR, RICTOR, IGF1, and PIK3R1 genes. Luciferase activity was measured in these cells 24 h after transfection. Effects of miR-128 overexpression on mRNA (C) and protein (D) expressions of mTOR, RICTOR, IGF1, and PIK3R1 genes. After cells were respectively transfected with the indicated dose of miR-128-expressing plasmids for 24 h, relative mRNA and protein levels of the mTOR, RICTOR, IGF1, and PIK3R1 genes were analyzed through real-time PCR and immunoblotting assays. Data are the mean ± SD of three experiments. * p < 0.05. (E) miR-128 is involved in TMZ-reduced mTOR signaling. (F) The effects of IGF-1 stimulation on miR-128-targeted genes expression levels. (G) IGF-1 stimulation attenuated miR-128-induced cytotoxicity. After cells were transfected with 750 ng of miR-128-expressing plasmids or 100 nM of a miR-128 inhibitor, 400 μM of TMZ was added for another 24 h. For IGF-1 stimulation assays, cells were treated with 200ng/mL of IGF-1 recombinant proteins for 24 h or transfected with 500 ng of miR-128-expressing plasmids combined with 200ng/mL of IGF-1 treatment for 24 h. Protein levels of mTOR, RICTOR, IGF1, and PIK3R1 were analyzed using immunoblotting assays. Cell viability was measured using the MTT assay. Data are the mean ± SD of three experiments. * p < 0.05.CC BY · PubMed Central

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Metadata

Authors
Chen, P.-H., Cheng, C.-H., Shih, C.-M., Ho, K.-H., Lin, C.-W., Lee, C.-C., Liu, A.-J., Chang, C.-K., & Chen, K.-C.
ORCID
Chen, Ku-Chung
Venue
PLOS ONE
Publisher
Public Library of Science (PLoS)
Published
2016-11-28
Volume
11
Issue
11
Pages
e0167096
ISSN
1932-6203
DOI
10.1371/journal.pone.0167096
PMC
PMC5125683
Cited by
41
References
0
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
Ministry of Science and Technology (MOST104-2320-B-038-046, MOST105-2320-B-038-019)

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CoChat. (2026). Citation check: The Inhibition of microRNA-128 on IGF-1-Activating mTOR Signaling Involves in Temozolomide-Induced Glioma Cell Apoptotic Death. https://app.cochat.ai/papers/10.1371/journal.pone.0167096
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Chen, P.-H., Cheng, C.-H., Shih, C.-M., Ho, K.-H., Lin, C.-W., Lee, C.-C., Liu, A.-J., Chang, C.-K., & Chen, K.-C. (2016). The Inhibition of microRNA-128 on IGF-1-Activating mTOR Signaling Involves in Temozolomide-Induced Glioma Cell Apoptotic Death. PLOS ONE. https://doi.org/10.1371/journal.pone.0167096