- RNA modifications and cancer
- Ferroptosis and cancer prognosis
- Cancer, Lipids, and Metabolism
- MicroRNA in disease regulation
- RNA Research and Splicing
- Cancer-related molecular mechanisms research
National Cancer Institute
2023
Center for Cancer Research
2023
University of York
2023
University of Maryland, College Park
2023
Mutations of the isocitrate dehydrogenase (IDH) gene are common genetic mutations in human malignancies. Increasing evidence indicates that IDH play critical roles malignant transformation and progression. However, therapeutic options for IDH-mutated cancers remain limited. In this study, investigation patient cohorts revealed PI3K/protein kinase B (AKT) signaling pathways were enhanced cancer cells.In we investigated expression profile cells using RNA sequencing after depletion AKT. Gene...
<p>(A) Immunoblotting analysis evaluated the siRNA knockdown efficiency of AKT in U87 cells. (B) Phase contrast imaging showed cytotoxicity ipatasertib (Ipa) IDH1WT and IDH1Mut NHA Bar = 100 mM. (C) Representative flow cytometric live/dead staining cells response to Ipa (0, 1, 2 mM) treatment. (D) Statistical dead/live cell ratio IDHMut after **p < 0.01.</p>
<div>AbstractPurpose:<p>Mutations of the isocitrate dehydrogenase (<i>IDH</i>) gene are common genetic mutations in human malignancies. Increasing evidence indicates that IDH play critical roles malignant transformation and progression. However, therapeutic options for IDH-mutated cancers remain limited. In this study, investigation patient cohorts revealed PI3K/protein kinase B (AKT) signaling pathways were enhanced cancer cells.</p>Experimental...
<p>(A) Heatmap of gene expression profile for glioma specimen. The leading edge the KEGG_MTOR_SIGNALING_PATHWAY geneset was shown. (B) Dose-response curve measured cell viability in IDH1WT NHA cells response to TMZ/Ipa combination treatment. (C) isobologram analysis showed synergistic effect TMZ and Ipa cells. (D) index (C.I.) calculated show additive Ipa.</p>
<p>(A) Gene expression profiling showed the of GPX4 and SLC7A11 in IDH-mutated NHA cells (B) ROS-Glo assay measured oxidative stress IDH1WT IDH1Mut response to ipatasertib (Ipa, 1 mM) treatment. (C) GSH, GSSG level was IDHWT Ipa (1 GSH/GSSG ratio calculated. (D) Immunoblotting analysis evaluated cleaved PARP with TMZ (200 and/or (1mM) b-actin used as an internal control. (E) Cell viability on under **p < 0.01.</p>
<p>(A) Phase contrast images showed the cytotoxicity of TMZ (400 mM)/ipatasertib (Ipa, 2 mM) combination treatment in brain tumor-initiating cells (BTICs). A ferroptosis inhibitor, Ferrstain-1 (Ferr-1, 5 mM), was used to rescue ferroptotic cell death. Bar = 100 mM. (B) Representative flow cytometric analysis live/dead staining BTICs response TMZ/Ipa treatment. (C) Statistical dead/live ratio BTICs. (D) The limiting dilution assay evaluated frequency generating spheres GSC827 and TSC603...
<p>(A) Immunoblotting analysis evaluated the siRNA knockdown efficiency of AKT in U87 cells. (B) Phase contrast imaging showed cytotoxicity ipatasertib (Ipa) IDH1WT and IDH1Mut NHA Bar = 100 mM. (C) Representative flow cytometric live/dead staining cells response to Ipa (0, 1, 2 mM) treatment. (D) Statistical dead/live cell ratio IDHMut after **p < 0.01.</p>
<p>(A) Phase contrast images showed the cytotoxicity of TMZ (400 mM)/ipatasertib (Ipa, 2 mM) combination treatment in brain tumor-initiating cells (BTICs). A ferroptosis inhibitor, Ferrstain-1 (Ferr-1, 5 mM), was used to rescue ferroptotic cell death. Bar = 100 mM. (B) Representative flow cytometric analysis live/dead staining BTICs response TMZ/Ipa treatment. (C) Statistical dead/live ratio BTICs. (D) The limiting dilution assay evaluated frequency generating spheres GSC827 and TSC603...
<p>(A) Heatmap of gene expression profile for glioma specimen. The leading edge the KEGG_MTOR_SIGNALING_PATHWAY geneset was shown. (B) Dose-response curve measured cell viability in IDH1WT NHA cells response to TMZ/Ipa combination treatment. (C) isobologram analysis showed synergistic effect TMZ and Ipa cells. (D) index (C.I.) calculated show additive Ipa.</p>
<p>(A) Gene expression profiling showed the of GPX4 and SLC7A11 in IDH-mutated NHA cells (B) ROS-Glo assay measured oxidative stress IDH1WT IDH1Mut response to ipatasertib (Ipa, 1 mM) treatment. (C) GSH, GSSG level was IDHWT Ipa (1 GSH/GSSG ratio calculated. (D) Immunoblotting analysis evaluated cleaved PARP with TMZ (200 and/or (1mM) b-actin used as an internal control. (E) Cell viability on under **p < 0.01.</p>
<p>(A) Heatmap of gene expression profile for glioma specimen. The leading edge the KEGG_MTOR_SIGNALING_PATHWAY geneset was shown. (B) Dose-response curve measured cell viability in IDH1WT NHA cells response to TMZ/Ipa combination treatment. (C) isobologram analysis showed synergistic effect TMZ and Ipa cells. (D) index (C.I.) calculated show additive Ipa.</p>
<p>(A) Gene expression profiling showed the of GPX4 and SLC7A11 in IDH-mutated NHA cells (B) ROS-Glo assay measured oxidative stress IDH1WT IDH1Mut response to ipatasertib (Ipa, 1 mM) treatment. (C) GSH, GSSG level was IDHWT Ipa (1 GSH/GSSG ratio calculated. (D) Immunoblotting analysis evaluated cleaved PARP with TMZ (200 and/or (1mM) b-actin used as an internal control. (E) Cell viability on under **p < 0.01.</p>
<p>(A) Phase contrast images showed the cytotoxicity of TMZ (400 mM)/ipatasertib (Ipa, 2 mM) combination treatment in brain tumor-initiating cells (BTICs). A ferroptosis inhibitor, Ferrstain-1 (Ferr-1, 5 mM), was used to rescue ferroptotic cell death. Bar = 100 mM. (B) Representative flow cytometric analysis live/dead staining BTICs response TMZ/Ipa treatment. (C) Statistical dead/live ratio BTICs. (D) The limiting dilution assay evaluated frequency generating spheres GSC827 and TSC603...
<p>(A) Immunoblotting analysis evaluated the siRNA knockdown efficiency of AKT in U87 cells. (B) Phase contrast imaging showed cytotoxicity ipatasertib (Ipa) IDH1WT and IDH1Mut NHA Bar = 100 mM. (C) Representative flow cytometric live/dead staining cells response to Ipa (0, 1, 2 mM) treatment. (D) Statistical dead/live cell ratio IDHMut after **p < 0.01.</p>
<p>(A) Gene expression profiling showed the of GPX4 and SLC7A11 in IDH-mutated NHA cells (B) ROS-Glo assay measured oxidative stress IDH1WT IDH1Mut response to ipatasertib (Ipa, 1 mM) treatment. (C) GSH, GSSG level was IDHWT Ipa (1 GSH/GSSG ratio calculated. (D) Immunoblotting analysis evaluated cleaved PARP with TMZ (200 and/or (1mM) b-actin used as an internal control. (E) Cell viability on under **p < 0.01.</p>
<div>AbstractPurpose:<p>Mutations of the isocitrate dehydrogenase (<i>IDH</i>) gene are common genetic mutations in human malignancies. Increasing evidence indicates that IDH play critical roles malignant transformation and progression. However, therapeutic options for IDH-mutated cancers remain limited. In this study, investigation patient cohorts revealed PI3K/protein kinase B (AKT) signaling pathways were enhanced cancer cells.</p>Experimental...
<p>(A) Heatmap of gene expression profile for glioma specimen. The leading edge the KEGG_MTOR_SIGNALING_PATHWAY geneset was shown. (B) Dose-response curve measured cell viability in IDH1WT NHA cells response to TMZ/Ipa combination treatment. (C) isobologram analysis showed synergistic effect TMZ and Ipa cells. (D) index (C.I.) calculated show additive Ipa.</p>
<p>(A) Phase contrast images showed the cytotoxicity of TMZ (400 mM)/ipatasertib (Ipa, 2 mM) combination treatment in brain tumor-initiating cells (BTICs). A ferroptosis inhibitor, Ferrstain-1 (Ferr-1, 5 mM), was used to rescue ferroptotic cell death. Bar = 100 mM. (B) Representative flow cytometric analysis live/dead staining BTICs response TMZ/Ipa treatment. (C) Statistical dead/live ratio BTICs. (D) The limiting dilution assay evaluated frequency generating spheres GSC827 and TSC603...
<p>(A) Immunoblotting analysis evaluated the siRNA knockdown efficiency of AKT in U87 cells. (B) Phase contrast imaging showed cytotoxicity ipatasertib (Ipa) IDH1WT and IDH1Mut NHA Bar = 100 mM. (C) Representative flow cytometric live/dead staining cells response to Ipa (0, 1, 2 mM) treatment. (D) Statistical dead/live cell ratio IDHMut after **p < 0.01.</p>
<div>AbstractPurpose:<p>Mutations of the isocitrate dehydrogenase (<i>IDH</i>) gene are common genetic mutations in human malignancies. Increasing evidence indicates that IDH play critical roles malignant transformation and progression. However, therapeutic options for IDH-mutated cancers remain limited. In this study, investigation patient cohorts revealed PI3K/protein kinase B (AKT) signaling pathways were enhanced cancer cells.</p>Experimental...