Journal: Behavioural brain research

Article Title: GSNO promotes functional recovery in experimental TBI by stabilizing HIF-1α

doi: 10.1016/j.bbr.2016.10.037

Figure Lengend Snippet: Effect of inhibition of HIF-1α by 2-ME on GSNO-induced improvement of neurobehavioral functions [rotarod task and novel object recognition (NOR) test] for 14 days. GSNO treatment of TBI animals improved motor function (rotarod task, A) and cognitive behavior (NOR, B) with increasing time whereas treatment with 2-ME of GSNO-treated TBI animals reversed the effects of GSNO. Sham animals showed deficits neither in rotarod task (base line latency 260±20 seconds) nor in NOR. Statistically significant differences were not observed between TBI and GSNO+2-ME group. Data are presented as mean±SE (n=7). *p<0.05 and ***p<0.001 vs. TBI and GSNO+2-ME.

Article Snippet: Enhancing the S-nitrosylation of HIF-1α with exogenous GSNO has been shown to stabilize HIF-1α, leading to induction and increased expression of VEGF, angiogenesis, and neurorepair [ 20 ; 29 ].

Techniques: Inhibition

Journal: Behavioural brain research

Article Title: GSNO promotes functional recovery in experimental TBI by stabilizing HIF-1α

doi: 10.1016/j.bbr.2016.10.037

Figure Lengend Snippet: Effect of inhibition of HIF-1α by 2-ME on GSNO-mediated stabilization of HIF-1α and stimulation of VEGF and BDNF at 14th day after TBI. TBI animals showed higher protein levels of both HIF-1α and VEGF; however, treatment of TBI animals with GSNO further increased the levels as shown by western blot studies (A) and densitometry (A’). 2-ME treatment of GSNO group animals reversed the effect of GSNO (A, A’). Similar effects of GSNO and 2-ME were observed on the levels of BDNF, as shown by western blot studies (B) and densitometry (B’). Data are presented as mean±SD (n=7). ##p<.01 vs. Sham, ***p<0.001 vs. TBI, +++p<0.001 vs. GSNO.

Article Snippet: Enhancing the S-nitrosylation of HIF-1α with exogenous GSNO has been shown to stabilize HIF-1α, leading to induction and increased expression of VEGF, angiogenesis, and neurorepair [ 20 ; 29 ].

Techniques: Inhibition, Western Blot

Journal: Behavioural brain research

Article Title: GSNO promotes functional recovery in experimental TBI by stabilizing HIF-1α

doi: 10.1016/j.bbr.2016.10.037

Figure Lengend Snippet: Effect of GSNO, HIF-1α inhibitor 2-ME, and denitrosylating agent DDT on the expression of VEGF and BDNF in endothelial (bEnd3) cells. GSNO treatment increased the mRNA expression levels of VEGF and BDNF in a dose dependent manner (A). Pretreatment (2 h) with 2-ME (5 μM) or DDT (200 μM) reversed the effect of GSNO on the expression levels of VEGF and BDNF (C). The expression of VEGF and BDNF was determined at 24 h using RT-PCR and normalized against β-actin. Under the described experimental conditions, cell viability was assayed using LDH release assay (B, D), showing no significant cell death. Data are presented as mean +SD. n=5. ***p<0.001, *p<0.05 vs. Untreated, +++p<0.001 vs. GSNO.

Article Snippet: Enhancing the S-nitrosylation of HIF-1α with exogenous GSNO has been shown to stabilize HIF-1α, leading to induction and increased expression of VEGF, angiogenesis, and neurorepair [ 20 ; 29 ].

Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Lactate Dehydrogenase Assay

Journal: Behavioural brain research

Article Title: GSNO promotes functional recovery in experimental TBI by stabilizing HIF-1α

doi: 10.1016/j.bbr.2016.10.037

Figure Lengend Snippet: Effect of GSNO (2 h treatment) on the total S-nitrosylated proteins, S-nitrosylation of HIF-1α using biotin switch assay and mRNA expression of PECAM-1 in endothelial (bEnd3) cells. Total S-nitrosylated proteins were determined by western blot analysis for biotin labeled proteins (A). A dose-wise effect of GSNO (100, 250, 500 μM) for 2 h treatment on increased S-nitrosylation of HIF-1α was examined by immunoblotting (B) and densitometry (C) and normalized with β-actin. mRNA expression of PECAM-1 was determined at 24 h using RT-PCR and normalized against β-actin (D). Data are presented as mean±SD. n=3. +p<0.05 vs. untreated (0 μM), ++p<0.01 vs. GSNO (100 μM), +++p<0.001 vs. GSNO (200 μM), ***p<0.001 vs. untreated (0 μM), *p<0.05 vs. GSNO (100, and200 μM).

Article Snippet: Enhancing the S-nitrosylation of HIF-1α with exogenous GSNO has been shown to stabilize HIF-1α, leading to induction and increased expression of VEGF, angiogenesis, and neurorepair [ 20 ; 29 ].

Techniques: Biotin Switch Assay, Expressing, Western Blot, Labeling, Reverse Transcription Polymerase Chain Reaction

Journal: Behavioural brain research

Article Title: GSNO promotes functional recovery in experimental TBI by stabilizing HIF-1α

doi: 10.1016/j.bbr.2016.10.037

Figure Lengend Snippet: Schematic showing the hypothesized deleterious events in a CCI rat model of TBI, GSNO-mediated stimulation of neurorepair mechanisms, and induction of functional recovery via stabilization of HIF-1α/VEGF following TBI. HIF-1α inhibitor 2-ME treatment of GSNO-treated TBI animals reverses the effect of GSNO.

Article Snippet: Enhancing the S-nitrosylation of HIF-1α with exogenous GSNO has been shown to stabilize HIF-1α, leading to induction and increased expression of VEGF, angiogenesis, and neurorepair [ 20 ; 29 ].

Techniques: Functional Assay

Journal: Nature Communications

Article Title: Host interneurons mediate plasticity reactivated by embryonic inhibitory cell transplantation in mouse visual cortex

doi: 10.1038/s41467-021-21097-4

Figure Lengend Snippet: a Left: schematic of experimental design for viral labeling PV interneurons in neonates at postnatal days (P) 2–5 and Ca 2+ imaging in critical period animals at P26-28. Right: in vivo image of visually responsive PV interneurons (green). Scale bar = 50 µm. This experiment was performed independently in eight animals total (6 saline group, 2 NRG1 group). b Visually evoked responses of PV interneurons through the deprived eye before and after monocular deprivation (MD) in saline controls. c Visually evoked responses of PV interneurons through the deprived eye before and after MD in neuregulin 1 (NRG1) treated mice. d 1D MD significantly decreased the percent of responsive PV interneurons (PreMD: n = 9 fields from 3 mice, solid green; PostMD: n = 10 fields from 3 mice, open green; * p = 0.027, t -test with Welch’s correction, two-tailed). Exogenous NRG1 prevented the reduction in PV cell responsiveness (PreMD: n = 7 fields from 2 mice, solid green; PostMD: n = 5 fields from 2 mice, dashed green; p = 0.876, Mann–Whitney U -test, two-tailed). e 1D MD also reduced the response amplitude of PV interneurons through the contralateral, deprived eye stimulation (Δ F / F 0 : PreMD, 0.401 ± 0.031, n = 78 cells from 5 mice, solid green; PostMD, 0.205 ± 0.022, n = 61 cells from 3 mice, open green; **** p = 0.00000046, Mann–Whitney U -test, two-tailed). Exogenous NRG1 blocked the reduction in response amplitude of PV interneurons. (Δ F / F 0 : PreMD, 0.449 ± 0.035, n = 73 cells from 3 mice, solid green; PostMD, 0.342 ± 0.028, n = 36 cells from 2 mice, dashed green; p = 0.266, Mann–Whitney U -test, two-tailed). Data in d and e are mean ± SEM.

Article Snippet: Exogenous NRG1 blocked the reduction in response amplitude of PV interneurons. (Δ F / F 0 : PreMD, 0.449 ± 0.035, n = 73 cells from 3 mice, solid green; PostMD, 0.342 ± 0.028, n = 36 cells from 2 mice, dashed green; p = 0.266, Mann–Whitney U -test, two-tailed).

Techniques: Labeling, Imaging, In Vivo, Saline, Two Tailed Test, MANN-WHITNEY

Journal: Nature Communications

Article Title: Host interneurons mediate plasticity reactivated by embryonic inhibitory cell transplantation in mouse visual cortex

doi: 10.1038/s41467-021-21097-4

Figure Lengend Snippet: a Experimental timeline. Top: calcium imaging of host PV interneurons in MGE transplant recipients (green, MGE), MGE recipients treated with NRG1 (dashed green, NRG1) or CGE transplant recipients (magenta, CGE) were performed at 33–35 days after transplantation. Bottom: imaging of PV interneurons in untreated adult control mice was performed around postnatal day (P) 115 (black, adult control). b In vivo image of GCaMP6s-labeled host PV interneurons in a MGE transplant recipient. Responsive cells are outlined in yellow and green. Scale bar = 50 µm. In vivo Ca 2+ imaging of PV interneurons were performed independently in 25 mice (17 transplant recipients and 8 wild-type mice). c Visually evoked responses at the peak spatial frequency for the cell outlined in green in b . d 1D MD reduced the overall responsiveness of host PV interneurons in 35DAT transplant recipients (MGE: n = 20 fields from 6 mice; adult control: n = 30 fields from 8 mice; 35DAT CGE: n = 9 fields from 5 mice; NRG1: n = 23 fields from 6 mice; 35DAT MGE vs. adult control: ** p = 0.0054; 35DAT MGE vs. 35DAT CGE: * p = 0.048; 35DAT MGE vs. NRG1: *** p = 0.0004, Brown–Forsythe ANOVA followed by Dunnett’s T3 multiple comparisons test). e , f 1D MD resulted in a large reduction in the response amplitude of 35DAT host PV interneurons through both the deprived ( e ) and open eyes ( f ). However, exogenous NRG1 did not prevent the reduction in the response amplitude of host PV interneurons (Contra: 35DAT MGE, n = 18 fields from 6 mice; adult control, n = 27 fields from 8 mice; CGE, n = 9 fields from 5 mice; NRG1, n = 23 fields from 6 mice; 35DAT MGE vs. adult control, * p = 0.019; 35DAT MGE vs. 35DAT CGE: p = 0.056; 35DAT MGE vs. NRG1: p = 0.914; Ipsi: 35DAT MGE, n = 16 fields from 6 mice; adult control, n = 23 fields from 8 mice; CGE, n = 10 fields from 5 mice; NRG1, n = 23 fields from 8 mice; 35DAT MGE vs. adult control, p = 0.125; 35DAT MGE vs. 35DAT CGE: p = 0.819; 35DAT MGE vs. NRG1: p = 0.746, Brown–Forsythe and Welch ANOVA followed by Dunnett’s T3 multiple comparisons test). Data in d , e , and f are mean ± SEM.

Article Snippet: Exogenous NRG1 blocked the reduction in response amplitude of PV interneurons. (Δ F / F 0 : PreMD, 0.449 ± 0.035, n = 73 cells from 3 mice, solid green; PostMD, 0.342 ± 0.028, n = 36 cells from 2 mice, dashed green; p = 0.266, Mann–Whitney U -test, two-tailed).

Techniques: Imaging, Transplantation Assay, Control, In Vivo, Labeling

Journal: Nature Communications

Article Title: Host interneurons mediate plasticity reactivated by embryonic inhibitory cell transplantation in mouse visual cortex

doi: 10.1038/s41467-021-21097-4

Figure Lengend Snippet: a , Example binocular responses from a host PV interneuron at 35DAT before MD. Gray boxes represent when the visual gratings were shown. Gray traces represent individual trials. Black represents averaged responses for contralateral eye stimulation. Red represents averaged responses for ipsilateral eye stimulation. The peak spatial frequency for the contralateral responses is 0.12 c/d and 0.06 c/d for the ipsilateral responses in the example shown. b Examples of different types of spatial frequency responses: binocular, contralateral monocular, and ipsilateral monocular cells. The average responses (solid line) at each spatial frequency are overlaid with a difference of Gaussians fit (dashed line). c No difference found in the overall responsiveness between all four experimental groups (MGE: n = 6 mice, 84.14% ± 3.63, solid green; Adult control: n = 8 mice, 82.51% ± 4.33, black; CGE: n = 5 mice, 79.48% ± 6.57, magenta; NRG1: n = 6 mice, 79.99% ± 5.68, dashed green; p = 0.910, one-way ANOVA) before MD. d No difference found in the percentage of responsive binocular responses (MGE: n = 6 mice, 45.23% ± 3.00; adult control: n = 8 mice, 46.22% ± 6.99; CGE: n = 5 mice, 48.87% ± 5.00; NRG1: n = 6 mice, 53.11% ± 7.47; p = 0.816, one-way ANOVA). e – h Single-cell ODI distribution of PV interneurons before and after MD. The colors of the lines are determined by the cell’s PostMD ODI. Non-responsive cells (NR): gray; contralateral only cells: dark green; binocular cells: medium green; ipsilateral cells: light green. e 35DAT host PV interneurons with MGE transplant ( n = 260 cells from 6 mice). f Untreated adult PV interneurons ( n = 435 cells from 8 mice). g 35DAT host PV interneurons with CGE transplant ( n = 150 cells from 5 mice). h 35DAT host PV interneurons treated with NRG1 ( n = 248 cells from 6 mice). i – l Same data as e – h but plotted by animal. i 1D MD selectively reduced the percentage of responsive binocular PV interneurons ( n = 6 mice, ** p = 0.0018, two-way ANOVA followed by Bonferroni’s multiple comparison test). j No significant reduction in the percentage of responsive binocular PV interneurons after 1D MD in untreated, age-matched adult control ( n = 8 mice, two-way ANOVA followed by Bonferroni’s multiple comparison test). k No significant reduction in the binocular host PV interneurons in adults with CGE transplant ( n = 5 mice, two-way ANOVA followed by Bonferroni’s multiple comparison test). l NRG1 treatment prevented the reduction in responsiveness of binocular PV interneurons after MD ( n = 6 mice, two-way ANOVA followed by Bonferroni’s multiple comparison test). Data in c , d , i , j , k , and l are mean ± SEM.

Article Snippet: Exogenous NRG1 blocked the reduction in response amplitude of PV interneurons. (Δ F / F 0 : PreMD, 0.449 ± 0.035, n = 73 cells from 3 mice, solid green; PostMD, 0.342 ± 0.028, n = 36 cells from 2 mice, dashed green; p = 0.266, Mann–Whitney U -test, two-tailed).

Techniques: Control, Comparison

Journal: Nature Communications

Article Title: Host interneurons mediate plasticity reactivated by embryonic inhibitory cell transplantation in mouse visual cortex

doi: 10.1038/s41467-021-21097-4

Figure Lengend Snippet: a Experimental timeline. b Intrinsic optical imaging was performed to measure ocular dominance plasticity (ODP) in adult transplant recipients around 33–35 days after transplantation (DAT). The wild-type adult recipients received either saline or soluble neuregulin 1 (NRG1) during 4 days of monocular deprivation (MD). c Examples of response amplitude before and after 4D MD in WT transplant recipients that received saline injections or were treated with NRG1 during deprivation. Scale bar = 500 µm. d Four-day MD resulted in a shift of ocular dominance index (ODI) in transplant recipients that received saline injections. Injections of exogenous NRG1 diminished transplant-induced ODI shift. Interneuron transplantation also failed to reactivate ODP in PV-cre;ErbB4 flx/flx adult recipients. However, WT adults that were transplanted with cells from PV-cre;ErbB4 flx/flx donor exhibited a significant shift in ODI after 4D MD. ODI is calculated as (Contra response amplitude − Ipsi response amplitude)/(Contra response amplitude + Ipsi response amplitude) (Saline n = 7 mice, red; NRG1 n = 6 mice, blue; PV-cre;ErbB4 flx/flx recipients n = 6 mice, orange; PV-cre;ErbB4 flx/flx donors PreMD: n = 7 mice, PostMD: n = 5 mice, yellow. Saline: ** p = 0.004; NRG1: p = 0.344; PV-cre;ErbB4 flx/flx recipients: p = 0.844; PV-cre;ErbB4 flx/flx donor: * p = 0.03, Mann–Whitney U -test, two-tailed). e Ocular dominance shift is calculated as (PreMD ODI–PostMD ODI). Ocular dominance shift was reduced in the transplant recipients treated with NRG1 and in PV-cre;ErbB4 flx/flx adult recipients (Saline n = 7 mice, red; NRG1 n = 6 mice, blue; PV-cre;ErbB4 flx/flx recipients n = 6 mice, orange; PV-cre;ErbB4 flx/flx donors n = 5, yellow). Data in d and e are mean ± SEM.

Article Snippet: Exogenous NRG1 blocked the reduction in response amplitude of PV interneurons. (Δ F / F 0 : PreMD, 0.449 ± 0.035, n = 73 cells from 3 mice, solid green; PostMD, 0.342 ± 0.028, n = 36 cells from 2 mice, dashed green; p = 0.266, Mann–Whitney U -test, two-tailed).

Techniques: Optical Imaging, Transplantation Assay, Saline, MANN-WHITNEY, Two Tailed Test

Journal: Frontiers in Oncology

Article Title: Circular RNA FNDC3B Protects Oral Squamous Cell Carcinoma Cells From Ferroptosis and Contributes to the Malignant Progression by Regulating miR-520d-5p/SLC7A11 Axis

doi: 10.3389/fonc.2021.672724

Figure Lengend Snippet: CircFNDC3B protects OSCC cells against ferroptosis. (A–F) The circFNDC3B shRNA treated the CAL27 and SCC15 cells. (A) The RT-qPCR analysis of circFNDC3B expression. (B) Western blot of GPX4 and SLC7A11 expression. (C–E) Analysis of ROS, iron, and Fe 2+ levels. (F) CCK-8 assays of cell viability. N = 3, mean ± SEM: ** P < 0.01, *** P < 0.001.

Article Snippet: The exogenous circFNDC3B and SLC7A11 were fully synthesized and purchased (GenScript, China).

Techniques: shRNA, Quantitative RT-PCR, Expressing, Western Blot, CCK-8 Assay

Journal: Frontiers in Oncology

Article Title: Circular RNA FNDC3B Protects Oral Squamous Cell Carcinoma Cells From Ferroptosis and Contributes to the Malignant Progression by Regulating miR-520d-5p/SLC7A11 Axis

doi: 10.3389/fonc.2021.672724

Figure Lengend Snippet: CircFNDC3B contributes to OSCC cell proliferation in vitro . (A) The expression of circFNDC3B was analyzed by qPCR in the clinical OSCC tissues and the OSCC samples were divided into two group according to the circFNDC3B expression. The correlation of circFNDC3B with the prognosis of OSCC patients was evaluated by the overall survival analysis. (B–F) The circFNDC3B shRNA treated the CAL27 and SCC15 cells. (B) CCK-8 assays of cell viability. (C, D) Colony formation assays of cell proliferation. (E, F) Flow cytometry analysis of cell apoptosis. N = 3, mean ± SEM: ** P < 0.01.

Article Snippet: The exogenous circFNDC3B and SLC7A11 were fully synthesized and purchased (GenScript, China).

Techniques: In Vitro, Expressing, shRNA, CCK-8 Assay, Flow Cytometry

Journal: Frontiers in Oncology

Article Title: Circular RNA FNDC3B Protects Oral Squamous Cell Carcinoma Cells From Ferroptosis and Contributes to the Malignant Progression by Regulating miR-520d-5p/SLC7A11 Axis

doi: 10.3389/fonc.2021.672724

Figure Lengend Snippet: CircFNDC3B promotes OSCC cell proliferation in vitro . (A–E) The pcDNA3.1-circFNDC3B overexpressing vectors treated the CAL27 and SCC15 cells. (A) CCK-8 assays of cell viability. (B, C) Colony formation assays of cell proliferation. (D, E) Flow cytometry analysis of cell apoptosis. N= 3, mean ± SEM: ** P < 0.01.

Article Snippet: The exogenous circFNDC3B and SLC7A11 were fully synthesized and purchased (GenScript, China).

Techniques: In Vitro, CCK-8 Assay, Flow Cytometry

Journal: Frontiers in Oncology

Article Title: Circular RNA FNDC3B Protects Oral Squamous Cell Carcinoma Cells From Ferroptosis and Contributes to the Malignant Progression by Regulating miR-520d-5p/SLC7A11 Axis

doi: 10.3389/fonc.2021.672724

Figure Lengend Snippet: CircFNDC3B enhances SLC7A11 expression by targeting miR-520d-5p. (A) The interaction of miR-520d-5p with circFNDC3B and SLC7A11 was identified in ENCORI online database. (B–D) MiR-520d-5p mimic or control mimic was used to treat CAL27 and SCC15 cells. (B) The RT-qPCR analysis of miR-520d-5p expression. (C, D) Dual luciferase reporter assays of luciferase activities of circFNDC3B and SLC7A11 mRNA 3’UTR, respectively. (E) The RT-qPCR analysis of miR-520d-5p expression in CAL27 and SCC15 cells treated with circFNDC3B shRNA. (F) The RT-qPCR analysis of SLC7A11 expression in CAL27 and SCC15 cells treated with miR-520d-5p mimic. (G) Western blot analysis of SLC7A11 expression in CAL27 and SCC15 cells treated with circFNDC3B shRNA and miR-520d-5p inhibitor. N = 6, mean ± SEM: ns no significance, ** P < 0.01. (H) The expression of circFNDC3B, SLC7A11, and miR-520d-5p was analyzed by qPCR in the clinical OSCC tissues and the related non-tumor tissues. (I) The correlation of circFNDC3B, SLC7A11, and miR-520d-5p was analyzed by qPCR in the clinical OSCC tissues. mean ± SEM: ** P < 0.01.

Article Snippet: The exogenous circFNDC3B and SLC7A11 were fully synthesized and purchased (GenScript, China).

Techniques: Expressing, Control, Quantitative RT-PCR, Luciferase, shRNA, Western Blot

Journal: Frontiers in Oncology

Article Title: Circular RNA FNDC3B Protects Oral Squamous Cell Carcinoma Cells From Ferroptosis and Contributes to the Malignant Progression by Regulating miR-520d-5p/SLC7A11 Axis

doi: 10.3389/fonc.2021.672724

Figure Lengend Snippet: CircFNDC3B represses ferroptosis of OSCC cells by inducing SLC7A11 expression. (A–E) The circFNDC3B shRNA and pcDNA3.1-SLC7A11 were applied to co-treat CAL27 and SCC15 cells. (A) Western blot of GPX4 and SLC7A11 expression. (B–D) Analysis of ROS, iron, and Fe 2+ levels. (E) CCK-8 assays of cell viability. N = 3, mean ± SEM: ** P < 0.01.

Article Snippet: The exogenous circFNDC3B and SLC7A11 were fully synthesized and purchased (GenScript, China).

Techniques: Expressing, shRNA, Western Blot, CCK-8 Assay

Journal: Frontiers in Oncology

Article Title: Circular RNA FNDC3B Protects Oral Squamous Cell Carcinoma Cells From Ferroptosis and Contributes to the Malignant Progression by Regulating miR-520d-5p/SLC7A11 Axis

doi: 10.3389/fonc.2021.672724

Figure Lengend Snippet: miR-520d-5p induces ferroptosis of OSCC cells by repressing SLC7A11 expression. (A–E) The miR-520d-5p mimic and pcDNA3.1-SLC7A11 were applied to co-treat CAL27 and SCC15 cells. (A–C) Analysis of ROS, iron, and Fe 2+ levels. (D) CCK-8 assays of cell viability. (E) The CAL27 and SCC15 cells were treated with circFNDC3B shRNA or co-treated with circFNDC3B shRNA and miR-520d-5p inhibitor and pcDNA3.1-SLC7A11. Colony formation assays of cell proliferation. N = 3, mean ± SEM: ** P < 0.01.

Article Snippet: The exogenous circFNDC3B and SLC7A11 were fully synthesized and purchased (GenScript, China).

Techniques: Expressing, CCK-8 Assay, shRNA

Journal: Frontiers in Oncology

Article Title: Circular RNA FNDC3B Protects Oral Squamous Cell Carcinoma Cells From Ferroptosis and Contributes to the Malignant Progression by Regulating miR-520d-5p/SLC7A11 Axis

doi: 10.3389/fonc.2021.672724

Figure Lengend Snippet: CircFNDC3B contributes to OSCC cells growth in vivo. (A–E) Tumorigenicity assays in nude mice injected with CAL27 cells, which were treated with control shRNA or circFNDC3B shRNA. (A) Representative images of dissected tumors. (B, C) The analysis of average tumor volume and tumor weight. (D) The RT-qPCR assays of miR-520d-5p expression. (E) Western blot analysis of SLC7A11 expression. (F) Schematic diagram of the proposed mechanism of circFNDC3B-mediated ferroptosis and progression of OSCC. N = 5, mean ± SEM: ** P < 0.01.

Article Snippet: The exogenous circFNDC3B and SLC7A11 were fully synthesized and purchased (GenScript, China).

Techniques: In Vivo, Injection, Control, shRNA, Quantitative RT-PCR, Expressing, Western Blot