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mnat1  (Proteintech)


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    Proteintech mnat1
    TDP-43 loss of function directly leads to cryptic splicing and reduced gene expression A. The levels of transcripts with cryptic exons in AKT3 , CACNA1E , CEP290 , KALRN , KCNQ2 , <t>MNAT1</t> , RAP1GAP , SETD5 , STXBP5L , and SYT7 were increased upon TDP-43 knockdown. qPCR experiments were performed in iNeurons treated with TDP-43 shRNAs for seven days. The level of GAPDH was used for normalization. The level in control condition was set to 1. Mean ± s.e.m., n=3, unpaired t-test, ** p<0.01, *** p<0.001, **** p<0.0001. B. The total transcript levels of AKT3 , CACNA1E , KALRN , KCNQ2 , RAP1GAP , SETD5 , and SYT7 were decreased upon TDP-43 knockdown while the total transcript level of STXBP5L was increased. qPCR experiments were performed in iNeurons treated with TDP-43 shRNAs for seven days. The level of GAPDH was used for normalization. The level in control condition was set to 1. Mean ± s.e.m., n=3, unpaired t-test, ** p<0.01, *** p<0.001, **** p<0.0001. C. The total protein levels of UNC13A , KALRN , MNAT1 , RAP1GAP , and SYT7 were decreased upon TDP-43 knockdown. Western blotting experiments were performed in iNeurons treated with TDP-43 shRNAs for twelve days. The level of GAPDH or Tubulin was used for normalization. The level in control condition was set to 1. Mean ± s.e.m., n=3, unpaired t-test, *** p<0.001, **** p<0.0001. D. TDP-43 binding sites or UG-rich motifs were detected in the cryptic splicing region of KALRN , KCNQ2 , MNAT1 , RAP1GAP , SETD5 , and SYT7 . Lane 1, RNA-seq track of TDP-43 positive nuclei from FTD/ALS patient brain tissues; Lane 2, RNA-seq track of TDP-43 negative nuclei from FTD/ALS patient brain tissues; Lane 3, CLIP-seq track of TDP-43 in SH-SY5Y cells; Lane 4, percentage of UG (TG) or GU (GT) dinucleotides in 20bp bins, displayed as IGV tracks with a data range of 0.4–1; red rectangle, cryptic exon.
    Mnat1, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 93 stars, based on 4 article reviews
    mnat1 - by Bioz Stars, 2026-07
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    1) Product Images from "Cryptic splicing in synaptic and membrane excitability genes links TDP-43 loss to neuronal dysfunction"

    Article Title: Cryptic splicing in synaptic and membrane excitability genes links TDP-43 loss to neuronal dysfunction

    Journal: bioRxiv

    doi: 10.1101/2025.08.28.672801

    TDP-43 loss of function directly leads to cryptic splicing and reduced gene expression A. The levels of transcripts with cryptic exons in AKT3 , CACNA1E , CEP290 , KALRN , KCNQ2 , MNAT1 , RAP1GAP , SETD5 , STXBP5L , and SYT7 were increased upon TDP-43 knockdown. qPCR experiments were performed in iNeurons treated with TDP-43 shRNAs for seven days. The level of GAPDH was used for normalization. The level in control condition was set to 1. Mean ± s.e.m., n=3, unpaired t-test, ** p<0.01, *** p<0.001, **** p<0.0001. B. The total transcript levels of AKT3 , CACNA1E , KALRN , KCNQ2 , RAP1GAP , SETD5 , and SYT7 were decreased upon TDP-43 knockdown while the total transcript level of STXBP5L was increased. qPCR experiments were performed in iNeurons treated with TDP-43 shRNAs for seven days. The level of GAPDH was used for normalization. The level in control condition was set to 1. Mean ± s.e.m., n=3, unpaired t-test, ** p<0.01, *** p<0.001, **** p<0.0001. C. The total protein levels of UNC13A , KALRN , MNAT1 , RAP1GAP , and SYT7 were decreased upon TDP-43 knockdown. Western blotting experiments were performed in iNeurons treated with TDP-43 shRNAs for twelve days. The level of GAPDH or Tubulin was used for normalization. The level in control condition was set to 1. Mean ± s.e.m., n=3, unpaired t-test, *** p<0.001, **** p<0.0001. D. TDP-43 binding sites or UG-rich motifs were detected in the cryptic splicing region of KALRN , KCNQ2 , MNAT1 , RAP1GAP , SETD5 , and SYT7 . Lane 1, RNA-seq track of TDP-43 positive nuclei from FTD/ALS patient brain tissues; Lane 2, RNA-seq track of TDP-43 negative nuclei from FTD/ALS patient brain tissues; Lane 3, CLIP-seq track of TDP-43 in SH-SY5Y cells; Lane 4, percentage of UG (TG) or GU (GT) dinucleotides in 20bp bins, displayed as IGV tracks with a data range of 0.4–1; red rectangle, cryptic exon.
    Figure Legend Snippet: TDP-43 loss of function directly leads to cryptic splicing and reduced gene expression A. The levels of transcripts with cryptic exons in AKT3 , CACNA1E , CEP290 , KALRN , KCNQ2 , MNAT1 , RAP1GAP , SETD5 , STXBP5L , and SYT7 were increased upon TDP-43 knockdown. qPCR experiments were performed in iNeurons treated with TDP-43 shRNAs for seven days. The level of GAPDH was used for normalization. The level in control condition was set to 1. Mean ± s.e.m., n=3, unpaired t-test, ** p<0.01, *** p<0.001, **** p<0.0001. B. The total transcript levels of AKT3 , CACNA1E , KALRN , KCNQ2 , RAP1GAP , SETD5 , and SYT7 were decreased upon TDP-43 knockdown while the total transcript level of STXBP5L was increased. qPCR experiments were performed in iNeurons treated with TDP-43 shRNAs for seven days. The level of GAPDH was used for normalization. The level in control condition was set to 1. Mean ± s.e.m., n=3, unpaired t-test, ** p<0.01, *** p<0.001, **** p<0.0001. C. The total protein levels of UNC13A , KALRN , MNAT1 , RAP1GAP , and SYT7 were decreased upon TDP-43 knockdown. Western blotting experiments were performed in iNeurons treated with TDP-43 shRNAs for twelve days. The level of GAPDH or Tubulin was used for normalization. The level in control condition was set to 1. Mean ± s.e.m., n=3, unpaired t-test, *** p<0.001, **** p<0.0001. D. TDP-43 binding sites or UG-rich motifs were detected in the cryptic splicing region of KALRN , KCNQ2 , MNAT1 , RAP1GAP , SETD5 , and SYT7 . Lane 1, RNA-seq track of TDP-43 positive nuclei from FTD/ALS patient brain tissues; Lane 2, RNA-seq track of TDP-43 negative nuclei from FTD/ALS patient brain tissues; Lane 3, CLIP-seq track of TDP-43 in SH-SY5Y cells; Lane 4, percentage of UG (TG) or GU (GT) dinucleotides in 20bp bins, displayed as IGV tracks with a data range of 0.4–1; red rectangle, cryptic exon.

    Techniques Used: Gene Expression, Knockdown, Control, Western Blot, Binding Assay, RNA Sequencing

    Cryptic splicing targets of TDP-43 are critical for maintaining neuronal activity A. Schematic diagrams show the experimental design of multielectrode array (MEA) recordings upon knockdown of TDP-43 or its cryptic splicing targets in iNeurons in two batches. Batch 1 examined the effects of a reduction in TDP-43, KALRN, RAP1GAP, SYT7, and UNC13A, and Batch 2 examined the effects of a reduction in TDP-43, KCNQ2, MNAT1, and STMN2. Knockdown or scramble shRNAs were administered on Day 21 in both batches. A first evaluation was conducted on Day 40 in Batch 1 and on Day 30 in Batch 2 (T1). A second evaluation was conducted on Day 48 in Batch 1 and on Day 35 in Batch 2 (T2). B. MEA analysis shows decreases in the weighted mean firing rate (spontaneous firing) and the number of bursts (excitability) upon reductions in TDP-43, RAP1GAP, SYT7, KCNQ2, and MNAT1 at T1, as well as decreases in the synchrony index (connectivity) upon reductions in TDP-43, KALRN, RAP1GAP, SYT7, UNC13A, KCNQ2, and MNAT1 at T2. Mean ± s.e.m., n=8, one-way ANOVA, * p<0.05, ** p<0.01, *** p<0.001, **** p<0.0001.
    Figure Legend Snippet: Cryptic splicing targets of TDP-43 are critical for maintaining neuronal activity A. Schematic diagrams show the experimental design of multielectrode array (MEA) recordings upon knockdown of TDP-43 or its cryptic splicing targets in iNeurons in two batches. Batch 1 examined the effects of a reduction in TDP-43, KALRN, RAP1GAP, SYT7, and UNC13A, and Batch 2 examined the effects of a reduction in TDP-43, KCNQ2, MNAT1, and STMN2. Knockdown or scramble shRNAs were administered on Day 21 in both batches. A first evaluation was conducted on Day 40 in Batch 1 and on Day 30 in Batch 2 (T1). A second evaluation was conducted on Day 48 in Batch 1 and on Day 35 in Batch 2 (T2). B. MEA analysis shows decreases in the weighted mean firing rate (spontaneous firing) and the number of bursts (excitability) upon reductions in TDP-43, RAP1GAP, SYT7, KCNQ2, and MNAT1 at T1, as well as decreases in the synchrony index (connectivity) upon reductions in TDP-43, KALRN, RAP1GAP, SYT7, UNC13A, KCNQ2, and MNAT1 at T2. Mean ± s.e.m., n=8, one-way ANOVA, * p<0.05, ** p<0.01, *** p<0.001, **** p<0.0001.

    Techniques Used: Activity Assay, Knockdown



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    TDP-43 loss of function directly leads to cryptic splicing and reduced gene expression A. The levels of transcripts with cryptic exons in AKT3 , CACNA1E , CEP290 , KALRN , KCNQ2 , MNAT1 , RAP1GAP , SETD5 , STXBP5L , and SYT7 were increased upon TDP-43 knockdown. qPCR experiments were performed in iNeurons treated with TDP-43 shRNAs for seven days. The level of GAPDH was used for normalization. The level in control condition was set to 1. Mean ± s.e.m., n=3, unpaired t-test, ** p<0.01, *** p<0.001, **** p<0.0001. B. The total transcript levels of AKT3 , CACNA1E , KALRN , KCNQ2 , RAP1GAP , SETD5 , and SYT7 were decreased upon TDP-43 knockdown while the total transcript level of STXBP5L was increased. qPCR experiments were performed in iNeurons treated with TDP-43 shRNAs for seven days. The level of GAPDH was used for normalization. The level in control condition was set to 1. Mean ± s.e.m., n=3, unpaired t-test, ** p<0.01, *** p<0.001, **** p<0.0001. C. The total protein levels of UNC13A , KALRN , MNAT1 , RAP1GAP , and SYT7 were decreased upon TDP-43 knockdown. Western blotting experiments were performed in iNeurons treated with TDP-43 shRNAs for twelve days. The level of GAPDH or Tubulin was used for normalization. The level in control condition was set to 1. Mean ± s.e.m., n=3, unpaired t-test, *** p<0.001, **** p<0.0001. D. TDP-43 binding sites or UG-rich motifs were detected in the cryptic splicing region of KALRN , KCNQ2 , MNAT1 , RAP1GAP , SETD5 , and SYT7 . Lane 1, RNA-seq track of TDP-43 positive nuclei from FTD/ALS patient brain tissues; Lane 2, RNA-seq track of TDP-43 negative nuclei from FTD/ALS patient brain tissues; Lane 3, CLIP-seq track of TDP-43 in SH-SY5Y cells; Lane 4, percentage of UG (TG) or GU (GT) dinucleotides in 20bp bins, displayed as IGV tracks with a data range of 0.4–1; red rectangle, cryptic exon.

    Journal: bioRxiv

    Article Title: Cryptic splicing in synaptic and membrane excitability genes links TDP-43 loss to neuronal dysfunction

    doi: 10.1101/2025.08.28.672801

    Figure Lengend Snippet: TDP-43 loss of function directly leads to cryptic splicing and reduced gene expression A. The levels of transcripts with cryptic exons in AKT3 , CACNA1E , CEP290 , KALRN , KCNQ2 , MNAT1 , RAP1GAP , SETD5 , STXBP5L , and SYT7 were increased upon TDP-43 knockdown. qPCR experiments were performed in iNeurons treated with TDP-43 shRNAs for seven days. The level of GAPDH was used for normalization. The level in control condition was set to 1. Mean ± s.e.m., n=3, unpaired t-test, ** p<0.01, *** p<0.001, **** p<0.0001. B. The total transcript levels of AKT3 , CACNA1E , KALRN , KCNQ2 , RAP1GAP , SETD5 , and SYT7 were decreased upon TDP-43 knockdown while the total transcript level of STXBP5L was increased. qPCR experiments were performed in iNeurons treated with TDP-43 shRNAs for seven days. The level of GAPDH was used for normalization. The level in control condition was set to 1. Mean ± s.e.m., n=3, unpaired t-test, ** p<0.01, *** p<0.001, **** p<0.0001. C. The total protein levels of UNC13A , KALRN , MNAT1 , RAP1GAP , and SYT7 were decreased upon TDP-43 knockdown. Western blotting experiments were performed in iNeurons treated with TDP-43 shRNAs for twelve days. The level of GAPDH or Tubulin was used for normalization. The level in control condition was set to 1. Mean ± s.e.m., n=3, unpaired t-test, *** p<0.001, **** p<0.0001. D. TDP-43 binding sites or UG-rich motifs were detected in the cryptic splicing region of KALRN , KCNQ2 , MNAT1 , RAP1GAP , SETD5 , and SYT7 . Lane 1, RNA-seq track of TDP-43 positive nuclei from FTD/ALS patient brain tissues; Lane 2, RNA-seq track of TDP-43 negative nuclei from FTD/ALS patient brain tissues; Lane 3, CLIP-seq track of TDP-43 in SH-SY5Y cells; Lane 4, percentage of UG (TG) or GU (GT) dinucleotides in 20bp bins, displayed as IGV tracks with a data range of 0.4–1; red rectangle, cryptic exon.

    Article Snippet: Primary antibodies used in this study were: TDP-43 (Proteintech, 10782-2-AP), Tubulin (Cell Signaling Technology, 2144S), GAPDH (Sigma-Aldrich, G8795), UNC13A (Proteintech, 68483-1-Ig), KALRN (Proteintech, 19740-1-AP), RAP1GAP (Abcam, ab32373), SYT7 (Thermo Scientific, PA5-52998), MNAT1 (Proteintech, 11719-1-AP).

    Techniques: Gene Expression, Knockdown, Control, Western Blot, Binding Assay, RNA Sequencing

    Cryptic splicing targets of TDP-43 are critical for maintaining neuronal activity A. Schematic diagrams show the experimental design of multielectrode array (MEA) recordings upon knockdown of TDP-43 or its cryptic splicing targets in iNeurons in two batches. Batch 1 examined the effects of a reduction in TDP-43, KALRN, RAP1GAP, SYT7, and UNC13A, and Batch 2 examined the effects of a reduction in TDP-43, KCNQ2, MNAT1, and STMN2. Knockdown or scramble shRNAs were administered on Day 21 in both batches. A first evaluation was conducted on Day 40 in Batch 1 and on Day 30 in Batch 2 (T1). A second evaluation was conducted on Day 48 in Batch 1 and on Day 35 in Batch 2 (T2). B. MEA analysis shows decreases in the weighted mean firing rate (spontaneous firing) and the number of bursts (excitability) upon reductions in TDP-43, RAP1GAP, SYT7, KCNQ2, and MNAT1 at T1, as well as decreases in the synchrony index (connectivity) upon reductions in TDP-43, KALRN, RAP1GAP, SYT7, UNC13A, KCNQ2, and MNAT1 at T2. Mean ± s.e.m., n=8, one-way ANOVA, * p<0.05, ** p<0.01, *** p<0.001, **** p<0.0001.

    Journal: bioRxiv

    Article Title: Cryptic splicing in synaptic and membrane excitability genes links TDP-43 loss to neuronal dysfunction

    doi: 10.1101/2025.08.28.672801

    Figure Lengend Snippet: Cryptic splicing targets of TDP-43 are critical for maintaining neuronal activity A. Schematic diagrams show the experimental design of multielectrode array (MEA) recordings upon knockdown of TDP-43 or its cryptic splicing targets in iNeurons in two batches. Batch 1 examined the effects of a reduction in TDP-43, KALRN, RAP1GAP, SYT7, and UNC13A, and Batch 2 examined the effects of a reduction in TDP-43, KCNQ2, MNAT1, and STMN2. Knockdown or scramble shRNAs were administered on Day 21 in both batches. A first evaluation was conducted on Day 40 in Batch 1 and on Day 30 in Batch 2 (T1). A second evaluation was conducted on Day 48 in Batch 1 and on Day 35 in Batch 2 (T2). B. MEA analysis shows decreases in the weighted mean firing rate (spontaneous firing) and the number of bursts (excitability) upon reductions in TDP-43, RAP1GAP, SYT7, KCNQ2, and MNAT1 at T1, as well as decreases in the synchrony index (connectivity) upon reductions in TDP-43, KALRN, RAP1GAP, SYT7, UNC13A, KCNQ2, and MNAT1 at T2. Mean ± s.e.m., n=8, one-way ANOVA, * p<0.05, ** p<0.01, *** p<0.001, **** p<0.0001.

    Article Snippet: Primary antibodies used in this study were: TDP-43 (Proteintech, 10782-2-AP), Tubulin (Cell Signaling Technology, 2144S), GAPDH (Sigma-Aldrich, G8795), UNC13A (Proteintech, 68483-1-Ig), KALRN (Proteintech, 19740-1-AP), RAP1GAP (Abcam, ab32373), SYT7 (Thermo Scientific, PA5-52998), MNAT1 (Proteintech, 11719-1-AP).

    Techniques: Activity Assay, Knockdown

    MNAT1 was upregulated in cisplatin-resistant LSCC cells and promotes cisplatin resistance. A-B ) CCK-8 assay was used to detect the survival rate and IC50 of LSCC cell lines and cisplatin-resistant cell lines. C ) The Venn diagram showed that the transcriptome sequencing of LSCC and LSCC/DDP up-regulated genes intersected with DDRs. D ) MNAT1 was analysed in LSCC and para-carcinoma tissues using IHC assay. E-F ) Western blotting was used to detect the expression of MNAT1 in LSCC tissues and adjacent tissues. G ) RT-PCR was used to detect the expression of MNAT1 in LSCC and HBE135-E6E7 cell lines. H) MNAT1 expression was detected in LSCC and HBE135-E6E7 cell lines using Western blotting. I ) Kaplan–Meier overall survival analysis of patients with HNSCC stratified by MNAT1 expression. G) Western blotting to analyse MNAT1 expression in LSCC cells and LSCC/DDP cells. K-L ) IC50 of MNAT1-OE against cisplatin in LSCC and IC50 of MNAT1/KD against cisplatin in LSCC/DDP. M) Colony formation assay to assess the rate of cell proliferation by MNAT1-KD. N—O) Invasive ability of LSCC and LSCC/DDP affected by MNAT1-OE and MNAT1-KD assessed by transwell. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Journal: Translational Oncology

    Article Title: Mitochondrial apoptosis induced by MNAT1 in laryngeal squamous cell carcinoma cells reverses drug resistance

    doi: 10.1016/j.tranon.2025.102460

    Figure Lengend Snippet: MNAT1 was upregulated in cisplatin-resistant LSCC cells and promotes cisplatin resistance. A-B ) CCK-8 assay was used to detect the survival rate and IC50 of LSCC cell lines and cisplatin-resistant cell lines. C ) The Venn diagram showed that the transcriptome sequencing of LSCC and LSCC/DDP up-regulated genes intersected with DDRs. D ) MNAT1 was analysed in LSCC and para-carcinoma tissues using IHC assay. E-F ) Western blotting was used to detect the expression of MNAT1 in LSCC tissues and adjacent tissues. G ) RT-PCR was used to detect the expression of MNAT1 in LSCC and HBE135-E6E7 cell lines. H) MNAT1 expression was detected in LSCC and HBE135-E6E7 cell lines using Western blotting. I ) Kaplan–Meier overall survival analysis of patients with HNSCC stratified by MNAT1 expression. G) Western blotting to analyse MNAT1 expression in LSCC cells and LSCC/DDP cells. K-L ) IC50 of MNAT1-OE against cisplatin in LSCC and IC50 of MNAT1/KD against cisplatin in LSCC/DDP. M) Colony formation assay to assess the rate of cell proliferation by MNAT1-KD. N—O) Invasive ability of LSCC and LSCC/DDP affected by MNAT1-OE and MNAT1-KD assessed by transwell. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Article Snippet: Blocking was conducted with goat serum, followed by an overnight incubation at 4 °C with primary antibodies against MNAT1 (YT2662, 1:100, Immunoway), GDF15 (sc377195, 1:100, Santa Cruz Biotechnology), and Ki67 (9027, 1:500, Cell Signaling Technology).

    Techniques: CCK-8 Assay, Sequencing, Western Blot, Expressing, Reverse Transcription Polymerase Chain Reaction, Colony Assay

    MNAT1 was involved in DNA damage and regulated mitochondrial apoptosis in LSCC cells and cisplatin-resistant cells. A-B ) DNA damage in MNAT1-OE and MNAT1-KD in cisplatin medium as assessed by γ-H2AX immunofluorescence. C-D ) DNA damage in MNAT1-OE in cisplatin medium assessed by comet assay. E ) Flow cytometry was used to analyse the effect of MNAT1-OE on the percentage of apoptosis in basal medium and cisplatin-induced medium in AMC—HN-8 and AMC—HN-8/DDP. F ) Immunoblots were used to analyse the effects of MNAT1 knockdown or overexpression on the mitochondrial apoptotic pathway in LSCC and LSCC/DDP, respectively. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Journal: Translational Oncology

    Article Title: Mitochondrial apoptosis induced by MNAT1 in laryngeal squamous cell carcinoma cells reverses drug resistance

    doi: 10.1016/j.tranon.2025.102460

    Figure Lengend Snippet: MNAT1 was involved in DNA damage and regulated mitochondrial apoptosis in LSCC cells and cisplatin-resistant cells. A-B ) DNA damage in MNAT1-OE and MNAT1-KD in cisplatin medium as assessed by γ-H2AX immunofluorescence. C-D ) DNA damage in MNAT1-OE in cisplatin medium assessed by comet assay. E ) Flow cytometry was used to analyse the effect of MNAT1-OE on the percentage of apoptosis in basal medium and cisplatin-induced medium in AMC—HN-8 and AMC—HN-8/DDP. F ) Immunoblots were used to analyse the effects of MNAT1 knockdown or overexpression on the mitochondrial apoptotic pathway in LSCC and LSCC/DDP, respectively. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Article Snippet: Blocking was conducted with goat serum, followed by an overnight incubation at 4 °C with primary antibodies against MNAT1 (YT2662, 1:100, Immunoway), GDF15 (sc377195, 1:100, Santa Cruz Biotechnology), and Ki67 (9027, 1:500, Cell Signaling Technology).

    Techniques: Immunofluorescence, Single Cell Gel Electrophoresis, Flow Cytometry, Western Blot, Knockdown, Over Expression

    Altered downstream genes after MNATI knockdown. A ) Heatmap of transcriptome of differentially expressed genes. B ) Volcano plot of differentially expressed genes. C ) Molecular docking of MNAT1 and GDF15.MNAT1 protein was shown in orange and GDF15 protein was shown in purple. D )Screening of target pathways. E ) Overall survival analysis of patients with high and low expression of GDF15 in the GEPIA database. F ) RT-PCR analysis of correlation between MNAT1 expression and GDF15 expression in LSCC patients. G-H) GDF15 expression in high/low MNAT1 expressing LSCC tissues was analysed using IHC and mIHC assays. I ) Co-IP of MNAT1 with GDF15 in AMC—HN-8. J ) Western blot analysis compared with the control group, the expression of GDF15 protein in MNAT1-OE and MNAT-KD. K ) Western Blotting analysis compared with the control group, the expression of mitochondrial apoptosis-related proteins in GDF15-OE or GDF15-KD. L ) Western Blotting analysis of GDF15-OE or GDF15-KD expression in the AMPK pathway compared to control. M ) Western Blotting analysis of Bcl-2 and Bax expression in LSCC/DDP cells treated with GDF15-KD and/or compound C compared to control. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Journal: Translational Oncology

    Article Title: Mitochondrial apoptosis induced by MNAT1 in laryngeal squamous cell carcinoma cells reverses drug resistance

    doi: 10.1016/j.tranon.2025.102460

    Figure Lengend Snippet: Altered downstream genes after MNATI knockdown. A ) Heatmap of transcriptome of differentially expressed genes. B ) Volcano plot of differentially expressed genes. C ) Molecular docking of MNAT1 and GDF15.MNAT1 protein was shown in orange and GDF15 protein was shown in purple. D )Screening of target pathways. E ) Overall survival analysis of patients with high and low expression of GDF15 in the GEPIA database. F ) RT-PCR analysis of correlation between MNAT1 expression and GDF15 expression in LSCC patients. G-H) GDF15 expression in high/low MNAT1 expressing LSCC tissues was analysed using IHC and mIHC assays. I ) Co-IP of MNAT1 with GDF15 in AMC—HN-8. J ) Western blot analysis compared with the control group, the expression of GDF15 protein in MNAT1-OE and MNAT-KD. K ) Western Blotting analysis compared with the control group, the expression of mitochondrial apoptosis-related proteins in GDF15-OE or GDF15-KD. L ) Western Blotting analysis of GDF15-OE or GDF15-KD expression in the AMPK pathway compared to control. M ) Western Blotting analysis of Bcl-2 and Bax expression in LSCC/DDP cells treated with GDF15-KD and/or compound C compared to control. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Article Snippet: Blocking was conducted with goat serum, followed by an overnight incubation at 4 °C with primary antibodies against MNAT1 (YT2662, 1:100, Immunoway), GDF15 (sc377195, 1:100, Santa Cruz Biotechnology), and Ki67 (9027, 1:500, Cell Signaling Technology).

    Techniques: Knockdown, Expressing, Reverse Transcription Polymerase Chain Reaction, Co-Immunoprecipitation Assay, Western Blot, Control

    MNAT1 inhibited the apoptosis of LSCC cells and promotes cisplatin resistance through GDF15, and affected the proliferation, migration and invasion of LSCC. A) CCK-8 assay was used to detect the relative IC50 of MNAT1 and GDF15 in LSCC cells treated with cisplatin for 24 h. B) Flow cytometry was used to analyze the effect of cisplatin on the apoptosis rate of LSCC cells through MNAT1 and GDF15 after 24 h of treatment. C-D) Colony formation assay and EDU were used to detect the effect of MNAT1 and GDF15 on cell proliferation rate. E) Scratch test was used to detect the effect of MNT1 and GDF15 on the migration of LSCC cells. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Journal: Translational Oncology

    Article Title: Mitochondrial apoptosis induced by MNAT1 in laryngeal squamous cell carcinoma cells reverses drug resistance

    doi: 10.1016/j.tranon.2025.102460

    Figure Lengend Snippet: MNAT1 inhibited the apoptosis of LSCC cells and promotes cisplatin resistance through GDF15, and affected the proliferation, migration and invasion of LSCC. A) CCK-8 assay was used to detect the relative IC50 of MNAT1 and GDF15 in LSCC cells treated with cisplatin for 24 h. B) Flow cytometry was used to analyze the effect of cisplatin on the apoptosis rate of LSCC cells through MNAT1 and GDF15 after 24 h of treatment. C-D) Colony formation assay and EDU were used to detect the effect of MNAT1 and GDF15 on cell proliferation rate. E) Scratch test was used to detect the effect of MNT1 and GDF15 on the migration of LSCC cells. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Article Snippet: Blocking was conducted with goat serum, followed by an overnight incubation at 4 °C with primary antibodies against MNAT1 (YT2662, 1:100, Immunoway), GDF15 (sc377195, 1:100, Santa Cruz Biotechnology), and Ki67 (9027, 1:500, Cell Signaling Technology).

    Techniques: Migration, CCK-8 Assay, Flow Cytometry, Colony Assay

    MNAT1 affected mitochondrial activity and mitochondrial apoptosis via GDF15 in laryngeal squamous cell carcinoma. A) Transwell assay was used to detect the invasion ability of LSCC cells by MNAT1 and GDF15. B ) Effects of ROS species in LSCC cells by MNAT1 and GDF15. C ) JC-1 assay was used to detect the effects of MNAT1 and GDF15 on mitochondrial membrane potential of LSCC cells. D) Mito Tracker assay was used to detect the effects of MNAT1 and GDF15 on mitochondria and lysosomes in LSCC cells. E) Western blot was used to analyze the expression of mitochondrial apoptosis-related proteins and AMPK pathway through MNAT1 and GDF15 in laryngeal squamous cell carcinoma tissues. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Journal: Translational Oncology

    Article Title: Mitochondrial apoptosis induced by MNAT1 in laryngeal squamous cell carcinoma cells reverses drug resistance

    doi: 10.1016/j.tranon.2025.102460

    Figure Lengend Snippet: MNAT1 affected mitochondrial activity and mitochondrial apoptosis via GDF15 in laryngeal squamous cell carcinoma. A) Transwell assay was used to detect the invasion ability of LSCC cells by MNAT1 and GDF15. B ) Effects of ROS species in LSCC cells by MNAT1 and GDF15. C ) JC-1 assay was used to detect the effects of MNAT1 and GDF15 on mitochondrial membrane potential of LSCC cells. D) Mito Tracker assay was used to detect the effects of MNAT1 and GDF15 on mitochondria and lysosomes in LSCC cells. E) Western blot was used to analyze the expression of mitochondrial apoptosis-related proteins and AMPK pathway through MNAT1 and GDF15 in laryngeal squamous cell carcinoma tissues. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Article Snippet: Blocking was conducted with goat serum, followed by an overnight incubation at 4 °C with primary antibodies against MNAT1 (YT2662, 1:100, Immunoway), GDF15 (sc377195, 1:100, Santa Cruz Biotechnology), and Ki67 (9027, 1:500, Cell Signaling Technology).

    Techniques: Activity Assay, Transwell Assay, Membrane, Western Blot, Expressing

    MNAT1 and GDF15 have a combined effect on cisplatin resistance in vivo. A ) and B ) KD+GDF15-KD transfected AMC—HN-8/DDP. C ) Weight of tumour. D ) Tumour growth curves based on tumour volume. E ) Effect of MNAT1 and GDF15 on LSCC/DDP subcellular structure. F ) Analysis of KI67 in the tumourome in the mouse xenograft model by IHC assay. G ) Schematic illustration of the effect of MNAT1 on cisplatin resistance through the regulation of mitochondrial apoptosis by GDF15. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Journal: Translational Oncology

    Article Title: Mitochondrial apoptosis induced by MNAT1 in laryngeal squamous cell carcinoma cells reverses drug resistance

    doi: 10.1016/j.tranon.2025.102460

    Figure Lengend Snippet: MNAT1 and GDF15 have a combined effect on cisplatin resistance in vivo. A ) and B ) KD+GDF15-KD transfected AMC—HN-8/DDP. C ) Weight of tumour. D ) Tumour growth curves based on tumour volume. E ) Effect of MNAT1 and GDF15 on LSCC/DDP subcellular structure. F ) Analysis of KI67 in the tumourome in the mouse xenograft model by IHC assay. G ) Schematic illustration of the effect of MNAT1 on cisplatin resistance through the regulation of mitochondrial apoptosis by GDF15. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Article Snippet: Blocking was conducted with goat serum, followed by an overnight incubation at 4 °C with primary antibodies against MNAT1 (YT2662, 1:100, Immunoway), GDF15 (sc377195, 1:100, Santa Cruz Biotechnology), and Ki67 (9027, 1:500, Cell Signaling Technology).

    Techniques: In Vivo, Transfection