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Proteintech primary antibodies against mnat1

<t>MNAT1</t> is upregulated in OS tissues and cell lines. a The mRNA expression of MNAT1 in OS cell lines (MG63, U2OS, Well5 and 143B) and control cells (HOBC and HFOB) was analyzed by qRT-PCR. b The protein expression of MNAT1 in OS cell lines and control cells. c The mRNA expression of MNAT1 in 30-paired OS tissues and adjacent normal tissues from affiliated hospital of qingdao university OS cohort was analyzed by qRT-PCR. d The protein expression of MNAT1 in 6-paired OS tissues (T) and adjacent normal tissues (N) was analyzed by western blot. * p < 0.05, ** p < 0.01

Primary Antibodies Against Mnat1, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/primary+antibodies+against+mnat1/MNAT1+Antibody/pmc07713032-49-0-4
Average 93 stars, based on 5 article reviews

primary antibodies against mnat1 - by Bioz Stars, 2026-08

93/100 stars

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1) Product Images from "MNAT1 promotes proliferation and the chemo-resistance of osteosarcoma cell to cisplatin through regulating PI3K/Akt/mTOR pathway"

Article Title: MNAT1 promotes proliferation and the chemo-resistance of osteosarcoma cell to cisplatin through regulating PI3K/Akt/mTOR pathway

Journal: BMC Cancer

doi: 10.1186/s12885-020-07687-3

MNAT1 is upregulated in OS tissues and cell lines. a The mRNA expression of MNAT1 in OS cell lines (MG63, U2OS, Well5 and 143B) and control cells (HOBC and HFOB) was analyzed by qRT-PCR. b The protein expression of MNAT1 in OS cell lines and control cells. c The mRNA expression of MNAT1 in 30-paired OS tissues and adjacent normal tissues from affiliated hospital of qingdao university OS cohort was analyzed by qRT-PCR. d The protein expression of MNAT1 in 6-paired OS tissues (T) and adjacent normal tissues (N) was analyzed by western blot. * p < 0.05, ** p < 0.01

Figure Legend Snippet: MNAT1 is upregulated in OS tissues and cell lines. a The mRNA expression of MNAT1 in OS cell lines (MG63, U2OS, Well5 and 143B) and control cells (HOBC and HFOB) was analyzed by qRT-PCR. b The protein expression of MNAT1 in OS cell lines and control cells. c The mRNA expression of MNAT1 in 30-paired OS tissues and adjacent normal tissues from affiliated hospital of qingdao university OS cohort was analyzed by qRT-PCR. d The protein expression of MNAT1 in 6-paired OS tissues (T) and adjacent normal tissues (N) was analyzed by western blot. * p < 0.05, ** p < 0.01

Techniques Used: Expressing, Control, Quantitative RT-PCR, Western Blot

MNAT1 expression in OS tissues and its prognostic value. a Representative MNAT1 staining patterns via IHC assays. b MNAT1 expression was significantly higher in OS tissues ( n = 78) compared with that in non-tumor tissues ( n = 40). The correlation of MNAT1 expression level with distant metastasis ( c ), vascular invasion ( d ), and TNM stage ( e ). f and g The OS and DFS were analyzed by Kaplan-Meier analysis. * p < 0.05, ** p < 0.01

Figure Legend Snippet: MNAT1 expression in OS tissues and its prognostic value. a Representative MNAT1 staining patterns via IHC assays. b MNAT1 expression was significantly higher in OS tissues ( n = 78) compared with that in non-tumor tissues ( n = 40). The correlation of MNAT1 expression level with distant metastasis ( c ), vascular invasion ( d ), and TNM stage ( e ). f and g The OS and DFS were analyzed by Kaplan-Meier analysis. * p < 0.05, ** p < 0.01

Techniques Used: Expressing, Staining

MNAT1 knockdown suppressed OS cell proliferation and migration. a The transfection efficiency of the MNAT1 siRNA was evaluated by qRT-PCR and western blot. b and c The changes in the proliferation of OS cells transfected with si-MNAT1 or NC were determined by the CCK-8 assay. d EdU staining assays (Scale bars, 50 μm) and e colony formation assays (Scale bars, 8 mm) were performed to determine the growth of U2OS and 143B cells. f Cell migration was assessed by wound-healing assay (Scale bars, 500 μm). g Cell invasion was assessed by transwell assay (Scale bars, 50 μm). * p < 0.05, ** p < 0.01

Figure Legend Snippet: MNAT1 knockdown suppressed OS cell proliferation and migration. a The transfection efficiency of the MNAT1 siRNA was evaluated by qRT-PCR and western blot. b and c The changes in the proliferation of OS cells transfected with si-MNAT1 or NC were determined by the CCK-8 assay. d EdU staining assays (Scale bars, 50 μm) and e colony formation assays (Scale bars, 8 mm) were performed to determine the growth of U2OS and 143B cells. f Cell migration was assessed by wound-healing assay (Scale bars, 500 μm). g Cell invasion was assessed by transwell assay (Scale bars, 50 μm). * p < 0.05, ** p < 0.01

Techniques Used: Knockdown, Migration, Transfection, Quantitative RT-PCR, Western Blot, CCK-8 Assay, Staining, Wound Healing Assay, Transwell Assay

Ectopic overexpression of MNAT1 promotes OS cell proliferation and invasion in vitro . U2OS and 143B cells were transfected with MNAT1 plasmid or negative control (NC). a The mRNA expression of MNAT1 was examined by qRT-PCR. b The transfection efficiency was evaluated by western blot assay and EdU staining assays (Scale bars, 50 μm) ( c ) and colony formation assays (Scale bars, 8 mm) ( d ) were performed to determine the proliferation of U2OS and 143B cells. e Cell migration was assessed by wound-healing assay (Scale bars, 500 μm). f Cell invasion was assessed by transwell assay (Scale bars, 50 μm). * p < 0.05, ** p < 0.01

Figure Legend Snippet: Ectopic overexpression of MNAT1 promotes OS cell proliferation and invasion in vitro . U2OS and 143B cells were transfected with MNAT1 plasmid or negative control (NC). a The mRNA expression of MNAT1 was examined by qRT-PCR. b The transfection efficiency was evaluated by western blot assay and EdU staining assays (Scale bars, 50 μm) ( c ) and colony formation assays (Scale bars, 8 mm) ( d ) were performed to determine the proliferation of U2OS and 143B cells. e Cell migration was assessed by wound-healing assay (Scale bars, 500 μm). f Cell invasion was assessed by transwell assay (Scale bars, 50 μm). * p < 0.05, ** p < 0.01

Techniques Used: Over Expression, In Vitro, Transfection, Plasmid Preparation, Negative Control, Expressing, Quantitative RT-PCR, Western Blot, Staining, Migration, Wound Healing Assay, Transwell Assay

In vivo functional analysis of MNAT1 in OS. a The strength of the luciferase signal of xenograft tumor was decreased by MNAT1 knockdown. b The relative photon flux of OS tumor in nude mice of NC or sh- MNAT1 group was analyzed by a live imaging system to measure the luciferase signal. Comparison of tumor volume ( c ) and weight ( d ) in NC and sh-MNAT1 infected U2OS cells. e and f Representative IHC staining images and relative expression levels for MNAT1 and ki-67 in tumor sections from sh-MNAT1 group and NC group. * p < 0.05, ** p < 0.01

Figure Legend Snippet: In vivo functional analysis of MNAT1 in OS. a The strength of the luciferase signal of xenograft tumor was decreased by MNAT1 knockdown. b The relative photon flux of OS tumor in nude mice of NC or sh- MNAT1 group was analyzed by a live imaging system to measure the luciferase signal. Comparison of tumor volume ( c ) and weight ( d ) in NC and sh-MNAT1 infected U2OS cells. e and f Representative IHC staining images and relative expression levels for MNAT1 and ki-67 in tumor sections from sh-MNAT1 group and NC group. * p < 0.05, ** p < 0.01

Techniques Used: In Vivo, Functional Assay, Luciferase, Knockdown, Imaging, Comparison, Infection, Immunohistochemistry, Expressing

MNAT1 regulated PI3K/Akt/mTOR signaling pathway in OS. a KEGG analysis the different regulated signaling pathways in OS tumor compared with adjacent non-tumor tissues. b GSEA analysis the enrichment of signature genes in MNAT1 high or low group. c PI3K/Akt/mTOR pathway related proteins were analyzed by western blot. d IHC staining of PI3K, AKT and mTOR in xenograft tumor tissues from NC or sh-MNAT1 group. e The expression of MNAT1 was evaluated by western blot assay. * p < 0.05; ** p < 0.01

Figure Legend Snippet: MNAT1 regulated PI3K/Akt/mTOR signaling pathway in OS. a KEGG analysis the different regulated signaling pathways in OS tumor compared with adjacent non-tumor tissues. b GSEA analysis the enrichment of signature genes in MNAT1 high or low group. c PI3K/Akt/mTOR pathway related proteins were analyzed by western blot. d IHC staining of PI3K, AKT and mTOR in xenograft tumor tissues from NC or sh-MNAT1 group. e The expression of MNAT1 was evaluated by western blot assay. * p < 0.05; ** p < 0.01

Techniques Used: Protein-Protein interactions, Western Blot, Immunohistochemistry, Expressing

MNAT1 regulated OS chemo-sensitivity to DDP-based therapy. U2OS and 143B cells were transfected with si-NC, si-MNAT1, VECTOR or MNAT1 plasmid. After 48 h cells were treated with different concentration of DDP. a and b Cell viability analysis of U2OS and 143B cells treated with si-MNAT1 or MNAT1 plasmid and different concentrations of DDP in comparison with the negative control. c and d Cell viability analysis of U2OS and 143B cells treated with PI3K inhibitor PF-04979064 or MNAT1 plasmid and different concentrations of DDP in comparison with the negative control. e and f Colony formation (Scale bars, 8 mm) and EdU assay (Scale bars, 50 μm) performed on U2OS cells treated with si-MNAT1 or MNAT1 plasmid and different concentration of DDP in comparison with the negative control

Figure Legend Snippet: MNAT1 regulated OS chemo-sensitivity to DDP-based therapy. U2OS and 143B cells were transfected with si-NC, si-MNAT1, VECTOR or MNAT1 plasmid. After 48 h cells were treated with different concentration of DDP. a and b Cell viability analysis of U2OS and 143B cells treated with si-MNAT1 or MNAT1 plasmid and different concentrations of DDP in comparison with the negative control. c and d Cell viability analysis of U2OS and 143B cells treated with PI3K inhibitor PF-04979064 or MNAT1 plasmid and different concentrations of DDP in comparison with the negative control. e and f Colony formation (Scale bars, 8 mm) and EdU assay (Scale bars, 50 μm) performed on U2OS cells treated with si-MNAT1 or MNAT1 plasmid and different concentration of DDP in comparison with the negative control

Techniques Used: Transfection, Plasmid Preparation, Concentration Assay, Comparison, Negative Control, EdU Assay

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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.

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.

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.

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.

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.

Techniques: In Vivo, Transfection

Journal: BMC Cancer

Article Title: MNAT1 promotes proliferation and the chemo-resistance of osteosarcoma cell to cisplatin through regulating PI3K/Akt/mTOR pathway

doi: 10.1186/s12885-020-07687-3

Figure Lengend Snippet: MNAT1 is upregulated in OS tissues and cell lines. a The mRNA expression of MNAT1 in OS cell lines (MG63, U2OS, Well5 and 143B) and control cells (HOBC and HFOB) was analyzed by qRT-PCR. b The protein expression of MNAT1 in OS cell lines and control cells. c The mRNA expression of MNAT1 in 30-paired OS tissues and adjacent normal tissues from affiliated hospital of qingdao university OS cohort was analyzed by qRT-PCR. d The protein expression of MNAT1 in 6-paired OS tissues (T) and adjacent normal tissues (N) was analyzed by western blot. * p < 0.05, ** p < 0.01

Article Snippet: Primary antibodies against MNAT1 (Proteintech, 11,719–1-AP), β-tubulin (Abcam, ab210797), PI3K (Proteintech, 20,584–1-AP), Akt (Proteintech, 10,176–2-AP) and mTOR (Proteintech, 20,657–1-AP).

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

Journal: BMC Cancer

Article Title: MNAT1 promotes proliferation and the chemo-resistance of osteosarcoma cell to cisplatin through regulating PI3K/Akt/mTOR pathway

doi: 10.1186/s12885-020-07687-3

Figure Lengend Snippet: MNAT1 expression in OS tissues and its prognostic value. a Representative MNAT1 staining patterns via IHC assays. b MNAT1 expression was significantly higher in OS tissues ( n = 78) compared with that in non-tumor tissues ( n = 40). The correlation of MNAT1 expression level with distant metastasis ( c ), vascular invasion ( d ), and TNM stage ( e ). f and g The OS and DFS were analyzed by Kaplan-Meier analysis. * p < 0.05, ** p < 0.01

Techniques: Expressing, Staining

Journal: BMC Cancer

Article Title: MNAT1 promotes proliferation and the chemo-resistance of osteosarcoma cell to cisplatin through regulating PI3K/Akt/mTOR pathway

doi: 10.1186/s12885-020-07687-3

Figure Lengend Snippet: MNAT1 knockdown suppressed OS cell proliferation and migration. a The transfection efficiency of the MNAT1 siRNA was evaluated by qRT-PCR and western blot. b and c The changes in the proliferation of OS cells transfected with si-MNAT1 or NC were determined by the CCK-8 assay. d EdU staining assays (Scale bars, 50 μm) and e colony formation assays (Scale bars, 8 mm) were performed to determine the growth of U2OS and 143B cells. f Cell migration was assessed by wound-healing assay (Scale bars, 500 μm). g Cell invasion was assessed by transwell assay (Scale bars, 50 μm). * p < 0.05, ** p < 0.01

Techniques: Knockdown, Migration, Transfection, Quantitative RT-PCR, Western Blot, CCK-8 Assay, Staining, Wound Healing Assay, Transwell Assay

Journal: BMC Cancer

Article Title: MNAT1 promotes proliferation and the chemo-resistance of osteosarcoma cell to cisplatin through regulating PI3K/Akt/mTOR pathway

doi: 10.1186/s12885-020-07687-3

Figure Lengend Snippet: Ectopic overexpression of MNAT1 promotes OS cell proliferation and invasion in vitro . U2OS and 143B cells were transfected with MNAT1 plasmid or negative control (NC). a The mRNA expression of MNAT1 was examined by qRT-PCR. b The transfection efficiency was evaluated by western blot assay and EdU staining assays (Scale bars, 50 μm) ( c ) and colony formation assays (Scale bars, 8 mm) ( d ) were performed to determine the proliferation of U2OS and 143B cells. e Cell migration was assessed by wound-healing assay (Scale bars, 500 μm). f Cell invasion was assessed by transwell assay (Scale bars, 50 μm). * p < 0.05, ** p < 0.01

Techniques: Over Expression, In Vitro, Transfection, Plasmid Preparation, Negative Control, Expressing, Quantitative RT-PCR, Western Blot, Staining, Migration, Wound Healing Assay, Transwell Assay

Journal: BMC Cancer

Article Title: MNAT1 promotes proliferation and the chemo-resistance of osteosarcoma cell to cisplatin through regulating PI3K/Akt/mTOR pathway

doi: 10.1186/s12885-020-07687-3

Figure Lengend Snippet: In vivo functional analysis of MNAT1 in OS. a The strength of the luciferase signal of xenograft tumor was decreased by MNAT1 knockdown. b The relative photon flux of OS tumor in nude mice of NC or sh- MNAT1 group was analyzed by a live imaging system to measure the luciferase signal. Comparison of tumor volume ( c ) and weight ( d ) in NC and sh-MNAT1 infected U2OS cells. e and f Representative IHC staining images and relative expression levels for MNAT1 and ki-67 in tumor sections from sh-MNAT1 group and NC group. * p < 0.05, ** p < 0.01

Techniques: In Vivo, Functional Assay, Luciferase, Knockdown, Imaging, Comparison, Infection, Immunohistochemistry, Expressing

Journal: BMC Cancer

Article Title: MNAT1 promotes proliferation and the chemo-resistance of osteosarcoma cell to cisplatin through regulating PI3K/Akt/mTOR pathway

doi: 10.1186/s12885-020-07687-3

Figure Lengend Snippet: MNAT1 regulated PI3K/Akt/mTOR signaling pathway in OS. a KEGG analysis the different regulated signaling pathways in OS tumor compared with adjacent non-tumor tissues. b GSEA analysis the enrichment of signature genes in MNAT1 high or low group. c PI3K/Akt/mTOR pathway related proteins were analyzed by western blot. d IHC staining of PI3K, AKT and mTOR in xenograft tumor tissues from NC or sh-MNAT1 group. e The expression of MNAT1 was evaluated by western blot assay. * p < 0.05; ** p < 0.01

Techniques: Protein-Protein interactions, Western Blot, Immunohistochemistry, Expressing

Journal: BMC Cancer

Article Title: MNAT1 promotes proliferation and the chemo-resistance of osteosarcoma cell to cisplatin through regulating PI3K/Akt/mTOR pathway

doi: 10.1186/s12885-020-07687-3

Figure Lengend Snippet: MNAT1 regulated OS chemo-sensitivity to DDP-based therapy. U2OS and 143B cells were transfected with si-NC, si-MNAT1, VECTOR or MNAT1 plasmid. After 48 h cells were treated with different concentration of DDP. a and b Cell viability analysis of U2OS and 143B cells treated with si-MNAT1 or MNAT1 plasmid and different concentrations of DDP in comparison with the negative control. c and d Cell viability analysis of U2OS and 143B cells treated with PI3K inhibitor PF-04979064 or MNAT1 plasmid and different concentrations of DDP in comparison with the negative control. e and f Colony formation (Scale bars, 8 mm) and EdU assay (Scale bars, 50 μm) performed on U2OS cells treated with si-MNAT1 or MNAT1 plasmid and different concentration of DDP in comparison with the negative control

Techniques: Transfection, Plasmid Preparation, Concentration Assay, Comparison, Negative Control, EdU Assay

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