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Fig. 6. MT1H induces p53-dependent <t>autophagy</t> via regulating the key genes in nutrient transportation. (A) Semi-qPCR to verify the downregulated or upregulated genes by MT1H in AGS cells. AGS-tetO-MT1H cells were treated with Dox (2 µg/ml) to induce the expression of ectopic MT1H. 24 h later, cells were harvested for total RNA extraction and reverse transcription followed by semi-qPCR. (B) The cells expressing tetO-MT1H were treated with Dox (2 µg/ml) to induce the expression of ectopic MT1H. 24 h later, cells were harvested for immunoblot analysis with indicated <t>antibodies.</t> NE-PER Nuclear and Cytoplasmic Extraction <t>kit</t> (Thermo) was used to fractionate cells into cytosol compartment and nuclear compartment. (C) MT1H biological functions by KEGG analysis. The participation in mineral absorption was predicted by KEGG-Pathway55 (https://www.genome.jp/kegg/). (D) Illustrative diagram of MT1H biological functions in gastric cells. The information in the diagram is the combination of our current research and KEGG-Pathway.
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Fig. 6. MT1H induces p53-dependent <t>autophagy</t> via regulating the key genes in nutrient transportation. (A) Semi-qPCR to verify the downregulated or upregulated genes by MT1H in AGS cells. AGS-tetO-MT1H cells were treated with Dox (2 µg/ml) to induce the expression of ectopic MT1H. 24 h later, cells were harvested for total RNA extraction and reverse transcription followed by semi-qPCR. (B) The cells expressing tetO-MT1H were treated with Dox (2 µg/ml) to induce the expression of ectopic MT1H. 24 h later, cells were harvested for immunoblot analysis with indicated <t>antibodies.</t> NE-PER Nuclear and Cytoplasmic Extraction <t>kit</t> (Thermo) was used to fractionate cells into cytosol compartment and nuclear compartment. (C) MT1H biological functions by KEGG analysis. The participation in mineral absorption was predicted by KEGG-Pathway55 (https://www.genome.jp/kegg/). (D) Illustrative diagram of MT1H biological functions in gastric cells. The information in the diagram is the combination of our current research and KEGG-Pathway.
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Fig. 6. MT1H induces p53-dependent <t>autophagy</t> via regulating the key genes in nutrient transportation. (A) Semi-qPCR to verify the downregulated or upregulated genes by MT1H in AGS cells. AGS-tetO-MT1H cells were treated with Dox (2 µg/ml) to induce the expression of ectopic MT1H. 24 h later, cells were harvested for total RNA extraction and reverse transcription followed by semi-qPCR. (B) The cells expressing tetO-MT1H were treated with Dox (2 µg/ml) to induce the expression of ectopic MT1H. 24 h later, cells were harvested for immunoblot analysis with indicated <t>antibodies.</t> NE-PER Nuclear and Cytoplasmic Extraction <t>kit</t> (Thermo) was used to fractionate cells into cytosol compartment and nuclear compartment. (C) MT1H biological functions by KEGG analysis. The participation in mineral absorption was predicted by KEGG-Pathway55 (https://www.genome.jp/kegg/). (D) Illustrative diagram of MT1H biological functions in gastric cells. The information in the diagram is the combination of our current research and KEGG-Pathway.
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Fig. 6. MT1H induces p53-dependent <t>autophagy</t> via regulating the key genes in nutrient transportation. (A) Semi-qPCR to verify the downregulated or upregulated genes by MT1H in AGS cells. AGS-tetO-MT1H cells were treated with Dox (2 µg/ml) to induce the expression of ectopic MT1H. 24 h later, cells were harvested for total RNA extraction and reverse transcription followed by semi-qPCR. (B) The cells expressing tetO-MT1H were treated with Dox (2 µg/ml) to induce the expression of ectopic MT1H. 24 h later, cells were harvested for immunoblot analysis with indicated <t>antibodies.</t> NE-PER Nuclear and Cytoplasmic Extraction <t>kit</t> (Thermo) was used to fractionate cells into cytosol compartment and nuclear compartment. (C) MT1H biological functions by KEGG analysis. The participation in mineral absorption was predicted by KEGG-Pathway55 (https://www.genome.jp/kegg/). (D) Illustrative diagram of MT1H biological functions in gastric cells. The information in the diagram is the combination of our current research and KEGG-Pathway.
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Fig. 6. MT1H induces p53-dependent <t>autophagy</t> via regulating the key genes in nutrient transportation. (A) Semi-qPCR to verify the downregulated or upregulated genes by MT1H in AGS cells. AGS-tetO-MT1H cells were treated with Dox (2 µg/ml) to induce the expression of ectopic MT1H. 24 h later, cells were harvested for total RNA extraction and reverse transcription followed by semi-qPCR. (B) The cells expressing tetO-MT1H were treated with Dox (2 µg/ml) to induce the expression of ectopic MT1H. 24 h later, cells were harvested for immunoblot analysis with indicated <t>antibodies.</t> NE-PER Nuclear and Cytoplasmic Extraction <t>kit</t> (Thermo) was used to fractionate cells into cytosol compartment and nuclear compartment. (C) MT1H biological functions by KEGG analysis. The participation in mineral absorption was predicted by KEGG-Pathway55 (https://www.genome.jp/kegg/). (D) Illustrative diagram of MT1H biological functions in gastric cells. The information in the diagram is the combination of our current research and KEGG-Pathway.
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Fig. 6. MT1H induces p53-dependent autophagy via regulating the key genes in nutrient transportation. (A) Semi-qPCR to verify the downregulated or upregulated genes by MT1H in AGS cells. AGS-tetO-MT1H cells were treated with Dox (2 µg/ml) to induce the expression of ectopic MT1H. 24 h later, cells were harvested for total RNA extraction and reverse transcription followed by semi-qPCR. (B) The cells expressing tetO-MT1H were treated with Dox (2 µg/ml) to induce the expression of ectopic MT1H. 24 h later, cells were harvested for immunoblot analysis with indicated antibodies. NE-PER Nuclear and Cytoplasmic Extraction kit (Thermo) was used to fractionate cells into cytosol compartment and nuclear compartment. (C) MT1H biological functions by KEGG analysis. The participation in mineral absorption was predicted by KEGG-Pathway55 (https://www.genome.jp/kegg/). (D) Illustrative diagram of MT1H biological functions in gastric cells. The information in the diagram is the combination of our current research and KEGG-Pathway.

Journal: Scientific reports

Article Title: MT1H inhibits the growth of gastric cancer by regulating SLC6A19/TTC39B/ADM2 and activating p53-dependent autophagy.

doi: 10.1038/s41598-025-91319-y

Figure Lengend Snippet: Fig. 6. MT1H induces p53-dependent autophagy via regulating the key genes in nutrient transportation. (A) Semi-qPCR to verify the downregulated or upregulated genes by MT1H in AGS cells. AGS-tetO-MT1H cells were treated with Dox (2 µg/ml) to induce the expression of ectopic MT1H. 24 h later, cells were harvested for total RNA extraction and reverse transcription followed by semi-qPCR. (B) The cells expressing tetO-MT1H were treated with Dox (2 µg/ml) to induce the expression of ectopic MT1H. 24 h later, cells were harvested for immunoblot analysis with indicated antibodies. NE-PER Nuclear and Cytoplasmic Extraction kit (Thermo) was used to fractionate cells into cytosol compartment and nuclear compartment. (C) MT1H biological functions by KEGG analysis. The participation in mineral absorption was predicted by KEGG-Pathway55 (https://www.genome.jp/kegg/). (D) Illustrative diagram of MT1H biological functions in gastric cells. The information in the diagram is the combination of our current research and KEGG-Pathway.

Article Snippet: For immunoblotting, LSD1 (2184), NF-κB p65 (8242T), RelB (4922T), Erk1/2 (9102), p-Erk1/2 (Thr202/Tyr204) (C4370S), and the Human Reactive Cell Death and Autophagy Antibody Sampler Kit (42867) were purchased from Cell Signaling Technology.

Techniques: Expressing, RNA Extraction, Reverse Transcription, Western Blot, Extraction