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ec cell lines kyse150  (Procell Inc)

 
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    Procell Inc ec cell lines kyse150
    METTL3 expression was upregulated in EC tissues and cells. (A and B) METTL3 expression was analyzed through the TCGA and TNMplot databases in esophageal cancer tissues and normal esophageal tissues. (C and D) METTL3 expression was detected by qRT‐PCR and western blotting assays in HEEC, <t>KYSE30,</t> <t>KYSE150,</t> KYSE180, <t>and</t> <t>TE1</t> cells. * p < 0.05.
    Ec Cell Lines Kyse150, supplied by Procell Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ec+cell+lines+kyse150/pmc11842509-32-3-17?v=Procell+Inc
    Average 90 stars, based on 1 article reviews
    ec cell lines kyse150 - by Bioz Stars, 2026-07
    90/100 stars

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    1) Product Images from "METTL3 / IGF2BP2 Promotes the Malignant Progression of Esophageal Cancer by Activating the PIK3CA / AKT Pathway"

    Article Title: METTL3 / IGF2BP2 Promotes the Malignant Progression of Esophageal Cancer by Activating the PIK3CA / AKT Pathway

    Journal: Thoracic Cancer

    doi: 10.1111/1759-7714.70022

    METTL3 expression was upregulated in EC tissues and cells. (A and B) METTL3 expression was analyzed through the TCGA and TNMplot databases in esophageal cancer tissues and normal esophageal tissues. (C and D) METTL3 expression was detected by qRT‐PCR and western blotting assays in HEEC, KYSE30, KYSE150, KYSE180, and TE1 cells. * p < 0.05.
    Figure Legend Snippet: METTL3 expression was upregulated in EC tissues and cells. (A and B) METTL3 expression was analyzed through the TCGA and TNMplot databases in esophageal cancer tissues and normal esophageal tissues. (C and D) METTL3 expression was detected by qRT‐PCR and western blotting assays in HEEC, KYSE30, KYSE150, KYSE180, and TE1 cells. * p < 0.05.

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

    METTL3 knockdown inhibited the proliferation, invasion, and migration of EC cells and angiogenesis and induced cell apoptosis. KYSE180 and TE1 cells were transfected with si‐NC, si‐METTL3#1, and si‐METTL3#2. (A) METTL3 protein expression was detected by western blotting assay. (B) Cell viability was assessed by CCK‐8 assay. (C and D) Cell proliferation was analyzed by EdU assay. (E) Cell apoptosis was analyzed by flow cytometry. (F) Cell invasion was analyzed by transwell invasion assay. (G and H) Wound‐healing assay was performed to analyze cell migration. (I) Angiogenesis was analyzed by tube formation assay. * p < 0.05.
    Figure Legend Snippet: METTL3 knockdown inhibited the proliferation, invasion, and migration of EC cells and angiogenesis and induced cell apoptosis. KYSE180 and TE1 cells were transfected with si‐NC, si‐METTL3#1, and si‐METTL3#2. (A) METTL3 protein expression was detected by western blotting assay. (B) Cell viability was assessed by CCK‐8 assay. (C and D) Cell proliferation was analyzed by EdU assay. (E) Cell apoptosis was analyzed by flow cytometry. (F) Cell invasion was analyzed by transwell invasion assay. (G and H) Wound‐healing assay was performed to analyze cell migration. (I) Angiogenesis was analyzed by tube formation assay. * p < 0.05.

    Techniques Used: Knockdown, Migration, Transfection, Expressing, Western Blot, CCK-8 Assay, EdU Assay, Flow Cytometry, Transwell Invasion Assay, Wound Healing Assay, Tube Formation Assay

    METTL3 maintained PIK3CA mRNA expression in an m6A‐dependent manner. (A) The GEO database (GSE254232) was used to predict the differently expressed genes in EC cells transfected with si‐METTL3 or si‐NC. (B and C) PIK3CA expression was detected by qRT‐PCR and western blotting assays in KYSE180 and TE1 cells transfected with si‐NC or si‐METTL3#2. (D and E) The TCGA and TNMplot databases were used to predict PIK3CA expression in esophageal cancer tissues and normal esophageal tissues. (F) The GEPIA database was used to predict the correlation of METTL3 and PIK3CA expression in esophageal cancer tissues. (G) The RMbase database predicted the presence of m6A methylation modification in PIK3CA. (H) The SRAMP website predicted the existence of methylation modification sites in PIK3CA. (I–M) The MeRIP, RIP, and Actinomycin D assays were used to identify the association of METTL3 and PIK3CA in KYSE180 and TE1 cells. * p < 0.05.
    Figure Legend Snippet: METTL3 maintained PIK3CA mRNA expression in an m6A‐dependent manner. (A) The GEO database (GSE254232) was used to predict the differently expressed genes in EC cells transfected with si‐METTL3 or si‐NC. (B and C) PIK3CA expression was detected by qRT‐PCR and western blotting assays in KYSE180 and TE1 cells transfected with si‐NC or si‐METTL3#2. (D and E) The TCGA and TNMplot databases were used to predict PIK3CA expression in esophageal cancer tissues and normal esophageal tissues. (F) The GEPIA database was used to predict the correlation of METTL3 and PIK3CA expression in esophageal cancer tissues. (G) The RMbase database predicted the presence of m6A methylation modification in PIK3CA. (H) The SRAMP website predicted the existence of methylation modification sites in PIK3CA. (I–M) The MeRIP, RIP, and Actinomycin D assays were used to identify the association of METTL3 and PIK3CA in KYSE180 and TE1 cells. * p < 0.05.

    Techniques Used: Expressing, Transfection, Quantitative RT-PCR, Western Blot, Methylation, Modification

    METTL3 maintained PIK3CA mRNA stability in an IGF2BP2‐dependent manner. (A) The ENCORI database was used to predict the association of IGF2BP2 and PIK3CA. (B) The GEPIA database was used to analyze the correlation of IGF2BP2 and PIK3CA in esophageal cancer tissues. (C and D) The protein expression of IGF2BP2 and PIK3CA was analyzed by western blotting assays in KYSE180 and TE1 cells transfected with si‐NC or si‐IGF2BP2. (E and F) The RIP assay was performed to analyze the association of IGF2BP2 with PIK3CA in KYSE180 and TE1 cells transfected with si‐NC or si‐METTL3#2. (G and H) Actinomycin D assay was used to detect the transcript half‐life of PIK3CA in KYSE180 and TE1 cells transfected with si‐NC or si‐IGF2BP2. * p < 0.05.
    Figure Legend Snippet: METTL3 maintained PIK3CA mRNA stability in an IGF2BP2‐dependent manner. (A) The ENCORI database was used to predict the association of IGF2BP2 and PIK3CA. (B) The GEPIA database was used to analyze the correlation of IGF2BP2 and PIK3CA in esophageal cancer tissues. (C and D) The protein expression of IGF2BP2 and PIK3CA was analyzed by western blotting assays in KYSE180 and TE1 cells transfected with si‐NC or si‐IGF2BP2. (E and F) The RIP assay was performed to analyze the association of IGF2BP2 with PIK3CA in KYSE180 and TE1 cells transfected with si‐NC or si‐METTL3#2. (G and H) Actinomycin D assay was used to detect the transcript half‐life of PIK3CA in KYSE180 and TE1 cells transfected with si‐NC or si‐IGF2BP2. * p < 0.05.

    Techniques Used: Expressing, Western Blot, Transfection

    PIK3CA overexpression attenuated METTL3 silencing‐induced effects on the malignant growth of KYSE180 and TE1 cells. (A) The efficiency of PIK3CA overexpression was analyzed by western blotting assay. KYSE180 and TE1 cells were transfected with si‐NC, si‐METTL3#2, si‐METTL3#2 + OE‐NC, or si‐METTL3#2 + OE‐PIK3CA. (B) Cell viability was assessed by CCK‐8 assay. (C and D) Cell proliferation was analyzed by EdU assay. (E) Cell apoptosis was analyzed by flow cytometry. (F and G) Cell invasion was analyzed by transwell invasion assay. (H) Wound‐healing assay was performed to analyze cell migration. (I) Angiogenesis was analyzed by tube formation assay. * p < 0.05.
    Figure Legend Snippet: PIK3CA overexpression attenuated METTL3 silencing‐induced effects on the malignant growth of KYSE180 and TE1 cells. (A) The efficiency of PIK3CA overexpression was analyzed by western blotting assay. KYSE180 and TE1 cells were transfected with si‐NC, si‐METTL3#2, si‐METTL3#2 + OE‐NC, or si‐METTL3#2 + OE‐PIK3CA. (B) Cell viability was assessed by CCK‐8 assay. (C and D) Cell proliferation was analyzed by EdU assay. (E) Cell apoptosis was analyzed by flow cytometry. (F and G) Cell invasion was analyzed by transwell invasion assay. (H) Wound‐healing assay was performed to analyze cell migration. (I) Angiogenesis was analyzed by tube formation assay. * p < 0.05.

    Techniques Used: Over Expression, Western Blot, Transfection, CCK-8 Assay, EdU Assay, Flow Cytometry, Transwell Invasion Assay, Wound Healing Assay, Migration, Tube Formation Assay

    METTL3 silencing inactivated the AKT pathway by regulating PIK3CA expression. (A and B) KYSE180 and TE1 cells were transfected with si‐NC, si‐METTL3#2, si‐METTL3#2 + OE‐NC, or si‐METTL3#2 + OE‐PIK3CA. The protein expression of p‐AKT and AKT was analyzed by western blotting assay. * p < 0.05.
    Figure Legend Snippet: METTL3 silencing inactivated the AKT pathway by regulating PIK3CA expression. (A and B) KYSE180 and TE1 cells were transfected with si‐NC, si‐METTL3#2, si‐METTL3#2 + OE‐NC, or si‐METTL3#2 + OE‐PIK3CA. The protein expression of p‐AKT and AKT was analyzed by western blotting assay. * p < 0.05.

    Techniques Used: Expressing, Transfection, Western Blot



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    ec cell lines kyse150  (Procell Inc)
    90
    Procell Inc ec cell lines kyse150
    METTL3 expression was upregulated in EC tissues and cells. (A and B) METTL3 expression was analyzed through the TCGA and TNMplot databases in esophageal cancer tissues and normal esophageal tissues. (C and D) METTL3 expression was detected by qRT‐PCR and western blotting assays in HEEC, <t>KYSE30,</t> <t>KYSE150,</t> KYSE180, <t>and</t> <t>TE1</t> cells. * p < 0.05.
    Ec Cell Lines Kyse150, supplied by Procell Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ec+cell+lines+kyse150/pmc11842509-32-3-17?v=Procell+Inc
    Average 90 stars, based on 1 article reviews
    ec cell lines kyse150 - by Bioz Stars, 2026-07
    90/100 stars
    		  Buy from Supplier

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    METTL3 expression was upregulated in EC tissues and cells. (A and B) METTL3 expression was analyzed through the TCGA and TNMplot databases in esophageal cancer tissues and normal esophageal tissues. (C and D) METTL3 expression was detected by qRT‐PCR and western blotting assays in HEEC, KYSE30, KYSE150, KYSE180, and TE1 cells. * p < 0.05.

    Journal: Thoracic Cancer

    Article Title: METTL3 / IGF2BP2 Promotes the Malignant Progression of Esophageal Cancer by Activating the PIK3CA / AKT Pathway

    doi: 10.1111/1759-7714.70022

    Figure Lengend Snippet: METTL3 expression was upregulated in EC tissues and cells. (A and B) METTL3 expression was analyzed through the TCGA and TNMplot databases in esophageal cancer tissues and normal esophageal tissues. (C and D) METTL3 expression was detected by qRT‐PCR and western blotting assays in HEEC, KYSE30, KYSE150, KYSE180, and TE1 cells. * p < 0.05.

    Article Snippet: EC cell lines (including KYSE30, TE‐1, and KYSE150) and human esophageal epithelial cells (HEECs) were provided by Procell (Wuhan, China).

    Techniques: Expressing, Quantitative RT-PCR, Western Blot

    METTL3 knockdown inhibited the proliferation, invasion, and migration of EC cells and angiogenesis and induced cell apoptosis. KYSE180 and TE1 cells were transfected with si‐NC, si‐METTL3#1, and si‐METTL3#2. (A) METTL3 protein expression was detected by western blotting assay. (B) Cell viability was assessed by CCK‐8 assay. (C and D) Cell proliferation was analyzed by EdU assay. (E) Cell apoptosis was analyzed by flow cytometry. (F) Cell invasion was analyzed by transwell invasion assay. (G and H) Wound‐healing assay was performed to analyze cell migration. (I) Angiogenesis was analyzed by tube formation assay. * p < 0.05.

    Journal: Thoracic Cancer

    Article Title: METTL3 / IGF2BP2 Promotes the Malignant Progression of Esophageal Cancer by Activating the PIK3CA / AKT Pathway

    doi: 10.1111/1759-7714.70022

    Figure Lengend Snippet: METTL3 knockdown inhibited the proliferation, invasion, and migration of EC cells and angiogenesis and induced cell apoptosis. KYSE180 and TE1 cells were transfected with si‐NC, si‐METTL3#1, and si‐METTL3#2. (A) METTL3 protein expression was detected by western blotting assay. (B) Cell viability was assessed by CCK‐8 assay. (C and D) Cell proliferation was analyzed by EdU assay. (E) Cell apoptosis was analyzed by flow cytometry. (F) Cell invasion was analyzed by transwell invasion assay. (G and H) Wound‐healing assay was performed to analyze cell migration. (I) Angiogenesis was analyzed by tube formation assay. * p < 0.05.

    Article Snippet: EC cell lines (including KYSE30, TE‐1, and KYSE150) and human esophageal epithelial cells (HEECs) were provided by Procell (Wuhan, China).

    Techniques: Knockdown, Migration, Transfection, Expressing, Western Blot, CCK-8 Assay, EdU Assay, Flow Cytometry, Transwell Invasion Assay, Wound Healing Assay, Tube Formation Assay

    METTL3 maintained PIK3CA mRNA expression in an m6A‐dependent manner. (A) The GEO database (GSE254232) was used to predict the differently expressed genes in EC cells transfected with si‐METTL3 or si‐NC. (B and C) PIK3CA expression was detected by qRT‐PCR and western blotting assays in KYSE180 and TE1 cells transfected with si‐NC or si‐METTL3#2. (D and E) The TCGA and TNMplot databases were used to predict PIK3CA expression in esophageal cancer tissues and normal esophageal tissues. (F) The GEPIA database was used to predict the correlation of METTL3 and PIK3CA expression in esophageal cancer tissues. (G) The RMbase database predicted the presence of m6A methylation modification in PIK3CA. (H) The SRAMP website predicted the existence of methylation modification sites in PIK3CA. (I–M) The MeRIP, RIP, and Actinomycin D assays were used to identify the association of METTL3 and PIK3CA in KYSE180 and TE1 cells. * p < 0.05.

    Journal: Thoracic Cancer

    Article Title: METTL3 / IGF2BP2 Promotes the Malignant Progression of Esophageal Cancer by Activating the PIK3CA / AKT Pathway

    doi: 10.1111/1759-7714.70022

    Figure Lengend Snippet: METTL3 maintained PIK3CA mRNA expression in an m6A‐dependent manner. (A) The GEO database (GSE254232) was used to predict the differently expressed genes in EC cells transfected with si‐METTL3 or si‐NC. (B and C) PIK3CA expression was detected by qRT‐PCR and western blotting assays in KYSE180 and TE1 cells transfected with si‐NC or si‐METTL3#2. (D and E) The TCGA and TNMplot databases were used to predict PIK3CA expression in esophageal cancer tissues and normal esophageal tissues. (F) The GEPIA database was used to predict the correlation of METTL3 and PIK3CA expression in esophageal cancer tissues. (G) The RMbase database predicted the presence of m6A methylation modification in PIK3CA. (H) The SRAMP website predicted the existence of methylation modification sites in PIK3CA. (I–M) The MeRIP, RIP, and Actinomycin D assays were used to identify the association of METTL3 and PIK3CA in KYSE180 and TE1 cells. * p < 0.05.

    Article Snippet: EC cell lines (including KYSE30, TE‐1, and KYSE150) and human esophageal epithelial cells (HEECs) were provided by Procell (Wuhan, China).

    Techniques: Expressing, Transfection, Quantitative RT-PCR, Western Blot, Methylation, Modification

    METTL3 maintained PIK3CA mRNA stability in an IGF2BP2‐dependent manner. (A) The ENCORI database was used to predict the association of IGF2BP2 and PIK3CA. (B) The GEPIA database was used to analyze the correlation of IGF2BP2 and PIK3CA in esophageal cancer tissues. (C and D) The protein expression of IGF2BP2 and PIK3CA was analyzed by western blotting assays in KYSE180 and TE1 cells transfected with si‐NC or si‐IGF2BP2. (E and F) The RIP assay was performed to analyze the association of IGF2BP2 with PIK3CA in KYSE180 and TE1 cells transfected with si‐NC or si‐METTL3#2. (G and H) Actinomycin D assay was used to detect the transcript half‐life of PIK3CA in KYSE180 and TE1 cells transfected with si‐NC or si‐IGF2BP2. * p < 0.05.

    Journal: Thoracic Cancer

    Article Title: METTL3 / IGF2BP2 Promotes the Malignant Progression of Esophageal Cancer by Activating the PIK3CA / AKT Pathway

    doi: 10.1111/1759-7714.70022

    Figure Lengend Snippet: METTL3 maintained PIK3CA mRNA stability in an IGF2BP2‐dependent manner. (A) The ENCORI database was used to predict the association of IGF2BP2 and PIK3CA. (B) The GEPIA database was used to analyze the correlation of IGF2BP2 and PIK3CA in esophageal cancer tissues. (C and D) The protein expression of IGF2BP2 and PIK3CA was analyzed by western blotting assays in KYSE180 and TE1 cells transfected with si‐NC or si‐IGF2BP2. (E and F) The RIP assay was performed to analyze the association of IGF2BP2 with PIK3CA in KYSE180 and TE1 cells transfected with si‐NC or si‐METTL3#2. (G and H) Actinomycin D assay was used to detect the transcript half‐life of PIK3CA in KYSE180 and TE1 cells transfected with si‐NC or si‐IGF2BP2. * p < 0.05.

    Article Snippet: EC cell lines (including KYSE30, TE‐1, and KYSE150) and human esophageal epithelial cells (HEECs) were provided by Procell (Wuhan, China).

    Techniques: Expressing, Western Blot, Transfection

    PIK3CA overexpression attenuated METTL3 silencing‐induced effects on the malignant growth of KYSE180 and TE1 cells. (A) The efficiency of PIK3CA overexpression was analyzed by western blotting assay. KYSE180 and TE1 cells were transfected with si‐NC, si‐METTL3#2, si‐METTL3#2 + OE‐NC, or si‐METTL3#2 + OE‐PIK3CA. (B) Cell viability was assessed by CCK‐8 assay. (C and D) Cell proliferation was analyzed by EdU assay. (E) Cell apoptosis was analyzed by flow cytometry. (F and G) Cell invasion was analyzed by transwell invasion assay. (H) Wound‐healing assay was performed to analyze cell migration. (I) Angiogenesis was analyzed by tube formation assay. * p < 0.05.

    Journal: Thoracic Cancer

    Article Title: METTL3 / IGF2BP2 Promotes the Malignant Progression of Esophageal Cancer by Activating the PIK3CA / AKT Pathway

    doi: 10.1111/1759-7714.70022

    Figure Lengend Snippet: PIK3CA overexpression attenuated METTL3 silencing‐induced effects on the malignant growth of KYSE180 and TE1 cells. (A) The efficiency of PIK3CA overexpression was analyzed by western blotting assay. KYSE180 and TE1 cells were transfected with si‐NC, si‐METTL3#2, si‐METTL3#2 + OE‐NC, or si‐METTL3#2 + OE‐PIK3CA. (B) Cell viability was assessed by CCK‐8 assay. (C and D) Cell proliferation was analyzed by EdU assay. (E) Cell apoptosis was analyzed by flow cytometry. (F and G) Cell invasion was analyzed by transwell invasion assay. (H) Wound‐healing assay was performed to analyze cell migration. (I) Angiogenesis was analyzed by tube formation assay. * p < 0.05.

    Article Snippet: EC cell lines (including KYSE30, TE‐1, and KYSE150) and human esophageal epithelial cells (HEECs) were provided by Procell (Wuhan, China).

    Techniques: Over Expression, Western Blot, Transfection, CCK-8 Assay, EdU Assay, Flow Cytometry, Transwell Invasion Assay, Wound Healing Assay, Migration, Tube Formation Assay

    METTL3 silencing inactivated the AKT pathway by regulating PIK3CA expression. (A and B) KYSE180 and TE1 cells were transfected with si‐NC, si‐METTL3#2, si‐METTL3#2 + OE‐NC, or si‐METTL3#2 + OE‐PIK3CA. The protein expression of p‐AKT and AKT was analyzed by western blotting assay. * p < 0.05.

    Journal: Thoracic Cancer

    Article Title: METTL3 / IGF2BP2 Promotes the Malignant Progression of Esophageal Cancer by Activating the PIK3CA / AKT Pathway

    doi: 10.1111/1759-7714.70022

    Figure Lengend Snippet: METTL3 silencing inactivated the AKT pathway by regulating PIK3CA expression. (A and B) KYSE180 and TE1 cells were transfected with si‐NC, si‐METTL3#2, si‐METTL3#2 + OE‐NC, or si‐METTL3#2 + OE‐PIK3CA. The protein expression of p‐AKT and AKT was analyzed by western blotting assay. * p < 0.05.

    Article Snippet: EC cell lines (including KYSE30, TE‐1, and KYSE150) and human esophageal epithelial cells (HEECs) were provided by Procell (Wuhan, China).

    Techniques: Expressing, Transfection, Western Blot