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Procell Inc human esca cell lines kyse150

High tumor expression of LINC01354 holds diagnostic potential in ESCA. ( A ) A comparative analysis of LINC01354 expression and prognosis revealed that LINC01354 was decreased in ESCA and BRCA and led to poor prognosis in patients. ( B , C ) The high expression of LINC01354 in ESCA was validated in additional two cohorts. ( D ) Paired analysis showed that LINC01354 was down-regulated in 95% of ESCA patients in GSE53622 cohort. ( E ) Further analysis depicted that LINC01354 was decreased in 89.9% of ESCA patients in GSE53624 cohort. ( F , G ) ROC analysis was used to evaluate the diagnostic potential of LINC01354 in the GSE53622 (95% confidence interval: 0.8317 to 0.9544) and GSE53624 (95% confidence interval: 0.8374 to 0.9277) cohorts. ( H ) The expression of LINC01354 in Het-1 A, TE1, KYSE70, <t>KYSE150,</t> and KYSE450 cells was examined by qRT-PCR, ** p < 0.01, *** p < 0.001, independent-samples T test. ( I ) FISH was employed to detect the expression of LINC01354 in ESCA TMA, scale bar = 800 μm.

Human Esca Cell Lines Kyse150, supplied by Procell Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human esca cell lines kyse150 - by Bioz Stars, 2026-05

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Article Title: Overexpression of LINC01354 predicts well prognosis and suppresses esophageal cancer progression

Journal: Scientific Reports

doi: 10.1038/s41598-025-20455-2

Figure Legend Snippet: High tumor expression of LINC01354 holds diagnostic potential in ESCA. ( A ) A comparative analysis of LINC01354 expression and prognosis revealed that LINC01354 was decreased in ESCA and BRCA and led to poor prognosis in patients. ( B , C ) The high expression of LINC01354 in ESCA was validated in additional two cohorts. ( D ) Paired analysis showed that LINC01354 was down-regulated in 95% of ESCA patients in GSE53622 cohort. ( E ) Further analysis depicted that LINC01354 was decreased in 89.9% of ESCA patients in GSE53624 cohort. ( F , G ) ROC analysis was used to evaluate the diagnostic potential of LINC01354 in the GSE53622 (95% confidence interval: 0.8317 to 0.9544) and GSE53624 (95% confidence interval: 0.8374 to 0.9277) cohorts. ( H ) The expression of LINC01354 in Het-1 A, TE1, KYSE70, KYSE150, and KYSE450 cells was examined by qRT-PCR, ** p < 0.01, *** p < 0.001, independent-samples T test. ( I ) FISH was employed to detect the expression of LINC01354 in ESCA TMA, scale bar = 800 μm.

Techniques Used: Expressing, Diagnostic Assay, Quantitative RT-PCR

LINC01354 is involved in cell-cycle regulation and curbs tumorigenesis in ESCA. ( A , B ) Functional enrichment analysis of LINC01354 associated genes in ESCA revealed the biological function of LINC01354. ( C – E ) The effect of overexpression of LINC01354 on ESCA tumor growth was evaluated in a nude mouse model, ** p < 0.01. ( F , G ) The inhibition of LINC01354 on KYSE150 cell cycle process was validated by flow cytometry analysis, **** p < 0.0001.

Figure Legend Snippet: LINC01354 is involved in cell-cycle regulation and curbs tumorigenesis in ESCA. ( A , B ) Functional enrichment analysis of LINC01354 associated genes in ESCA revealed the biological function of LINC01354. ( C – E ) The effect of overexpression of LINC01354 on ESCA tumor growth was evaluated in a nude mouse model, ** p < 0.01. ( F , G ) The inhibition of LINC01354 on KYSE150 cell cycle process was validated by flow cytometry analysis, **** p < 0.0001.

Techniques Used: Functional Assay, Over Expression, Inhibition, Flow Cytometry

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Journal: Scientific Reports

Article Title: Overexpression of LINC01354 predicts well prognosis and suppresses esophageal cancer progression

doi: 10.1038/s41598-025-20455-2

Figure Lengend Snippet: High tumor expression of LINC01354 holds diagnostic potential in ESCA. ( A ) A comparative analysis of LINC01354 expression and prognosis revealed that LINC01354 was decreased in ESCA and BRCA and led to poor prognosis in patients. ( B , C ) The high expression of LINC01354 in ESCA was validated in additional two cohorts. ( D ) Paired analysis showed that LINC01354 was down-regulated in 95% of ESCA patients in GSE53622 cohort. ( E ) Further analysis depicted that LINC01354 was decreased in 89.9% of ESCA patients in GSE53624 cohort. ( F , G ) ROC analysis was used to evaluate the diagnostic potential of LINC01354 in the GSE53622 (95% confidence interval: 0.8317 to 0.9544) and GSE53624 (95% confidence interval: 0.8374 to 0.9277) cohorts. ( H ) The expression of LINC01354 in Het-1 A, TE1, KYSE70, KYSE150, and KYSE450 cells was examined by qRT-PCR, ** p < 0.01, *** p < 0.001, independent-samples T test. ( I ) FISH was employed to detect the expression of LINC01354 in ESCA TMA, scale bar = 800 μm.

Article Snippet: Human ESCA cell lines KYSE150 and TE1 were purchased from Procell (Wuhan, China).

Techniques: Expressing, Diagnostic Assay, Quantitative RT-PCR

Journal: Scientific Reports

Article Title: Overexpression of LINC01354 predicts well prognosis and suppresses esophageal cancer progression

doi: 10.1038/s41598-025-20455-2

Figure Lengend Snippet: LINC01354 is involved in cell-cycle regulation and curbs tumorigenesis in ESCA. ( A , B ) Functional enrichment analysis of LINC01354 associated genes in ESCA revealed the biological function of LINC01354. ( C – E ) The effect of overexpression of LINC01354 on ESCA tumor growth was evaluated in a nude mouse model, ** p < 0.01. ( F , G ) The inhibition of LINC01354 on KYSE150 cell cycle process was validated by flow cytometry analysis, **** p < 0.0001.

Article Snippet: Human ESCA cell lines KYSE150 and TE1 were purchased from Procell (Wuhan, China).

Techniques: Functional Assay, Over Expression, Inhibition, Flow Cytometry

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

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