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Knockdown of MUC16 Suppresses Tumor Proliferation and Invasion. (A) WB analysis showing higher MUC16 protein expression <t>in</t> <t>endometrial</t> cancer tumor tissues compared with matched adjacent non-tumor tissues. (B, C) Constructing a shMUC16 lentiviral vector to knockdown MUC16 in the Ishikawa and <t>KLE</t> cell lines. The knockdown efficiency was verified by qRT-PCR and WB. (D) CCK-8 assay demonstrated that MUC16 knockdown significantly inhibited cell viability and proliferation in both Ishikawa and KLE cell lines. (E) The MUC16-knockdown cells showed a significant decrease in colony formation, indicating suppression of cell proliferation. (F) Transwell assay confirms that MUC16 knockdown inhibits cell migration. (G) The wound healing assay shows that MUC16 knockdown suppresses cell invasion in both cell lines. Bar: 200 μm. Statistical significance was calculated using two-way ANOVA (D) or one-way ANOVA with Tukey's post-test (B, C) or two-tailed unpaired t -test (A, E-G). * p < 0.05, ** p < 0.01, and *** p < 0.001.

Kle, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 446 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/kle/pmc13125919-65-7-11?v=ATCC
Average 96 stars, based on 446 article reviews

kle - by Bioz Stars, 2026-06

96/100 stars

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1) Product Images from "MUC16 promotes endometrial cancer progression and modulates sensitivity to lapatinib through the ESR1/PI3K/AKT axis"

Article Title: MUC16 promotes endometrial cancer progression and modulates sensitivity to lapatinib through the ESR1/PI3K/AKT axis

Journal: Translational Oncology

doi: 10.1016/j.tranon.2026.102774

Knockdown of MUC16 Suppresses Tumor Proliferation and Invasion. (A) WB analysis showing higher MUC16 protein expression in endometrial cancer tumor tissues compared with matched adjacent non-tumor tissues. (B, C) Constructing a shMUC16 lentiviral vector to knockdown MUC16 in the Ishikawa and KLE cell lines. The knockdown efficiency was verified by qRT-PCR and WB. (D) CCK-8 assay demonstrated that MUC16 knockdown significantly inhibited cell viability and proliferation in both Ishikawa and KLE cell lines. (E) The MUC16-knockdown cells showed a significant decrease in colony formation, indicating suppression of cell proliferation. (F) Transwell assay confirms that MUC16 knockdown inhibits cell migration. (G) The wound healing assay shows that MUC16 knockdown suppresses cell invasion in both cell lines. Bar: 200 μm. Statistical significance was calculated using two-way ANOVA (D) or one-way ANOVA with Tukey's post-test (B, C) or two-tailed unpaired t -test (A, E-G). * p < 0.05, ** p < 0.01, and *** p < 0.001.

Figure Legend Snippet: Knockdown of MUC16 Suppresses Tumor Proliferation and Invasion. (A) WB analysis showing higher MUC16 protein expression in endometrial cancer tumor tissues compared with matched adjacent non-tumor tissues. (B, C) Constructing a shMUC16 lentiviral vector to knockdown MUC16 in the Ishikawa and KLE cell lines. The knockdown efficiency was verified by qRT-PCR and WB. (D) CCK-8 assay demonstrated that MUC16 knockdown significantly inhibited cell viability and proliferation in both Ishikawa and KLE cell lines. (E) The MUC16-knockdown cells showed a significant decrease in colony formation, indicating suppression of cell proliferation. (F) Transwell assay confirms that MUC16 knockdown inhibits cell migration. (G) The wound healing assay shows that MUC16 knockdown suppresses cell invasion in both cell lines. Bar: 200 μm. Statistical significance was calculated using two-way ANOVA (D) or one-way ANOVA with Tukey's post-test (B, C) or two-tailed unpaired t -test (A, E-G). * p < 0.05, ** p < 0.01, and *** p < 0.001.

Techniques Used: Knockdown, Expressing, Plasmid Preparation, Quantitative RT-PCR, CCK-8 Assay, Transwell Assay, Migration, Wound Healing Assay, Two Tailed Test

Overexpression of MUC16 Promotes Tumor Proliferation and Invasion. (A, B) The MUC16 overexpression plasmid was transfected into the Ishikawa and KLE cells, and the efficiency of MUC16 overexpression was verified by qRT-PCR (A) and WB (B). (C) CCK-8 proliferation assays show significantly increased cell viability in MUC16-overexpressing cells. (D) Colony formation assays reveal enhanced clonogenic growth upon MUC16 overexpression. (E) Transwell assay confirms that MUC16 overexpression enhances cell migration. Bar: 200 μm. (F) The wound healing assay indicates that MUC16 overexpression promotes cell invasion in both cell lines. Bar: 200 μm. Statistical significance was calculated using two-way ANOVA (C) or one-way ANOVA with Tukey's post-test (A, B) or two-tailed unpaired t -test (D-F). *p < 0.05, **p < 0.01, and ***p < 0.001.

Figure Legend Snippet: Overexpression of MUC16 Promotes Tumor Proliferation and Invasion. (A, B) The MUC16 overexpression plasmid was transfected into the Ishikawa and KLE cells, and the efficiency of MUC16 overexpression was verified by qRT-PCR (A) and WB (B). (C) CCK-8 proliferation assays show significantly increased cell viability in MUC16-overexpressing cells. (D) Colony formation assays reveal enhanced clonogenic growth upon MUC16 overexpression. (E) Transwell assay confirms that MUC16 overexpression enhances cell migration. Bar: 200 μm. (F) The wound healing assay indicates that MUC16 overexpression promotes cell invasion in both cell lines. Bar: 200 μm. Statistical significance was calculated using two-way ANOVA (C) or one-way ANOVA with Tukey's post-test (A, B) or two-tailed unpaired t -test (D-F). *p < 0.05, **p < 0.01, and ***p < 0.001.

Techniques Used: Over Expression, Plasmid Preparation, Transfection, Quantitative RT-PCR, CCK-8 Assay, Transwell Assay, Migration, Wound Healing Assay, Two Tailed Test

MUC16 Interacts with ESR1 and Modulates the PI3K/AKT Signaling Pathway. (A) Through pan-cancer analysis, it was found that MUC16 has a high mutation frequency in various malignancies. (B) KEGG pathway enrichment analysis suggests that MUC16 may have potential biological functions and participate in certain signaling pathways. (C, D) Immunoprecipitation experiments with anti-MUC16 (C) or anti-ESR1 (D) as primary antibody confirm the interaction between MUC16 C-terminal fragment and ESR1 in Ishikawa cells. (E, F) Co-transfection of Flag-MUC16 and HA-ESR1 plasmids was performed, and the binding between MUC16 and ESR1 proteins was confirmed through immunoprecipitation experiment in HEK293T cells. (G) Knockdown of MUC16 reducing ESR1 expression and PI3K/AKT pathway. (H) WB analysis shows that overexpression of MUC16 increases the expression of ESR1 and phosphorylation of PI3K, AKT and mTOR in KLE and Ishikawa cell lines.

Figure Legend Snippet: MUC16 Interacts with ESR1 and Modulates the PI3K/AKT Signaling Pathway. (A) Through pan-cancer analysis, it was found that MUC16 has a high mutation frequency in various malignancies. (B) KEGG pathway enrichment analysis suggests that MUC16 may have potential biological functions and participate in certain signaling pathways. (C, D) Immunoprecipitation experiments with anti-MUC16 (C) or anti-ESR1 (D) as primary antibody confirm the interaction between MUC16 C-terminal fragment and ESR1 in Ishikawa cells. (E, F) Co-transfection of Flag-MUC16 and HA-ESR1 plasmids was performed, and the binding between MUC16 and ESR1 proteins was confirmed through immunoprecipitation experiment in HEK293T cells. (G) Knockdown of MUC16 reducing ESR1 expression and PI3K/AKT pathway. (H) WB analysis shows that overexpression of MUC16 increases the expression of ESR1 and phosphorylation of PI3K, AKT and mTOR in KLE and Ishikawa cell lines.

Techniques Used: Mutagenesis, Protein-Protein interactions, Immunoprecipitation, Cotransfection, Binding Assay, Knockdown, Expressing, Over Expression, Phospho-proteomics

MUC16 Promotes Endometrial Cancer Progression via ESR1/PI3K/AKT Axis. (A) MUC16 promotes the phosphorylation of mTOR through the PI3K/AKT pathway. (B and C) MUC16 promotes the proliferation and growth of Ishikawa and KLE cells through the PI3K/AKT/mTOR signaling pathway. (D and E) The rescue experiment has shown that MUC16 promotes the invasion and metastasis of Ishikawa and KLE cells through the PI3K/AKT/mTOR signaling pathway. (F) MUC16 knockdown inhibited the growth of subcutaneous tumors in mice, and ESR1 overexpression can reverse the effect of shMUC16. (G) The weight of subcutaneous xenograft tumors. (H) The growth curve of subcutaneous xenograft tumors in nude mice. (I) Gross specimens of lungs. (J) Number of lung metastatic nodules. (K) Representative images of H&E staining of lung metastasis. Statistical significance was calculated using two-way ANOVA (B, H) or one-way ANOVA with Tukey's post-test (G, J). *p < 0.05, **p < 0.01, and ***p < 0.001.

Figure Legend Snippet: MUC16 Promotes Endometrial Cancer Progression via ESR1/PI3K/AKT Axis. (A) MUC16 promotes the phosphorylation of mTOR through the PI3K/AKT pathway. (B and C) MUC16 promotes the proliferation and growth of Ishikawa and KLE cells through the PI3K/AKT/mTOR signaling pathway. (D and E) The rescue experiment has shown that MUC16 promotes the invasion and metastasis of Ishikawa and KLE cells through the PI3K/AKT/mTOR signaling pathway. (F) MUC16 knockdown inhibited the growth of subcutaneous tumors in mice, and ESR1 overexpression can reverse the effect of shMUC16. (G) The weight of subcutaneous xenograft tumors. (H) The growth curve of subcutaneous xenograft tumors in nude mice. (I) Gross specimens of lungs. (J) Number of lung metastatic nodules. (K) Representative images of H&E staining of lung metastasis. Statistical significance was calculated using two-way ANOVA (B, H) or one-way ANOVA with Tukey's post-test (G, J). *p < 0.05, **p < 0.01, and ***p < 0.001.

Techniques Used: Phospho-proteomics, Knockdown, Over Expression, Staining

MUC16 Mutation Influences Sensitivity to Targeted Therapies in Endometrial Cancer. (A) Filter genes that related to MUC16 mutation status, display the top 10 genes with the most obvious differences. (B) Based on MUC16 mutation-related gene screening, identify drugs that may have their efficacy affected by MUC16 mutations. (C) The IC50 of lapatinib, Neratinib, Afatinib and Pazopanib in Ishikawa and KLE cells were measured. (D) A molecular docking model of MUC16 protein with lapatinib was generated. (E) The IC50 of lapatinib is lower in cells with MUC16 knockdown. (F) Flow cytometry detection revealed that knockdown of MUC16 can enhance lapatinib-induced apoptosis in Ishikawa cells, whereas MUC16 overexpression significantly reduces lapatinib-induced apoptosis. Statistical significance was calculated using one-way ANOVA. *p < 0.05, **p < 0.01, and ***p < 0.001.

Figure Legend Snippet: MUC16 Mutation Influences Sensitivity to Targeted Therapies in Endometrial Cancer. (A) Filter genes that related to MUC16 mutation status, display the top 10 genes with the most obvious differences. (B) Based on MUC16 mutation-related gene screening, identify drugs that may have their efficacy affected by MUC16 mutations. (C) The IC50 of lapatinib, Neratinib, Afatinib and Pazopanib in Ishikawa and KLE cells were measured. (D) A molecular docking model of MUC16 protein with lapatinib was generated. (E) The IC50 of lapatinib is lower in cells with MUC16 knockdown. (F) Flow cytometry detection revealed that knockdown of MUC16 can enhance lapatinib-induced apoptosis in Ishikawa cells, whereas MUC16 overexpression significantly reduces lapatinib-induced apoptosis. Statistical significance was calculated using one-way ANOVA. *p < 0.05, **p < 0.01, and ***p < 0.001.

Techniques Used: Mutagenesis, Generated, Knockdown, Flow Cytometry, Over Expression

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Journal: Translational Oncology

Article Title: MUC16 promotes endometrial cancer progression and modulates sensitivity to lapatinib through the ESR1/PI3K/AKT axis

doi: 10.1016/j.tranon.2026.102774

Figure Lengend Snippet: Knockdown of MUC16 Suppresses Tumor Proliferation and Invasion. (A) WB analysis showing higher MUC16 protein expression in endometrial cancer tumor tissues compared with matched adjacent non-tumor tissues. (B, C) Constructing a shMUC16 lentiviral vector to knockdown MUC16 in the Ishikawa and KLE cell lines. The knockdown efficiency was verified by qRT-PCR and WB. (D) CCK-8 assay demonstrated that MUC16 knockdown significantly inhibited cell viability and proliferation in both Ishikawa and KLE cell lines. (E) The MUC16-knockdown cells showed a significant decrease in colony formation, indicating suppression of cell proliferation. (F) Transwell assay confirms that MUC16 knockdown inhibits cell migration. (G) The wound healing assay shows that MUC16 knockdown suppresses cell invasion in both cell lines. Bar: 200 μm. Statistical significance was calculated using two-way ANOVA (D) or one-way ANOVA with Tukey's post-test (B, C) or two-tailed unpaired t -test (A, E-G). * p < 0.05, ** p < 0.01, and *** p < 0.001.

Article Snippet: Human endometrial cancer cell lines, Ishikawa and KLE, were obtained from American Type Culture Collection (ATCC).

Techniques: Knockdown, Expressing, Plasmid Preparation, Quantitative RT-PCR, CCK-8 Assay, Transwell Assay, Migration, Wound Healing Assay, Two Tailed Test

Journal: Translational Oncology

Article Title: MUC16 promotes endometrial cancer progression and modulates sensitivity to lapatinib through the ESR1/PI3K/AKT axis

doi: 10.1016/j.tranon.2026.102774

Figure Lengend Snippet: Overexpression of MUC16 Promotes Tumor Proliferation and Invasion. (A, B) The MUC16 overexpression plasmid was transfected into the Ishikawa and KLE cells, and the efficiency of MUC16 overexpression was verified by qRT-PCR (A) and WB (B). (C) CCK-8 proliferation assays show significantly increased cell viability in MUC16-overexpressing cells. (D) Colony formation assays reveal enhanced clonogenic growth upon MUC16 overexpression. (E) Transwell assay confirms that MUC16 overexpression enhances cell migration. Bar: 200 μm. (F) The wound healing assay indicates that MUC16 overexpression promotes cell invasion in both cell lines. Bar: 200 μm. Statistical significance was calculated using two-way ANOVA (C) or one-way ANOVA with Tukey's post-test (A, B) or two-tailed unpaired t -test (D-F). *p < 0.05, **p < 0.01, and ***p < 0.001.

Article Snippet: Human endometrial cancer cell lines, Ishikawa and KLE, were obtained from American Type Culture Collection (ATCC).

Techniques: Over Expression, Plasmid Preparation, Transfection, Quantitative RT-PCR, CCK-8 Assay, Transwell Assay, Migration, Wound Healing Assay, Two Tailed Test

Journal: Translational Oncology

Article Title: MUC16 promotes endometrial cancer progression and modulates sensitivity to lapatinib through the ESR1/PI3K/AKT axis

doi: 10.1016/j.tranon.2026.102774

Figure Lengend Snippet: MUC16 Interacts with ESR1 and Modulates the PI3K/AKT Signaling Pathway. (A) Through pan-cancer analysis, it was found that MUC16 has a high mutation frequency in various malignancies. (B) KEGG pathway enrichment analysis suggests that MUC16 may have potential biological functions and participate in certain signaling pathways. (C, D) Immunoprecipitation experiments with anti-MUC16 (C) or anti-ESR1 (D) as primary antibody confirm the interaction between MUC16 C-terminal fragment and ESR1 in Ishikawa cells. (E, F) Co-transfection of Flag-MUC16 and HA-ESR1 plasmids was performed, and the binding between MUC16 and ESR1 proteins was confirmed through immunoprecipitation experiment in HEK293T cells. (G) Knockdown of MUC16 reducing ESR1 expression and PI3K/AKT pathway. (H) WB analysis shows that overexpression of MUC16 increases the expression of ESR1 and phosphorylation of PI3K, AKT and mTOR in KLE and Ishikawa cell lines.

Article Snippet: Human endometrial cancer cell lines, Ishikawa and KLE, were obtained from American Type Culture Collection (ATCC).

Techniques: Mutagenesis, Protein-Protein interactions, Immunoprecipitation, Cotransfection, Binding Assay, Knockdown, Expressing, Over Expression, Phospho-proteomics

Journal: Translational Oncology

Article Title: MUC16 promotes endometrial cancer progression and modulates sensitivity to lapatinib through the ESR1/PI3K/AKT axis

doi: 10.1016/j.tranon.2026.102774

Figure Lengend Snippet: MUC16 Promotes Endometrial Cancer Progression via ESR1/PI3K/AKT Axis. (A) MUC16 promotes the phosphorylation of mTOR through the PI3K/AKT pathway. (B and C) MUC16 promotes the proliferation and growth of Ishikawa and KLE cells through the PI3K/AKT/mTOR signaling pathway. (D and E) The rescue experiment has shown that MUC16 promotes the invasion and metastasis of Ishikawa and KLE cells through the PI3K/AKT/mTOR signaling pathway. (F) MUC16 knockdown inhibited the growth of subcutaneous tumors in mice, and ESR1 overexpression can reverse the effect of shMUC16. (G) The weight of subcutaneous xenograft tumors. (H) The growth curve of subcutaneous xenograft tumors in nude mice. (I) Gross specimens of lungs. (J) Number of lung metastatic nodules. (K) Representative images of H&E staining of lung metastasis. Statistical significance was calculated using two-way ANOVA (B, H) or one-way ANOVA with Tukey's post-test (G, J). *p < 0.05, **p < 0.01, and ***p < 0.001.

Article Snippet: Human endometrial cancer cell lines, Ishikawa and KLE, were obtained from American Type Culture Collection (ATCC).

Techniques: Phospho-proteomics, Knockdown, Over Expression, Staining

Journal: Translational Oncology

Article Title: MUC16 promotes endometrial cancer progression and modulates sensitivity to lapatinib through the ESR1/PI3K/AKT axis

doi: 10.1016/j.tranon.2026.102774

Figure Lengend Snippet: MUC16 Mutation Influences Sensitivity to Targeted Therapies in Endometrial Cancer. (A) Filter genes that related to MUC16 mutation status, display the top 10 genes with the most obvious differences. (B) Based on MUC16 mutation-related gene screening, identify drugs that may have their efficacy affected by MUC16 mutations. (C) The IC50 of lapatinib, Neratinib, Afatinib and Pazopanib in Ishikawa and KLE cells were measured. (D) A molecular docking model of MUC16 protein with lapatinib was generated. (E) The IC50 of lapatinib is lower in cells with MUC16 knockdown. (F) Flow cytometry detection revealed that knockdown of MUC16 can enhance lapatinib-induced apoptosis in Ishikawa cells, whereas MUC16 overexpression significantly reduces lapatinib-induced apoptosis. Statistical significance was calculated using one-way ANOVA. *p < 0.05, **p < 0.01, and ***p < 0.001.

Article Snippet: Human endometrial cancer cell lines, Ishikawa and KLE, were obtained from American Type Culture Collection (ATCC).

Techniques: Mutagenesis, Generated, Knockdown, Flow Cytometry, Over Expression

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