emt 9782 Search Results


epithelial mesenchymal transition emt antibody  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc epithelial mesenchymal transition emt antibody
( A–B ) Knockdown of TAK1 by Map3k7 shRNA. ECA-109 cells were transduced with lentivirus bearing Map3k7 shRNA (LV- Map3k7 shRNA) or NC shRNA (LV-NC). 48 hr post-transduction, cells were harvested for analyzing TAK1 expression by quantitative real time-PCR (qRT-PCR) ( A ) and western blot ( B ). n = 3 biologically independent replicates. ( C–E ) Decreased expression of TAK1 facilitates cell migration and invasion. ECA-109 cells were transduced with LV- Map3k7 shRNA or LV-NC. 48 hr post-transduction, cells were subjected to transwell ( C, D ) or wound healing ( E ) assay. n=5 biologically independent replicates. Scale bar = 500 µm ( C ); scale bar = 100 µm ( E ). ( F – G ) Reduced expression of TAK1 increases mesenchymal marker expression and decreases epithelial marker expression. n=3 biologically independent replicates. ( H ) Reduced expression of TAK1 in ECA-109 cells affects epithelial-mesenchymal <t>transition</t> <t>(EMT)</t> related gene expression. Protein levels were analyzed by western blot, and Actin was used as a loading control. Gene expression was detected by qRT-PCR, and Gapdh was used as a house-keeping gene. n=4 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by unpaired Student’s t-test. *p<0.05, **p<0.01, and ***p<0.001. Figure 1—figure supplement 3—source data 1. TAK1 knockdown facilitates esophageal squamous cell carcinoma (ESCC) migration and invasion. Figure 1—figure supplement 3—source data 2. PDF file containing original western blots for , indicating the relevant bands. Figure 1—figure supplement 3—source data 3. Original files for western blot analysis displayed in .
Epithelial Mesenchymal Transition Emt Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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epithelialmesenchymal transition emt antibody sampler kit  (Cell Signaling Technology Inc)
93
Cell Signaling Technology Inc epithelialmesenchymal transition emt antibody sampler kit
( A–B ) Knockdown of TAK1 by Map3k7 shRNA. ECA-109 cells were transduced with lentivirus bearing Map3k7 shRNA (LV- Map3k7 shRNA) or NC shRNA (LV-NC). 48 hr post-transduction, cells were harvested for analyzing TAK1 expression by quantitative real time-PCR (qRT-PCR) ( A ) and western blot ( B ). n = 3 biologically independent replicates. ( C–E ) Decreased expression of TAK1 facilitates cell migration and invasion. ECA-109 cells were transduced with LV- Map3k7 shRNA or LV-NC. 48 hr post-transduction, cells were subjected to transwell ( C, D ) or wound healing ( E ) assay. n=5 biologically independent replicates. Scale bar = 500 µm ( C ); scale bar = 100 µm ( E ). ( F – G ) Reduced expression of TAK1 increases mesenchymal marker expression and decreases epithelial marker expression. n=3 biologically independent replicates. ( H ) Reduced expression of TAK1 in ECA-109 cells affects epithelial-mesenchymal <t>transition</t> <t>(EMT)</t> related gene expression. Protein levels were analyzed by western blot, and Actin was used as a loading control. Gene expression was detected by qRT-PCR, and Gapdh was used as a house-keeping gene. n=4 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by unpaired Student’s t-test. *p<0.05, **p<0.01, and ***p<0.001. Figure 1—figure supplement 3—source data 1. TAK1 knockdown facilitates esophageal squamous cell carcinoma (ESCC) migration and invasion. Figure 1—figure supplement 3—source data 2. PDF file containing original western blots for , indicating the relevant bands. Figure 1—figure supplement 3—source data 3. Original files for western blot analysis displayed in .
Epithelialmesenchymal Transition Emt Antibody Sampler Kit, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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emt antibody sampler kit #9782  (Cell Signaling Technology Inc)
90
Cell Signaling Technology Inc emt antibody sampler kit #9782
( A–B ) Knockdown of TAK1 by Map3k7 shRNA. ECA-109 cells were transduced with lentivirus bearing Map3k7 shRNA (LV- Map3k7 shRNA) or NC shRNA (LV-NC). 48 hr post-transduction, cells were harvested for analyzing TAK1 expression by quantitative real time-PCR (qRT-PCR) ( A ) and western blot ( B ). n = 3 biologically independent replicates. ( C–E ) Decreased expression of TAK1 facilitates cell migration and invasion. ECA-109 cells were transduced with LV- Map3k7 shRNA or LV-NC. 48 hr post-transduction, cells were subjected to transwell ( C, D ) or wound healing ( E ) assay. n=5 biologically independent replicates. Scale bar = 500 µm ( C ); scale bar = 100 µm ( E ). ( F – G ) Reduced expression of TAK1 increases mesenchymal marker expression and decreases epithelial marker expression. n=3 biologically independent replicates. ( H ) Reduced expression of TAK1 in ECA-109 cells affects epithelial-mesenchymal <t>transition</t> <t>(EMT)</t> related gene expression. Protein levels were analyzed by western blot, and Actin was used as a loading control. Gene expression was detected by qRT-PCR, and Gapdh was used as a house-keeping gene. n=4 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by unpaired Student’s t-test. *p<0.05, **p<0.01, and ***p<0.001. Figure 1—figure supplement 3—source data 1. TAK1 knockdown facilitates esophageal squamous cell carcinoma (ESCC) migration and invasion. Figure 1—figure supplement 3—source data 2. PDF file containing original western blots for , indicating the relevant bands. Figure 1—figure supplement 3—source data 3. Original files for western blot analysis displayed in .
Emt Antibody Sampler Kit #9782, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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parp 13371-1-ap  (Proteintech)
90
Proteintech parp 13371-1-ap
( A–B ) Knockdown of TAK1 by Map3k7 shRNA. ECA-109 cells were transduced with lentivirus bearing Map3k7 shRNA (LV- Map3k7 shRNA) or NC shRNA (LV-NC). 48 hr post-transduction, cells were harvested for analyzing TAK1 expression by quantitative real time-PCR (qRT-PCR) ( A ) and western blot ( B ). n = 3 biologically independent replicates. ( C–E ) Decreased expression of TAK1 facilitates cell migration and invasion. ECA-109 cells were transduced with LV- Map3k7 shRNA or LV-NC. 48 hr post-transduction, cells were subjected to transwell ( C, D ) or wound healing ( E ) assay. n=5 biologically independent replicates. Scale bar = 500 µm ( C ); scale bar = 100 µm ( E ). ( F – G ) Reduced expression of TAK1 increases mesenchymal marker expression and decreases epithelial marker expression. n=3 biologically independent replicates. ( H ) Reduced expression of TAK1 in ECA-109 cells affects epithelial-mesenchymal <t>transition</t> <t>(EMT)</t> related gene expression. Protein levels were analyzed by western blot, and Actin was used as a loading control. Gene expression was detected by qRT-PCR, and Gapdh was used as a house-keeping gene. n=4 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by unpaired Student’s t-test. *p<0.05, **p<0.01, and ***p<0.001. Figure 1—figure supplement 3—source data 1. TAK1 knockdown facilitates esophageal squamous cell carcinoma (ESCC) migration and invasion. Figure 1—figure supplement 3—source data 2. PDF file containing original western blots for , indicating the relevant bands. Figure 1—figure supplement 3—source data 3. Original files for western blot analysis displayed in .
Parp 13371 1 Ap, supplied by Proteintech, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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epithelial mesenchymal transition emt antibody sample kit  (Cell Signaling Technology Inc)
98
Cell Signaling Technology Inc epithelial mesenchymal transition emt antibody sample kit
( A–B ) Knockdown of TAK1 by Map3k7 shRNA. ECA-109 cells were transduced with lentivirus bearing Map3k7 shRNA (LV- Map3k7 shRNA) or NC shRNA (LV-NC). 48 hr post-transduction, cells were harvested for analyzing TAK1 expression by quantitative real time-PCR (qRT-PCR) ( A ) and western blot ( B ). n = 3 biologically independent replicates. ( C–E ) Decreased expression of TAK1 facilitates cell migration and invasion. ECA-109 cells were transduced with LV- Map3k7 shRNA or LV-NC. 48 hr post-transduction, cells were subjected to transwell ( C, D ) or wound healing ( E ) assay. n=5 biologically independent replicates. Scale bar = 500 µm ( C ); scale bar = 100 µm ( E ). ( F – G ) Reduced expression of TAK1 increases mesenchymal marker expression and decreases epithelial marker expression. n=3 biologically independent replicates. ( H ) Reduced expression of TAK1 in ECA-109 cells affects epithelial-mesenchymal <t>transition</t> <t>(EMT)</t> related gene expression. Protein levels were analyzed by western blot, and Actin was used as a loading control. Gene expression was detected by qRT-PCR, and Gapdh was used as a house-keeping gene. n=4 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by unpaired Student’s t-test. *p<0.05, **p<0.01, and ***p<0.001. Figure 1—figure supplement 3—source data 1. TAK1 knockdown facilitates esophageal squamous cell carcinoma (ESCC) migration and invasion. Figure 1—figure supplement 3—source data 2. PDF file containing original western blots for , indicating the relevant bands. Figure 1—figure supplement 3—source data 3. Original files for western blot analysis displayed in .
Epithelial Mesenchymal Transition Emt Antibody Sample Kit, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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emt pcr arrays  (Qiagen)
90
Qiagen emt pcr arrays
( A–B ) Knockdown of TAK1 by Map3k7 shRNA. ECA-109 cells were transduced with lentivirus bearing Map3k7 shRNA (LV- Map3k7 shRNA) or NC shRNA (LV-NC). 48 hr post-transduction, cells were harvested for analyzing TAK1 expression by quantitative real time-PCR (qRT-PCR) ( A ) and western blot ( B ). n = 3 biologically independent replicates. ( C–E ) Decreased expression of TAK1 facilitates cell migration and invasion. ECA-109 cells were transduced with LV- Map3k7 shRNA or LV-NC. 48 hr post-transduction, cells were subjected to transwell ( C, D ) or wound healing ( E ) assay. n=5 biologically independent replicates. Scale bar = 500 µm ( C ); scale bar = 100 µm ( E ). ( F – G ) Reduced expression of TAK1 increases mesenchymal marker expression and decreases epithelial marker expression. n=3 biologically independent replicates. ( H ) Reduced expression of TAK1 in ECA-109 cells affects epithelial-mesenchymal <t>transition</t> <t>(EMT)</t> related gene expression. Protein levels were analyzed by western blot, and Actin was used as a loading control. Gene expression was detected by qRT-PCR, and Gapdh was used as a house-keeping gene. n=4 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by unpaired Student’s t-test. *p<0.05, **p<0.01, and ***p<0.001. Figure 1—figure supplement 3—source data 1. TAK1 knockdown facilitates esophageal squamous cell carcinoma (ESCC) migration and invasion. Figure 1—figure supplement 3—source data 2. PDF file containing original western blots for , indicating the relevant bands. Figure 1—figure supplement 3—source data 3. Original files for western blot analysis displayed in .
Emt Pcr Arrays, supplied by Qiagen, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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efemp2 12004-1-ap antibody  (Proteintech)
90
Proteintech efemp2 12004-1-ap antibody
( A–B ) Knockdown of TAK1 by Map3k7 shRNA. ECA-109 cells were transduced with lentivirus bearing Map3k7 shRNA (LV- Map3k7 shRNA) or NC shRNA (LV-NC). 48 hr post-transduction, cells were harvested for analyzing TAK1 expression by quantitative real time-PCR (qRT-PCR) ( A ) and western blot ( B ). n = 3 biologically independent replicates. ( C–E ) Decreased expression of TAK1 facilitates cell migration and invasion. ECA-109 cells were transduced with LV- Map3k7 shRNA or LV-NC. 48 hr post-transduction, cells were subjected to transwell ( C, D ) or wound healing ( E ) assay. n=5 biologically independent replicates. Scale bar = 500 µm ( C ); scale bar = 100 µm ( E ). ( F – G ) Reduced expression of TAK1 increases mesenchymal marker expression and decreases epithelial marker expression. n=3 biologically independent replicates. ( H ) Reduced expression of TAK1 in ECA-109 cells affects epithelial-mesenchymal <t>transition</t> <t>(EMT)</t> related gene expression. Protein levels were analyzed by western blot, and Actin was used as a loading control. Gene expression was detected by qRT-PCR, and Gapdh was used as a house-keeping gene. n=4 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by unpaired Student’s t-test. *p<0.05, **p<0.01, and ***p<0.001. Figure 1—figure supplement 3—source data 1. TAK1 knockdown facilitates esophageal squamous cell carcinoma (ESCC) migration and invasion. Figure 1—figure supplement 3—source data 2. PDF file containing original western blots for , indicating the relevant bands. Figure 1—figure supplement 3—source data 3. Original files for western blot analysis displayed in .
Efemp2 12004 1 Ap Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti-p-akt  (Cell Signaling Technology Inc)
90
Cell Signaling Technology Inc anti-p-akt
( A–B ) Knockdown of TAK1 by Map3k7 shRNA. ECA-109 cells were transduced with lentivirus bearing Map3k7 shRNA (LV- Map3k7 shRNA) or NC shRNA (LV-NC). 48 hr post-transduction, cells were harvested for analyzing TAK1 expression by quantitative real time-PCR (qRT-PCR) ( A ) and western blot ( B ). n = 3 biologically independent replicates. ( C–E ) Decreased expression of TAK1 facilitates cell migration and invasion. ECA-109 cells were transduced with LV- Map3k7 shRNA or LV-NC. 48 hr post-transduction, cells were subjected to transwell ( C, D ) or wound healing ( E ) assay. n=5 biologically independent replicates. Scale bar = 500 µm ( C ); scale bar = 100 µm ( E ). ( F – G ) Reduced expression of TAK1 increases mesenchymal marker expression and decreases epithelial marker expression. n=3 biologically independent replicates. ( H ) Reduced expression of TAK1 in ECA-109 cells affects epithelial-mesenchymal <t>transition</t> <t>(EMT)</t> related gene expression. Protein levels were analyzed by western blot, and Actin was used as a loading control. Gene expression was detected by qRT-PCR, and Gapdh was used as a house-keeping gene. n=4 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by unpaired Student’s t-test. *p<0.05, **p<0.01, and ***p<0.001. Figure 1—figure supplement 3—source data 1. TAK1 knockdown facilitates esophageal squamous cell carcinoma (ESCC) migration and invasion. Figure 1—figure supplement 3—source data 2. PDF file containing original western blots for , indicating the relevant bands. Figure 1—figure supplement 3—source data 3. Original files for western blot analysis displayed in .
Anti P Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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emt  (Cell Signaling Technology Inc)
94
Cell Signaling Technology Inc emt
Figure 4. Comparison between CM and FM on cell survival, autophagy, and <t>EMT</t> in TNBC cells. (A–C) Comparative effects of CM and FM on protein expression levels related to cell survival, autophagy, and EMT in MB-231, MB-468, and PY8119 cells, respectively. Cells were treated with CM and FM for 24 h. Whole-cell lysates were prepared, and Western blots were carried out <t>using</t> <t>antibodies</t> specific to cell survival-, autophagy-, and EMT-related proteins. β-actin was used as a loading control. Representative pictures are shown. (D) A significant difference between CM and FM on vimentin and β-catenin expression levels in MB-231, MB-468, and PY8119 cells. Experiments were performed at least in triplicate (n = 3), and all data are shown as mean ± SD. # p < 0.05 in each group as calculated by the paired Student’s t-test. CM: complete conditioned media with 4 g/L glucose and 10% FBS; FM: fasting-mimicking conditioned media with 1 g/L glucose and 1% FBS; EGFR: epidermal growth factor receptor; pEGFR: phospho-EGFR; PCNA: proliferating cell nuclear antigen; LC3A/B: light chain 3A/B.
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anti atg7 antibodies  (Cell Signaling Technology Inc)
95
Cell Signaling Technology Inc anti atg7 antibodies
Figure 4. Comparison between CM and FM on cell survival, autophagy, and <t>EMT</t> in TNBC cells. (A–C) Comparative effects of CM and FM on protein expression levels related to cell survival, autophagy, and EMT in MB-231, MB-468, and PY8119 cells, respectively. Cells were treated with CM and FM for 24 h. Whole-cell lysates were prepared, and Western blots were carried out <t>using</t> <t>antibodies</t> specific to cell survival-, autophagy-, and EMT-related proteins. β-actin was used as a loading control. Representative pictures are shown. (D) A significant difference between CM and FM on vimentin and β-catenin expression levels in MB-231, MB-468, and PY8119 cells. Experiments were performed at least in triplicate (n = 3), and all data are shown as mean ± SD. # p < 0.05 in each group as calculated by the paired Student’s t-test. CM: complete conditioned media with 4 g/L glucose and 10% FBS; FM: fasting-mimicking conditioned media with 1 g/L glucose and 1% FBS; EGFR: epidermal growth factor receptor; pEGFR: phospho-EGFR; PCNA: proliferating cell nuclear antigen; LC3A/B: light chain 3A/B.
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emt kit  (Cell Signaling Technology Inc)
99
Cell Signaling Technology Inc emt kit
Figure 4. Comparison between CM and FM on cell survival, autophagy, and <t>EMT</t> in TNBC cells. (A–C) Comparative effects of CM and FM on protein expression levels related to cell survival, autophagy, and EMT in MB-231, MB-468, and PY8119 cells, respectively. Cells were treated with CM and FM for 24 h. Whole-cell lysates were prepared, and Western blots were carried out <t>using</t> <t>antibodies</t> specific to cell survival-, autophagy-, and EMT-related proteins. β-actin was used as a loading control. Representative pictures are shown. (D) A significant difference between CM and FM on vimentin and β-catenin expression levels in MB-231, MB-468, and PY8119 cells. Experiments were performed at least in triplicate (n = 3), and all data are shown as mean ± SD. # p < 0.05 in each group as calculated by the paired Student’s t-test. CM: complete conditioned media with 4 g/L glucose and 10% FBS; FM: fasting-mimicking conditioned media with 1 g/L glucose and 1% FBS; EGFR: epidermal growth factor receptor; pEGFR: phospho-EGFR; PCNA: proliferating cell nuclear antigen; LC3A/B: light chain 3A/B.
Emt Kit, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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emt marker antibodies #9782  (Cell Signaling Technology Inc)
90
Cell Signaling Technology Inc emt marker antibodies #9782
Figure 4. Comparison between CM and FM on cell survival, autophagy, and <t>EMT</t> in TNBC cells. (A–C) Comparative effects of CM and FM on protein expression levels related to cell survival, autophagy, and EMT in MB-231, MB-468, and PY8119 cells, respectively. Cells were treated with CM and FM for 24 h. Whole-cell lysates were prepared, and Western blots were carried out <t>using</t> <t>antibodies</t> specific to cell survival-, autophagy-, and EMT-related proteins. β-actin was used as a loading control. Representative pictures are shown. (D) A significant difference between CM and FM on vimentin and β-catenin expression levels in MB-231, MB-468, and PY8119 cells. Experiments were performed at least in triplicate (n = 3), and all data are shown as mean ± SD. # p < 0.05 in each group as calculated by the paired Student’s t-test. CM: complete conditioned media with 4 g/L glucose and 10% FBS; FM: fasting-mimicking conditioned media with 1 g/L glucose and 1% FBS; EGFR: epidermal growth factor receptor; pEGFR: phospho-EGFR; PCNA: proliferating cell nuclear antigen; LC3A/B: light chain 3A/B.
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Image Search Results


( A–B ) Knockdown of TAK1 by Map3k7 shRNA. ECA-109 cells were transduced with lentivirus bearing Map3k7 shRNA (LV- Map3k7 shRNA) or NC shRNA (LV-NC). 48 hr post-transduction, cells were harvested for analyzing TAK1 expression by quantitative real time-PCR (qRT-PCR) ( A ) and western blot ( B ). n = 3 biologically independent replicates. ( C–E ) Decreased expression of TAK1 facilitates cell migration and invasion. ECA-109 cells were transduced with LV- Map3k7 shRNA or LV-NC. 48 hr post-transduction, cells were subjected to transwell ( C, D ) or wound healing ( E ) assay. n=5 biologically independent replicates. Scale bar = 500 µm ( C ); scale bar = 100 µm ( E ). ( F – G ) Reduced expression of TAK1 increases mesenchymal marker expression and decreases epithelial marker expression. n=3 biologically independent replicates. ( H ) Reduced expression of TAK1 in ECA-109 cells affects epithelial-mesenchymal transition (EMT) related gene expression. Protein levels were analyzed by western blot, and Actin was used as a loading control. Gene expression was detected by qRT-PCR, and Gapdh was used as a house-keeping gene. n=4 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by unpaired Student’s t-test. *p<0.05, **p<0.01, and ***p<0.001. Figure 1—figure supplement 3—source data 1. TAK1 knockdown facilitates esophageal squamous cell carcinoma (ESCC) migration and invasion. Figure 1—figure supplement 3—source data 2. PDF file containing original western blots for , indicating the relevant bands. Figure 1—figure supplement 3—source data 3. Original files for western blot analysis displayed in .

Journal: eLife

Article Title: TAK1-mediated phosphorylation of PLCE1 represses PIP2 hydrolysis to impede esophageal squamous cancer metastasis

doi: 10.7554/eLife.97373

Figure Lengend Snippet: ( A–B ) Knockdown of TAK1 by Map3k7 shRNA. ECA-109 cells were transduced with lentivirus bearing Map3k7 shRNA (LV- Map3k7 shRNA) or NC shRNA (LV-NC). 48 hr post-transduction, cells were harvested for analyzing TAK1 expression by quantitative real time-PCR (qRT-PCR) ( A ) and western blot ( B ). n = 3 biologically independent replicates. ( C–E ) Decreased expression of TAK1 facilitates cell migration and invasion. ECA-109 cells were transduced with LV- Map3k7 shRNA or LV-NC. 48 hr post-transduction, cells were subjected to transwell ( C, D ) or wound healing ( E ) assay. n=5 biologically independent replicates. Scale bar = 500 µm ( C ); scale bar = 100 µm ( E ). ( F – G ) Reduced expression of TAK1 increases mesenchymal marker expression and decreases epithelial marker expression. n=3 biologically independent replicates. ( H ) Reduced expression of TAK1 in ECA-109 cells affects epithelial-mesenchymal transition (EMT) related gene expression. Protein levels were analyzed by western blot, and Actin was used as a loading control. Gene expression was detected by qRT-PCR, and Gapdh was used as a house-keeping gene. n=4 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by unpaired Student’s t-test. *p<0.05, **p<0.01, and ***p<0.001. Figure 1—figure supplement 3—source data 1. TAK1 knockdown facilitates esophageal squamous cell carcinoma (ESCC) migration and invasion. Figure 1—figure supplement 3—source data 2. PDF file containing original western blots for , indicating the relevant bands. Figure 1—figure supplement 3—source data 3. Original files for western blot analysis displayed in .

Article Snippet: Rabbit monoclonal antibodies against TAK1 (#5206), phospho-TAK1 (Ser412, #9339), PKCα (#2056), phospho-PKC (pan) (gamma Thr514) (#38938), GSK-3β (#9315), phospho-GSK-3β (Ser9) (#5558), β-Catenin (#8480), phospho-β-Catenin (Ser33/37/Thr41) (#9561), MMP-2 (#87809), mouse monoclonal antibodies against Actin (#3700), Myc-Tag (Sepharose Bead Conjugate) (#55464), Epithelial-Mesenchymal Transition (EMT) antibody sample kit (#9782), phosphor-IKK (#2078), IKK (#61294), phosphor-JNK (#4668), JNK (#9252), phospho-ERK (#4370), ERK (#9102), phospho-P38 MAPK (#9211), P38 MPAK (#9212), and normal rabbit IgG (#2729) were from Cell Signaling Technology (Beverley, MA, USA).

Techniques: Knockdown, shRNA, Transduction, Expressing, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Western Blot, Migration, Marker, Gene Expression, Control

( A–B ) TAK1 expression was decreased by Map3k7 gRNA in ECA-109 cells. TAK1 knockout was achieved by CRISPR-Cas9. (B–D) Knockout of TAK1 expression in ECA-109 cells accelerates cell migration and invasion as analyzed by transwell ( B, C ) and wound healing ( D ) assays. Scale bar = 500 µm ( B ); scale bar = 100 µm ( D ). ( E – F ) Loss of TAK1 increases mesenchymal protein marker expression and reduces epithelial protein marker expression. ECA-109 cells were treated with Map3k7 gRNA, and then cells were harvested for western blot analysis. n=3 biologically independent replicates. ( G ) Knockout of TAK1 expression in ECA-109 cells alters epithelial-mesenchymal transition (EMT) related gene expression as analyzed by quantitative real time-PCR (qRT-PCR). Gapdh was used as a house-keeping gene. n=4 biologically independent replicates. Protein levels were analyzed by western blot, and Actin was used as a loading control. Data are presented as mean ± SD. Statistical significance was tested by unpaired Student’s t-test. *p<0.05, **p<0.01, and ***p<0.001. Figure 1—figure supplement 4—source data 1. TAK1 knockout accelerates esophageal squamous cell carcinoma (ESCC) migration and invasion. Figure 1—figure supplement 4—source data 2. PDF file containing original western blots for , indicating the relevant bands. Figure 1—figure supplement 4—source data 3. Original files for western blot analysis displayed in .

Journal: eLife

Article Title: TAK1-mediated phosphorylation of PLCE1 represses PIP2 hydrolysis to impede esophageal squamous cancer metastasis

doi: 10.7554/eLife.97373

Figure Lengend Snippet: ( A–B ) TAK1 expression was decreased by Map3k7 gRNA in ECA-109 cells. TAK1 knockout was achieved by CRISPR-Cas9. (B–D) Knockout of TAK1 expression in ECA-109 cells accelerates cell migration and invasion as analyzed by transwell ( B, C ) and wound healing ( D ) assays. Scale bar = 500 µm ( B ); scale bar = 100 µm ( D ). ( E – F ) Loss of TAK1 increases mesenchymal protein marker expression and reduces epithelial protein marker expression. ECA-109 cells were treated with Map3k7 gRNA, and then cells were harvested for western blot analysis. n=3 biologically independent replicates. ( G ) Knockout of TAK1 expression in ECA-109 cells alters epithelial-mesenchymal transition (EMT) related gene expression as analyzed by quantitative real time-PCR (qRT-PCR). Gapdh was used as a house-keeping gene. n=4 biologically independent replicates. Protein levels were analyzed by western blot, and Actin was used as a loading control. Data are presented as mean ± SD. Statistical significance was tested by unpaired Student’s t-test. *p<0.05, **p<0.01, and ***p<0.001. Figure 1—figure supplement 4—source data 1. TAK1 knockout accelerates esophageal squamous cell carcinoma (ESCC) migration and invasion. Figure 1—figure supplement 4—source data 2. PDF file containing original western blots for , indicating the relevant bands. Figure 1—figure supplement 4—source data 3. Original files for western blot analysis displayed in .

Article Snippet: Rabbit monoclonal antibodies against TAK1 (#5206), phospho-TAK1 (Ser412, #9339), PKCα (#2056), phospho-PKC (pan) (gamma Thr514) (#38938), GSK-3β (#9315), phospho-GSK-3β (Ser9) (#5558), β-Catenin (#8480), phospho-β-Catenin (Ser33/37/Thr41) (#9561), MMP-2 (#87809), mouse monoclonal antibodies against Actin (#3700), Myc-Tag (Sepharose Bead Conjugate) (#55464), Epithelial-Mesenchymal Transition (EMT) antibody sample kit (#9782), phosphor-IKK (#2078), IKK (#61294), phosphor-JNK (#4668), JNK (#9252), phospho-ERK (#4370), ERK (#9102), phospho-P38 MAPK (#9211), P38 MPAK (#9212), and normal rabbit IgG (#2729) were from Cell Signaling Technology (Beverley, MA, USA).

Techniques: Expressing, Knock-Out, CRISPR, Migration, Marker, Western Blot, Gene Expression, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Control

( A–D ) IP3R blocking inhibits PLCE1 promoted cell migration and invasion. ECA-109 cells were transfected with the plasmid expressing Plce1 for 6 hr and then cells were treated with 2-APB (10 µM) for additional 18 hr. Cell migration and invasion were analyzed by transwell ( A, B ) or wound healing ( C, D ) assay. n=5 biologically independent replicates. Scale bar = 500 µm ( A ) and 100 µm ( C ). (E) IP3R blocking counteracts PLCE1-induced changes in epithelial-mesenchymal transition (EMT) gene expression. The levels of mRNA were analyzed by quantitative real time-PCR (qRT-PCR), and Gapdh was used as a house-keeping gene. n=3 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by two-tailed one-way ANOVA test. * p<0.05, **p<0.01 , and *** p < 0.001. Figure 5—figure supplement 2—source data 1. 2-APB treatment counteracts PLCE1-induced cell migration.

Journal: eLife

Article Title: TAK1-mediated phosphorylation of PLCE1 represses PIP2 hydrolysis to impede esophageal squamous cancer metastasis

doi: 10.7554/eLife.97373

Figure Lengend Snippet: ( A–D ) IP3R blocking inhibits PLCE1 promoted cell migration and invasion. ECA-109 cells were transfected with the plasmid expressing Plce1 for 6 hr and then cells were treated with 2-APB (10 µM) for additional 18 hr. Cell migration and invasion were analyzed by transwell ( A, B ) or wound healing ( C, D ) assay. n=5 biologically independent replicates. Scale bar = 500 µm ( A ) and 100 µm ( C ). (E) IP3R blocking counteracts PLCE1-induced changes in epithelial-mesenchymal transition (EMT) gene expression. The levels of mRNA were analyzed by quantitative real time-PCR (qRT-PCR), and Gapdh was used as a house-keeping gene. n=3 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by two-tailed one-way ANOVA test. * p<0.05, **p<0.01 , and *** p < 0.001. Figure 5—figure supplement 2—source data 1. 2-APB treatment counteracts PLCE1-induced cell migration.

Article Snippet: Rabbit monoclonal antibodies against TAK1 (#5206), phospho-TAK1 (Ser412, #9339), PKCα (#2056), phospho-PKC (pan) (gamma Thr514) (#38938), GSK-3β (#9315), phospho-GSK-3β (Ser9) (#5558), β-Catenin (#8480), phospho-β-Catenin (Ser33/37/Thr41) (#9561), MMP-2 (#87809), mouse monoclonal antibodies against Actin (#3700), Myc-Tag (Sepharose Bead Conjugate) (#55464), Epithelial-Mesenchymal Transition (EMT) antibody sample kit (#9782), phosphor-IKK (#2078), IKK (#61294), phosphor-JNK (#4668), JNK (#9252), phospho-ERK (#4370), ERK (#9102), phospho-P38 MAPK (#9211), P38 MPAK (#9212), and normal rabbit IgG (#2729) were from Cell Signaling Technology (Beverley, MA, USA).

Techniques: Blocking Assay, Migration, Transfection, Plasmid Preparation, Expressing, Gene Expression, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Two Tailed Test

Cells were transfected with plasmid expressing Plce1 for 6 hr and then treated with 2-APB (10 µM) for additional 18 hr. ( A–B ) Transwell assay showing the application of 2-APB attenuates cell migration and invasion induced by PLCE1. Scale bar = 500 µm. n=5 biologically independent replicates. ( C–D ) Wound healing assay showing the treatment of 2-APB represses cell migration induced by PLCE1. Scale bar = 100 µm. n=5 biologically independent replicates. ( E ) 2-APB counteracts PLCE1-induced changes in epithelial-mesenchymal transition (EMT) gene expression. The mRNA levels were detected by quantitative real time-PCR (qRT-PCR), and Gapdh was used as a house-keeping gene. n=3 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by two-tailed one-way ANOVA test. * p < 0.05, ** p<0.01, and *** p<0.001. Figure 5—figure supplement 3—source data 1. IP3R inhibition represses PLCE1-stimulated cell migration and invasion in KYSE-150 cells.

Journal: eLife

Article Title: TAK1-mediated phosphorylation of PLCE1 represses PIP2 hydrolysis to impede esophageal squamous cancer metastasis

doi: 10.7554/eLife.97373

Figure Lengend Snippet: Cells were transfected with plasmid expressing Plce1 for 6 hr and then treated with 2-APB (10 µM) for additional 18 hr. ( A–B ) Transwell assay showing the application of 2-APB attenuates cell migration and invasion induced by PLCE1. Scale bar = 500 µm. n=5 biologically independent replicates. ( C–D ) Wound healing assay showing the treatment of 2-APB represses cell migration induced by PLCE1. Scale bar = 100 µm. n=5 biologically independent replicates. ( E ) 2-APB counteracts PLCE1-induced changes in epithelial-mesenchymal transition (EMT) gene expression. The mRNA levels were detected by quantitative real time-PCR (qRT-PCR), and Gapdh was used as a house-keeping gene. n=3 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by two-tailed one-way ANOVA test. * p < 0.05, ** p<0.01, and *** p<0.001. Figure 5—figure supplement 3—source data 1. IP3R inhibition represses PLCE1-stimulated cell migration and invasion in KYSE-150 cells.

Article Snippet: Rabbit monoclonal antibodies against TAK1 (#5206), phospho-TAK1 (Ser412, #9339), PKCα (#2056), phospho-PKC (pan) (gamma Thr514) (#38938), GSK-3β (#9315), phospho-GSK-3β (Ser9) (#5558), β-Catenin (#8480), phospho-β-Catenin (Ser33/37/Thr41) (#9561), MMP-2 (#87809), mouse monoclonal antibodies against Actin (#3700), Myc-Tag (Sepharose Bead Conjugate) (#55464), Epithelial-Mesenchymal Transition (EMT) antibody sample kit (#9782), phosphor-IKK (#2078), IKK (#61294), phosphor-JNK (#4668), JNK (#9252), phospho-ERK (#4370), ERK (#9102), phospho-P38 MAPK (#9211), P38 MPAK (#9212), and normal rabbit IgG (#2729) were from Cell Signaling Technology (Beverley, MA, USA).

Techniques: Transfection, Plasmid Preparation, Expressing, Transwell Assay, Migration, Wound Healing Assay, Gene Expression, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Two Tailed Test, Inhibition

Cells were transfected with plasmid expressing Plce1 for 6 hr and then treated with 2-APB (10 µM) for additional 18 hr. ( A–D ) Cell migration and invasion induced by PLCE1 were repressed by the application of 2-APB in TE-1 cells. Cell migration and invasion were analyzed by transwell assay (A–B, scale bar = 500 µm) and wound healing assay (C–D, scale bar = 100 µm). n=5 biologically independent replicates. ( E ) 2-APB abolishes PLCE1-induced changes in epithelial-mesenchymal transition (EMT) gene expression in TE-1 cells. Gene expression was analyzed by quantitative real time-PCR (qRT-PCR), and Gapdh was used as a house-keeping gene. n=3 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by two-tailed one-way ANOVA test. ** p<0.01 and *** p<0.001 . Figure 5—figure supplement 4—source data 1. IP3R inhibition reduces PLCE1-stimulated cell migration and invasion in TE-1 cells.

Journal: eLife

Article Title: TAK1-mediated phosphorylation of PLCE1 represses PIP2 hydrolysis to impede esophageal squamous cancer metastasis

doi: 10.7554/eLife.97373

Figure Lengend Snippet: Cells were transfected with plasmid expressing Plce1 for 6 hr and then treated with 2-APB (10 µM) for additional 18 hr. ( A–D ) Cell migration and invasion induced by PLCE1 were repressed by the application of 2-APB in TE-1 cells. Cell migration and invasion were analyzed by transwell assay (A–B, scale bar = 500 µm) and wound healing assay (C–D, scale bar = 100 µm). n=5 biologically independent replicates. ( E ) 2-APB abolishes PLCE1-induced changes in epithelial-mesenchymal transition (EMT) gene expression in TE-1 cells. Gene expression was analyzed by quantitative real time-PCR (qRT-PCR), and Gapdh was used as a house-keeping gene. n=3 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by two-tailed one-way ANOVA test. ** p<0.01 and *** p<0.001 . Figure 5—figure supplement 4—source data 1. IP3R inhibition reduces PLCE1-stimulated cell migration and invasion in TE-1 cells.

Article Snippet: Rabbit monoclonal antibodies against TAK1 (#5206), phospho-TAK1 (Ser412, #9339), PKCα (#2056), phospho-PKC (pan) (gamma Thr514) (#38938), GSK-3β (#9315), phospho-GSK-3β (Ser9) (#5558), β-Catenin (#8480), phospho-β-Catenin (Ser33/37/Thr41) (#9561), MMP-2 (#87809), mouse monoclonal antibodies against Actin (#3700), Myc-Tag (Sepharose Bead Conjugate) (#55464), Epithelial-Mesenchymal Transition (EMT) antibody sample kit (#9782), phosphor-IKK (#2078), IKK (#61294), phosphor-JNK (#4668), JNK (#9252), phospho-ERK (#4370), ERK (#9102), phospho-P38 MAPK (#9211), P38 MPAK (#9212), and normal rabbit IgG (#2729) were from Cell Signaling Technology (Beverley, MA, USA).

Techniques: Transfection, Plasmid Preparation, Expressing, Migration, Transwell Assay, Wound Healing Assay, Gene Expression, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Two Tailed Test, Inhibition

Journal: eLife

Article Title: TAK1-mediated phosphorylation of PLCE1 represses PIP2 hydrolysis to impede esophageal squamous cancer metastasis

doi: 10.7554/eLife.97373

Figure Lengend Snippet:

Article Snippet: Rabbit monoclonal antibodies against TAK1 (#5206), phospho-TAK1 (Ser412, #9339), PKCα (#2056), phospho-PKC (pan) (gamma Thr514) (#38938), GSK-3β (#9315), phospho-GSK-3β (Ser9) (#5558), β-Catenin (#8480), phospho-β-Catenin (Ser33/37/Thr41) (#9561), MMP-2 (#87809), mouse monoclonal antibodies against Actin (#3700), Myc-Tag (Sepharose Bead Conjugate) (#55464), Epithelial-Mesenchymal Transition (EMT) antibody sample kit (#9782), phosphor-IKK (#2078), IKK (#61294), phosphor-JNK (#4668), JNK (#9252), phospho-ERK (#4370), ERK (#9102), phospho-P38 MAPK (#9211), P38 MPAK (#9212), and normal rabbit IgG (#2729) were from Cell Signaling Technology (Beverley, MA, USA).

Techniques: Transfection, Construct, shRNA, Recombinant, Plasmid Preparation, Sequencing, Activity Assay, Enzyme-linked Immunosorbent Assay, Software

Figure 4. Comparison between CM and FM on cell survival, autophagy, and EMT in TNBC cells. (A–C) Comparative effects of CM and FM on protein expression levels related to cell survival, autophagy, and EMT in MB-231, MB-468, and PY8119 cells, respectively. Cells were treated with CM and FM for 24 h. Whole-cell lysates were prepared, and Western blots were carried out using antibodies specific to cell survival-, autophagy-, and EMT-related proteins. β-actin was used as a loading control. Representative pictures are shown. (D) A significant difference between CM and FM on vimentin and β-catenin expression levels in MB-231, MB-468, and PY8119 cells. Experiments were performed at least in triplicate (n = 3), and all data are shown as mean ± SD. # p < 0.05 in each group as calculated by the paired Student’s t-test. CM: complete conditioned media with 4 g/L glucose and 10% FBS; FM: fasting-mimicking conditioned media with 1 g/L glucose and 1% FBS; EGFR: epidermal growth factor receptor; pEGFR: phospho-EGFR; PCNA: proliferating cell nuclear antigen; LC3A/B: light chain 3A/B.

Journal: Nutrients

Article Title: Intermittent Fasting Attenuates Obesity-Induced Triple-Negative Breast Cancer Progression by Disrupting Cell Cycle, Epithelial-Mesenchymal Transition, Immune Contexture, and Proinflammatory Signature.

doi: 10.3390/nu16132101

Figure Lengend Snippet: Figure 4. Comparison between CM and FM on cell survival, autophagy, and EMT in TNBC cells. (A–C) Comparative effects of CM and FM on protein expression levels related to cell survival, autophagy, and EMT in MB-231, MB-468, and PY8119 cells, respectively. Cells were treated with CM and FM for 24 h. Whole-cell lysates were prepared, and Western blots were carried out using antibodies specific to cell survival-, autophagy-, and EMT-related proteins. β-actin was used as a loading control. Representative pictures are shown. (D) A significant difference between CM and FM on vimentin and β-catenin expression levels in MB-231, MB-468, and PY8119 cells. Experiments were performed at least in triplicate (n = 3), and all data are shown as mean ± SD. # p < 0.05 in each group as calculated by the paired Student’s t-test. CM: complete conditioned media with 4 g/L glucose and 10% FBS; FM: fasting-mimicking conditioned media with 1 g/L glucose and 1% FBS; EGFR: epidermal growth factor receptor; pEGFR: phospho-EGFR; PCNA: proliferating cell nuclear antigen; LC3A/B: light chain 3A/B.

Article Snippet: Antibodies for Akt (#4060/4691), MAPK (#9910/9926), Autophagy (#4445), EMT (#9782), and Cell Cycle Phase (#17498) were obtained from Cell Signaling Technology (Danvers, MA, USA).

Techniques: Comparison, Expressing, Western Blot, Control