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Procell Inc human pancreatic cancer cells sw1990
Human Pancreatic Cancer Cells Sw1990, 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/human+pancreatic+cancer+cells+sw1990/sw1990+cells/pm36801507-71-0-14
Average 90 stars, based on 1 article reviews
human pancreatic cancer cells sw1990 - by Bioz Stars, 2026-10
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Article Title: Comprehensive pan-cancer analysis of role of GPRASP1, associated with clinical outcomes, immune microenvironment, and immunotherapeutic efficiency in pancreatic cancer.
Article Snippet: Human pancreatic cancer cells PANC-1, MIA PaCa-2, BxPC-3, SW1990, and AsPC-1 were obtained from Procell (Wuhan, China), Biobaiye (Shanghai, China), and BIOON (Shanghai, China).



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ATCC human pancreatic cancer cell line sw1990
Human Pancreatic Cancer Cell Line Sw1990, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+pancreatic+cancer+cells+sw1990/SW+1990/pm39983554-470-30-36
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ATCC sw1990 human pancreatic cancer cell lines
Figure 3. Safety evaluation of SMSN@G NPs in vitro. (a) CCK8 absorbance at different concentrations of SMSN@G NPs with or without light; (b) apoptotic assay at different concentrations of SMSN@G NPs; (c)Histogram of apoptosis rates of <t>SW1990</t> and PANC1 cells treated with different concentrations of SMSN@G NPs; Annexin V+/PI+ were defined as late apoptosis or necrosis, Annexin V+/PI−were defined as early apoptosis, *compared with SMSN without irradiation group. NS: No statistical difference, *p < 0.05, **p < 0.01, ***p < 0.001, analyzed using student’s t-test.
Sw1990 Human Pancreatic Cancer Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+pancreatic+cancer+cells+sw1990/SW+1990/pm38452386-142-2-12
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ATCC human pancreatic cancer cell lines sw1990
Figure 2. EBF2 is downregulated in PDAC tissues and inhibits cell proliferation and metastasis. A) H&E and IHC staining of EBF2 protein in PDAC and adjacent normal tissues. Scale bar, 10 μm. B) H scores of EBF2 in PDAC and adjacent normal tissues. C–E) Correlations of EBF2 expression with tumor stage (C), lymph node metastasis (D), and distal metastasis (E) in PDAC patients. Data in B–E are presented as mean ± SEM, *p < 0.05, **p < 0.01 by Student’s t-test. F) Kaplan–Meier plot of overall survival in 90 patients with PDAC, stratified by EBF2 expression (Log-rank test, p < 0.0001). G, H) The mRNA (G) and protein (H) levels of EBF2 in <t>SW1990</t> cells treated with EBF2 shRNAs (EBF2-KD) or negative control (SCR) verified by qPCR and Western
Human Pancreatic Cancer Cell Lines Sw1990, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+pancreatic+cancer+cells+sw1990/SW+1990/pm38015024-249-2-14
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human pancreatic cancer cell lines sw1990 - by Bioz Stars, 2026-10
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Procell Inc human pancreatic cancer cells sw1990
Figure 2. EBF2 is downregulated in PDAC tissues and inhibits cell proliferation and metastasis. A) H&E and IHC staining of EBF2 protein in PDAC and adjacent normal tissues. Scale bar, 10 μm. B) H scores of EBF2 in PDAC and adjacent normal tissues. C–E) Correlations of EBF2 expression with tumor stage (C), lymph node metastasis (D), and distal metastasis (E) in PDAC patients. Data in B–E are presented as mean ± SEM, *p < 0.05, **p < 0.01 by Student’s t-test. F) Kaplan–Meier plot of overall survival in 90 patients with PDAC, stratified by EBF2 expression (Log-rank test, p < 0.0001). G, H) The mRNA (G) and protein (H) levels of EBF2 in <t>SW1990</t> cells treated with EBF2 shRNAs (EBF2-KD) or negative control (SCR) verified by qPCR and Western
Human Pancreatic Cancer Cells Sw1990, 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/human+pancreatic+cancer+cells+sw1990/sw1990+cells/pm36801507-71-0-14
Average 90 stars, based on 1 article reviews
human pancreatic cancer cells sw1990 - by Bioz Stars, 2026-10
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Figure 3. Safety evaluation of SMSN@G NPs in vitro. (a) CCK8 absorbance at different concentrations of SMSN@G NPs with or without light; (b) apoptotic assay at different concentrations of SMSN@G NPs; (c)Histogram of apoptosis rates of SW1990 and PANC1 cells treated with different concentrations of SMSN@G NPs; Annexin V+/PI+ were defined as late apoptosis or necrosis, Annexin V+/PI−were defined as early apoptosis, *compared with SMSN without irradiation group. NS: No statistical difference, *p < 0.05, **p < 0.01, ***p < 0.001, analyzed using student’s t-test.

Journal: Nanotechnology

Article Title: Novel silicene-mesoporous silica nanoparticles conjugated gemcitabine induced cellular apoptosis via upregulating NF- κ B p65 nuclear translocation suppresses pancreatic cancer growth in vitro and in vivo .

doi: 10.1088/1361-6528/ad312a

Figure Lengend Snippet: Figure 3. Safety evaluation of SMSN@G NPs in vitro. (a) CCK8 absorbance at different concentrations of SMSN@G NPs with or without light; (b) apoptotic assay at different concentrations of SMSN@G NPs; (c)Histogram of apoptosis rates of SW1990 and PANC1 cells treated with different concentrations of SMSN@G NPs; Annexin V+/PI+ were defined as late apoptosis or necrosis, Annexin V+/PI−were defined as early apoptosis, *compared with SMSN without irradiation group. NS: No statistical difference, *p < 0.05, **p < 0.01, ***p < 0.001, analyzed using student’s t-test.

Article Snippet: PANC1 and SW1990 human pancreatic cancer cell lines were obtained from the American Type Culture Collection (ATCC, USA).

Techniques: In Vitro, Irradiation

Figure 4. Functional verification of SMSN@G NPs in vitro. (a) CCK8 experiment of different treatments. (b) Flow cytometry analyses of SW1990 and PANC1 cells that received different treatments: SMSN, SMSN@G NPs, SMSN@G NPs with NIR irradiation (200 pm, 808 nm, 1 W cm−2, 15 min), and SMSN@G NPs with NIR irradiation (200 pm, 808 nm, 1 W cm−2, 30 min). (c) Histogram of apoptosis rate of SW1990 and PANC1 cells intervened by different treatments. Annexin V+/PI+ was defined as late apoptosis or necrosis, while Annexin V+/PI−was defined as early apoptosis. NS: No statistical difference; *p < 0.05, ****p < 0.0001, analyzed using student’s t-test.

Journal: Nanotechnology

Article Title: Novel silicene-mesoporous silica nanoparticles conjugated gemcitabine induced cellular apoptosis via upregulating NF- κ B p65 nuclear translocation suppresses pancreatic cancer growth in vitro and in vivo .

doi: 10.1088/1361-6528/ad312a

Figure Lengend Snippet: Figure 4. Functional verification of SMSN@G NPs in vitro. (a) CCK8 experiment of different treatments. (b) Flow cytometry analyses of SW1990 and PANC1 cells that received different treatments: SMSN, SMSN@G NPs, SMSN@G NPs with NIR irradiation (200 pm, 808 nm, 1 W cm−2, 15 min), and SMSN@G NPs with NIR irradiation (200 pm, 808 nm, 1 W cm−2, 30 min). (c) Histogram of apoptosis rate of SW1990 and PANC1 cells intervened by different treatments. Annexin V+/PI+ was defined as late apoptosis or necrosis, while Annexin V+/PI−was defined as early apoptosis. NS: No statistical difference; *p < 0.05, ****p < 0.0001, analyzed using student’s t-test.

Article Snippet: PANC1 and SW1990 human pancreatic cancer cell lines were obtained from the American Type Culture Collection (ATCC, USA).

Techniques: Functional Assay, In Vitro, Flow Cytometry, Irradiation

Figure 5. Evaluation of BCL2, BID, p21, NF-κB p65 total lysate, NF-κB p65 nuclear fraction, GAPDH (as internal control) in SW1990 (5a) and PANC1 (5b) cells in the SMSN without irradiation group, SMSN@G NPs without irradiation group, SMSN@G NPs with irradiation for 15 min group, and SMSN@G NPs with irradiation for 30 min group. The histogram illustrates the relative expression levels of apoptosis- related proteins in SW1990 and PANC1 cells under various treatment conditions. *compared with SMSN without irradiation group, #compared with SMSN@G NPs without irradiation group. NS: No statistical difference, **p < 0.01, ***p < 0.001, ****p < 0.0001, ###p < 0.001, ####p < 0.0001, analyzed using student’s t-test.

Journal: Nanotechnology

Article Title: Novel silicene-mesoporous silica nanoparticles conjugated gemcitabine induced cellular apoptosis via upregulating NF- κ B p65 nuclear translocation suppresses pancreatic cancer growth in vitro and in vivo .

doi: 10.1088/1361-6528/ad312a

Figure Lengend Snippet: Figure 5. Evaluation of BCL2, BID, p21, NF-κB p65 total lysate, NF-κB p65 nuclear fraction, GAPDH (as internal control) in SW1990 (5a) and PANC1 (5b) cells in the SMSN without irradiation group, SMSN@G NPs without irradiation group, SMSN@G NPs with irradiation for 15 min group, and SMSN@G NPs with irradiation for 30 min group. The histogram illustrates the relative expression levels of apoptosis- related proteins in SW1990 and PANC1 cells under various treatment conditions. *compared with SMSN without irradiation group, #compared with SMSN@G NPs without irradiation group. NS: No statistical difference, **p < 0.01, ***p < 0.001, ****p < 0.0001, ###p < 0.001, ####p < 0.0001, analyzed using student’s t-test.

Article Snippet: PANC1 and SW1990 human pancreatic cancer cell lines were obtained from the American Type Culture Collection (ATCC, USA).

Techniques: Control, Irradiation, Expressing

Figure 6. (a) A schematic depiction of murine xenograft establishment and intervention. (b) Thermal images captured during 808 nm laser irradiation (1.5 W m−2) of SW1990 xenograft in various groups. (c) Relative tumor volume (V/V0) was observed in the various treatment groups, V: the tumor volume at each time point, V0: the tumor volume on the first day of treatment. (d) Body weight measurements of SW1990 xenograft in each group. (e) Representative photographs showcasing SW1990 xenograft subjected to different treatments.

Journal: Nanotechnology

Article Title: Novel silicene-mesoporous silica nanoparticles conjugated gemcitabine induced cellular apoptosis via upregulating NF- κ B p65 nuclear translocation suppresses pancreatic cancer growth in vitro and in vivo .

doi: 10.1088/1361-6528/ad312a

Figure Lengend Snippet: Figure 6. (a) A schematic depiction of murine xenograft establishment and intervention. (b) Thermal images captured during 808 nm laser irradiation (1.5 W m−2) of SW1990 xenograft in various groups. (c) Relative tumor volume (V/V0) was observed in the various treatment groups, V: the tumor volume at each time point, V0: the tumor volume on the first day of treatment. (d) Body weight measurements of SW1990 xenograft in each group. (e) Representative photographs showcasing SW1990 xenograft subjected to different treatments.

Article Snippet: PANC1 and SW1990 human pancreatic cancer cell lines were obtained from the American Type Culture Collection (ATCC, USA).

Techniques: Irradiation

Figure 2. EBF2 is downregulated in PDAC tissues and inhibits cell proliferation and metastasis. A) H&E and IHC staining of EBF2 protein in PDAC and adjacent normal tissues. Scale bar, 10 μm. B) H scores of EBF2 in PDAC and adjacent normal tissues. C–E) Correlations of EBF2 expression with tumor stage (C), lymph node metastasis (D), and distal metastasis (E) in PDAC patients. Data in B–E are presented as mean ± SEM, *p < 0.05, **p < 0.01 by Student’s t-test. F) Kaplan–Meier plot of overall survival in 90 patients with PDAC, stratified by EBF2 expression (Log-rank test, p < 0.0001). G, H) The mRNA (G) and protein (H) levels of EBF2 in SW1990 cells treated with EBF2 shRNAs (EBF2-KD) or negative control (SCR) verified by qPCR and Western

Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

Article Title: EBF2 Links KMT2D-Mediated H3K4me1 to Suppress Pancreatic Cancer Progression via Upregulating KLLN.

doi: 10.1002/advs.202302037

Figure Lengend Snippet: Figure 2. EBF2 is downregulated in PDAC tissues and inhibits cell proliferation and metastasis. A) H&E and IHC staining of EBF2 protein in PDAC and adjacent normal tissues. Scale bar, 10 μm. B) H scores of EBF2 in PDAC and adjacent normal tissues. C–E) Correlations of EBF2 expression with tumor stage (C), lymph node metastasis (D), and distal metastasis (E) in PDAC patients. Data in B–E are presented as mean ± SEM, *p < 0.05, **p < 0.01 by Student’s t-test. F) Kaplan–Meier plot of overall survival in 90 patients with PDAC, stratified by EBF2 expression (Log-rank test, p < 0.0001). G, H) The mRNA (G) and protein (H) levels of EBF2 in SW1990 cells treated with EBF2 shRNAs (EBF2-KD) or negative control (SCR) verified by qPCR and Western

Article Snippet: Cell Culture: Human pancreatic cancer cell lines SW1990 and PANC-1 were purchased from the American Type Culture Collection (ATCC, USA), and cultured in Dulbecco’s modified Eagle’s medium (DMEM; Gibco, USA) or Roswell Park Memorial Institute 1640 medium (RPMI-1640; Gibco) supplemented with 10% fetal calf serum (FCS; Wisent, Canada) and penicillin-streptomycin solution (100 μg mL−1; Beyotime, China) in a humidified chamber with 5% CO2 at 37 °C.

Techniques: Immunohistochemistry, Expressing, Negative Control, Western Blot

Figure 4. KLLN is a common transcriptional target of KMT2D and EBF2 in PDAC cells. A) Heatmaps from RNA-seq data showing overlapping of differentially expressed genes (DEGs) of SW1990-luc cells with EBF2 overexpression (EBF2-OE) or H3K4me1 activation by GSK-LSD1. B) Gene Set Enrichment Analysis (GSEA) reveals that the DEGs are enriched in genes regulated by p53. C, D) The mRNA (C) and protein (D) levels of EBF2 and KLLN in negative control (Vector) and EBF2 overexpressed (EBF2-OE) SW1990 cells verified by qPCR and Western blot analysis. Data in C are presented as mean ± SEM, **p < 0.01 by Student’s t-test. E,F) The mRNA (E) and protein (F) levels of KLLN in negative control (Vector) and GSK-LSD1-treated SW1990 cells verified by qPCR and Western blot analysis. Data in E are presented as mean ± SEM, **p < 0.01 by Student’s t-test. G) H&E and IHC staining of KLLN protein in PDAC and adjacent normal tissues. Scale bar, 10 μm. H) H score of KLLN in PDAC and tumor adjacent tissues. I–K) Correlations of KLLN expression with tumor stage (I), lymph node metastasis (J), and distal metastasis (K) in PDAC patients. Data in I–K are presented as mean ± SEM, **p < 0.01 by Student’s t-test. L) Kaplan–Meier plot of overall survival of 90 patients with PDAC, stratified by KLLN expression (Log-rank test, p = 0.001). M) Spearman correlation analysis of KMT2D and KLLN levels in PDAC tissues (n = 90, r = 0.6838, p < 0.0001). N) Spearman correlation analysis of EBF2 and KLLN levels in PDAC tissues (n = 90, r = 0.7541, p < 0.0001). O) Western blot analysis of KLLN and H3K4me1 levels in SCR, KMT2D-KD, or EBF2-KD xenografts. P) H&E and IHC staining of KLLN and Ki67 in SCR, KMT2D-KD, or EBF2-KD xenografts. Scale bar, 20 μm.

Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

Article Title: EBF2 Links KMT2D-Mediated H3K4me1 to Suppress Pancreatic Cancer Progression via Upregulating KLLN.

doi: 10.1002/advs.202302037

Figure Lengend Snippet: Figure 4. KLLN is a common transcriptional target of KMT2D and EBF2 in PDAC cells. A) Heatmaps from RNA-seq data showing overlapping of differentially expressed genes (DEGs) of SW1990-luc cells with EBF2 overexpression (EBF2-OE) or H3K4me1 activation by GSK-LSD1. B) Gene Set Enrichment Analysis (GSEA) reveals that the DEGs are enriched in genes regulated by p53. C, D) The mRNA (C) and protein (D) levels of EBF2 and KLLN in negative control (Vector) and EBF2 overexpressed (EBF2-OE) SW1990 cells verified by qPCR and Western blot analysis. Data in C are presented as mean ± SEM, **p < 0.01 by Student’s t-test. E,F) The mRNA (E) and protein (F) levels of KLLN in negative control (Vector) and GSK-LSD1-treated SW1990 cells verified by qPCR and Western blot analysis. Data in E are presented as mean ± SEM, **p < 0.01 by Student’s t-test. G) H&E and IHC staining of KLLN protein in PDAC and adjacent normal tissues. Scale bar, 10 μm. H) H score of KLLN in PDAC and tumor adjacent tissues. I–K) Correlations of KLLN expression with tumor stage (I), lymph node metastasis (J), and distal metastasis (K) in PDAC patients. Data in I–K are presented as mean ± SEM, **p < 0.01 by Student’s t-test. L) Kaplan–Meier plot of overall survival of 90 patients with PDAC, stratified by KLLN expression (Log-rank test, p = 0.001). M) Spearman correlation analysis of KMT2D and KLLN levels in PDAC tissues (n = 90, r = 0.6838, p < 0.0001). N) Spearman correlation analysis of EBF2 and KLLN levels in PDAC tissues (n = 90, r = 0.7541, p < 0.0001). O) Western blot analysis of KLLN and H3K4me1 levels in SCR, KMT2D-KD, or EBF2-KD xenografts. P) H&E and IHC staining of KLLN and Ki67 in SCR, KMT2D-KD, or EBF2-KD xenografts. Scale bar, 20 μm.

Article Snippet: Cell Culture: Human pancreatic cancer cell lines SW1990 and PANC-1 were purchased from the American Type Culture Collection (ATCC, USA), and cultured in Dulbecco’s modified Eagle’s medium (DMEM; Gibco, USA) or Roswell Park Memorial Institute 1640 medium (RPMI-1640; Gibco) supplemented with 10% fetal calf serum (FCS; Wisent, Canada) and penicillin-streptomycin solution (100 μg mL−1; Beyotime, China) in a humidified chamber with 5% CO2 at 37 °C.

Techniques: RNA Sequencing, Over Expression, Activation Assay, Negative Control, Plasmid Preparation, Western Blot, Immunohistochemistry, Expressing

Figure 5. GSK-LSD1 inhibits the proliferation, migration, and invasion of PDAC cells. A) Diagram of flag-tagged KMT2D-C, KMT2Dfusion and mKMT2Dfusion plasmid models. B) Western blot analysis of KLLN and H3K4me1 levels in SW1990 cells transfected with KMT2D-C, KMT2Dfusion, and mKMT2Dfusion. C, D) Colony-formation (C) and Transwell (D) assays of SW1990 cells transfected with KMT2D-C, KMT2Dfusion, and mKMT2Dfusion. Data in C and D are presented as mean ± SEM, **p < 0.01 by one-way ANOVA test. E) Western blot analysis of H3K4me1 and KLLN levels in SW1990 cells treated with 0, 1, 10, or 100 μm GSK-LSD1. F–H) Colony-formation (F), CCK-8 (G), and Transwell (H) assays of SW1990 cells treated with Vehicle

Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

Article Title: EBF2 Links KMT2D-Mediated H3K4me1 to Suppress Pancreatic Cancer Progression via Upregulating KLLN.

doi: 10.1002/advs.202302037

Figure Lengend Snippet: Figure 5. GSK-LSD1 inhibits the proliferation, migration, and invasion of PDAC cells. A) Diagram of flag-tagged KMT2D-C, KMT2Dfusion and mKMT2Dfusion plasmid models. B) Western blot analysis of KLLN and H3K4me1 levels in SW1990 cells transfected with KMT2D-C, KMT2Dfusion, and mKMT2Dfusion. C, D) Colony-formation (C) and Transwell (D) assays of SW1990 cells transfected with KMT2D-C, KMT2Dfusion, and mKMT2Dfusion. Data in C and D are presented as mean ± SEM, **p < 0.01 by one-way ANOVA test. E) Western blot analysis of H3K4me1 and KLLN levels in SW1990 cells treated with 0, 1, 10, or 100 μm GSK-LSD1. F–H) Colony-formation (F), CCK-8 (G), and Transwell (H) assays of SW1990 cells treated with Vehicle

Article Snippet: Cell Culture: Human pancreatic cancer cell lines SW1990 and PANC-1 were purchased from the American Type Culture Collection (ATCC, USA), and cultured in Dulbecco’s modified Eagle’s medium (DMEM; Gibco, USA) or Roswell Park Memorial Institute 1640 medium (RPMI-1640; Gibco) supplemented with 10% fetal calf serum (FCS; Wisent, Canada) and penicillin-streptomycin solution (100 μg mL−1; Beyotime, China) in a humidified chamber with 5% CO2 at 37 °C.

Techniques: Migration, Plasmid Preparation, Western Blot, Transfection, CCK-8 Assay

Figure 6. KMT2D and EBF2 cooperate to regulate the expression of KLLN. A) Western blot of KLLN and H3K4me1 in SW1990 cells transfected with KMT2D-C, KMT2Dfusion, or EBF2. B) Western blot of KLLN and H3K4me1 in SW1990 cells transfected with mKMT2Dfusion, KMT2Dfusion or EBF2. C) Western blot of KLLN and H3K4me1 in SW1990 cells transfected with KMT2D-C, KMT2Dfusion or EBF2-KD. D) Western blot of KLLN and H3K4me1 in SW1990 cells transfected with mKMT2Dfusion, KMT2Dfusion, or EBF2-KD. 𝛽-actin and H3 were used as loading control. E–G) Colony-formation (E), migration (F), and invasion (G) of SW1990 cells treated with KMT2D-C, KMT2Dfusion, mKMT2Dfusion, EBF2, KMT2Dfusion+EBF2, mKMT2Dfusion+EBF2. H,I) Colony-formation assays (H) and Transwell (I) assays of SW1990 cells transfected with control (NC), KMT2D-KD or KMT2D-KD + KLLN. J-K) Colony- formation assays (J) and Transwell (K) assays of SW1990 cells transfected with control (NC), EBF2-KD or EBF2-KD+KLLN. Scale bar,100 μm. Data in E–K are presented as mean ± SEM, **p < 0.01 by one-way ANOVA test.

Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

Article Title: EBF2 Links KMT2D-Mediated H3K4me1 to Suppress Pancreatic Cancer Progression via Upregulating KLLN.

doi: 10.1002/advs.202302037

Figure Lengend Snippet: Figure 6. KMT2D and EBF2 cooperate to regulate the expression of KLLN. A) Western blot of KLLN and H3K4me1 in SW1990 cells transfected with KMT2D-C, KMT2Dfusion, or EBF2. B) Western blot of KLLN and H3K4me1 in SW1990 cells transfected with mKMT2Dfusion, KMT2Dfusion or EBF2. C) Western blot of KLLN and H3K4me1 in SW1990 cells transfected with KMT2D-C, KMT2Dfusion or EBF2-KD. D) Western blot of KLLN and H3K4me1 in SW1990 cells transfected with mKMT2Dfusion, KMT2Dfusion, or EBF2-KD. 𝛽-actin and H3 were used as loading control. E–G) Colony-formation (E), migration (F), and invasion (G) of SW1990 cells treated with KMT2D-C, KMT2Dfusion, mKMT2Dfusion, EBF2, KMT2Dfusion+EBF2, mKMT2Dfusion+EBF2. H,I) Colony-formation assays (H) and Transwell (I) assays of SW1990 cells transfected with control (NC), KMT2D-KD or KMT2D-KD + KLLN. J-K) Colony- formation assays (J) and Transwell (K) assays of SW1990 cells transfected with control (NC), EBF2-KD or EBF2-KD+KLLN. Scale bar,100 μm. Data in E–K are presented as mean ± SEM, **p < 0.01 by one-way ANOVA test.

Article Snippet: Cell Culture: Human pancreatic cancer cell lines SW1990 and PANC-1 were purchased from the American Type Culture Collection (ATCC, USA), and cultured in Dulbecco’s modified Eagle’s medium (DMEM; Gibco, USA) or Roswell Park Memorial Institute 1640 medium (RPMI-1640; Gibco) supplemented with 10% fetal calf serum (FCS; Wisent, Canada) and penicillin-streptomycin solution (100 μg mL−1; Beyotime, China) in a humidified chamber with 5% CO2 at 37 °C.

Techniques: Expressing, Western Blot, Transfection, Control, Migration