pl45 human pdac cell lines  (ATCC)

Journal: Cell Communication and Signaling : CCS

Article Title: Transcriptional deregulation by FOXM1–JUP signaling confers dual oncogenic drivers for pancreatic tumorigenesis and therapeutic resistance

doi: 10.1186/s12964-025-02512-5

Figure Lengend Snippet: JUP is highly expressed in PDAC and precancerous lesions. A The expression of JUP in normal and PDAC tissues were detected by IHC and IFS. Compared with normal tissues, JUP was highly expressed in PDAC tissues (n=25). B IFS of JUP in mouse pancreatic tissue samples ( n =6). Orange, JUP; green, CK-19; purple, Amylase; blue, DAPI. JUP co-localized mainly with CK-19, and increased in ADM, PanIN and PDAC. C Quantitative and statistical analyses of IHC and IFS results in human pancreatic tissues. D Quantitative and statistical analyses of relative expression levels of JUP, CK-19 and Amylase in mouse pancreatic tissues. All data were expressed as mean ± SD. Statistical analysis: student t-test or ANOVA, * P < 0.05, ** P < 0.01 and *** P < 0.001 vs. control group. Scale bars, 100 μm

Article Snippet: HPNE and HPDE human normal ductal epithelial cell lines, AsPC-1, BxPC-3, CaPan-2, CFPAC-1, HPAC, HPAF-II, MIA PaCa-2, PANC-1 and PL45 human PDAC cell lines, and Panc02 murine PDAC cell line were originally purchased from the American Type Culture Collection (ATCC, Virgin Islands, USA).

Techniques: Expressing, Control

Journal: Cell Communication and Signaling : CCS

Article Title: Transcriptional deregulation by FOXM1–JUP signaling confers dual oncogenic drivers for pancreatic tumorigenesis and therapeutic resistance

doi: 10.1186/s12964-025-02512-5

Figure Lengend Snippet: JUP is essential for the growth of PDAC cells. Proliferative capacity of AsPC-1, PL45 and Panc02 cells with JUP knockdown or overexpression. A , CCK-8 assay: JUP knockdown suppressed PDAC cell proliferation ( A 1), overexpression of JUP promoted PDAC cell proliferation ( A 2). B , Clonogenic assay: siJUP suppressed the colony formation ( B 1). pJUP promoted the colony formation. ( B 2). C , EdU assay: JUP silence suppressed EdU incorporation ( C 1), JUP overexpression enhanced EdU incorporation ( C 2). All data were expressed as mean ± SD, n = 3. Statistical analysis: student t-test or ANOVA, * P < 0.05, ** P < 0.01 and *** P < 0.001 vs. control group

Article Snippet: HPNE and HPDE human normal ductal epithelial cell lines, AsPC-1, BxPC-3, CaPan-2, CFPAC-1, HPAC, HPAF-II, MIA PaCa-2, PANC-1 and PL45 human PDAC cell lines, and Panc02 murine PDAC cell line were originally purchased from the American Type Culture Collection (ATCC, Virgin Islands, USA).

Techniques: Knockdown, Over Expression, CCK-8 Assay, Clonogenic Assay, EdU Assay, Control

Journal: Cell Communication and Signaling : CCS

Article Title: Transcriptional deregulation by FOXM1–JUP signaling confers dual oncogenic drivers for pancreatic tumorigenesis and therapeutic resistance

doi: 10.1186/s12964-025-02512-5

Figure Lengend Snippet: JUP enhances the migration and invasion of PDAC cells. Scratch and transwell assays of PDAC cells with JUP knockdown ( A ) or overexpression ( B ). Silencing JUP attenuated the invasion and migration ability of PDAC cells, whereas overexpression of JUP enhanced the invasion and migration ability of PDAC cells. ( C , D ) Representative HE staining and CA199 staining of liver tissues. JUP promoted the formation of liver metastasis in mice. All data are expressed as mean ± SD, n = 4. Statistical analysis: student t-test or ANOVA, * P < 0.05, ** P < 0.01 and *** P < 0.001 vs. control group

Article Snippet: HPNE and HPDE human normal ductal epithelial cell lines, AsPC-1, BxPC-3, CaPan-2, CFPAC-1, HPAC, HPAF-II, MIA PaCa-2, PANC-1 and PL45 human PDAC cell lines, and Panc02 murine PDAC cell line were originally purchased from the American Type Culture Collection (ATCC, Virgin Islands, USA).

Techniques: Migration, Knockdown, Over Expression, Staining, Control

Journal: Cell Communication and Signaling : CCS

Article Title: Transcriptional deregulation by FOXM1–JUP signaling confers dual oncogenic drivers for pancreatic tumorigenesis and therapeutic resistance

doi: 10.1186/s12964-025-02512-5

Figure Lengend Snippet: FOXM1 transcriptionally regulates JUP in PDAC. A , IHC: Levels of JUP and FOXM1 protein expression in PDAC ( A1 ). Linear regression analysis: the correlation of FOXM1 and JUP ( n = 16) ( A2 ). Correlation analysis of FOXM1 and JUP expression in PDAC ( http://gepia.cancer-pku.cn/ ) ( n = 329) ( A3 ). B-C , Expression of FOXM1 was altered by transfection with siRNA or expression vectors. The impact of FOXM1 on JUP expression in PDAC cells by WB ( B ) and RT-qPCR ( C ) analyses. Note that FOXM1 inhibited the expression of JUP mRNA and protein in AsPC-1 and PL45, while the overexpression of FOXM1 increased the JUP mRNA and protein in AsPC-1 and PL45. FOXM1 regulated the expression of both JUP protein and mRNA. D , Direct binding of JUP to FOXM1 promoter. Sequences and positions of putative FOXM1-binding elements on JUP promoter (#1 and #2) ( D1 ). Normal IgG was used as a control, and 1.5% of the total cell lysates was subjected to PCR before immunoprecipitation. The ChIP assay to test the direct binding of FOXM1 on the genomic locus of JUP promoter regions ( D2 ). Quantitative analysis of ChIP results ( D3 ). All data are expressed as mean ± SD, n = 3. Statistical analysis: student t-test or ANOVA, * P < 0.05, ** P < 0.01 and *** P < 0.001 vs. control group

Article Snippet: HPNE and HPDE human normal ductal epithelial cell lines, AsPC-1, BxPC-3, CaPan-2, CFPAC-1, HPAC, HPAF-II, MIA PaCa-2, PANC-1 and PL45 human PDAC cell lines, and Panc02 murine PDAC cell line were originally purchased from the American Type Culture Collection (ATCC, Virgin Islands, USA).

Techniques: Expressing, Transfection, Quantitative RT-PCR, Over Expression, Binding Assay, Control, Immunoprecipitation

Journal: Cell Communication and Signaling : CCS

Article Title: Transcriptional deregulation by FOXM1–JUP signaling confers dual oncogenic drivers for pancreatic tumorigenesis and therapeutic resistance

doi: 10.1186/s12964-025-02512-5

Figure Lengend Snippet: FOXM1-mediated cancer cell proliferation requires JUP expression. A - C , FOXM1-silenced and JUP-overexpressing PDAC cells were established. The protein levels of FOXM1 and JUP were determined by Western blot ( A1 ) and the mRNA levels by RT-qPCR ( A2 ); cell viability by CCK-8 ( B ), and colony formation assay and the number of clones by ImageJ software. Note that JUP mediated FOXM1-induced PDAC cell proliferation and colony formation ( C ). D , PDAC cells were injected subcutaneously into mice. Tumor sizes were measured weekly ( D1 ). The mice were sacrificed and the tumors were removed and weighed ( D2 , D3 ). All data were expressed as mean ± SD, n = 3. Statistical analysis: student t-test or ANOVA, * P < 0.05, ** P < 0.01 and *** P < 0.001 vs. control group

Article Snippet: HPNE and HPDE human normal ductal epithelial cell lines, AsPC-1, BxPC-3, CaPan-2, CFPAC-1, HPAC, HPAF-II, MIA PaCa-2, PANC-1 and PL45 human PDAC cell lines, and Panc02 murine PDAC cell line were originally purchased from the American Type Culture Collection (ATCC, Virgin Islands, USA).

Techniques: Expressing, Western Blot, Quantitative RT-PCR, CCK-8 Assay, Colony Assay, Clone Assay, Software, Injection, Control

Journal: Cell Communication and Signaling : CCS

Article Title: Transcriptional deregulation by FOXM1–JUP signaling confers dual oncogenic drivers for pancreatic tumorigenesis and therapeutic resistance

doi: 10.1186/s12964-025-02512-5

Figure Lengend Snippet: FOXM1-mediated therapeutic resistance requires JUP expression. AsPC-1, PL45 and Panc02 cells were either transfection with siRNA (NC or siJUP) or expression vectors (p3.1 or pJUP) to alter the expression levels of JUP. A , The cells were then treated in vitro with different concentrations of GEM and OXA for 48 h and cell viability was determined by CCK8 assay. Note that increased expression of JUP significantly enhanced PDAC cells resistance to both GEM and OXA, whereas reduced expression of JUP did the opposite. B , GEM/OXA in vivo treatment model scheme. C , D , The cells with altered expression of JUP were subcutaneously injected into groups of mice, which then received treatment of drugs ( C , GEM; D , OXA) for indicated times. The tumor growth curves ( C1 , D1 ), subcutaneous tumors from mice ( C2 , D2 ) and tumor weights ( C3 , D3 ) were shown. Note that increased JUP expression significantly reduced the therapeutic efficacy of both GEM and OXA. All data were expressed as mean ± SD, n = 5. Statistical analysis: student t-test or ANOVA, * P < 0.05, ** P < 0.01 and *** P < 0.001 vs. control group

Article Snippet: HPNE and HPDE human normal ductal epithelial cell lines, AsPC-1, BxPC-3, CaPan-2, CFPAC-1, HPAC, HPAF-II, MIA PaCa-2, PANC-1 and PL45 human PDAC cell lines, and Panc02 murine PDAC cell line were originally purchased from the American Type Culture Collection (ATCC, Virgin Islands, USA).

Techniques: Expressing, Transfection, In Vitro, CCK-8 Assay, In Vivo, Injection, Drug discovery, Control

Journal: Molecular Medicine Reports

Article Title: Downregulation of LINC01638 lncRNA inhibits migration and invasion of pancreatic ductal adenocarcinoma cells by reducing TGF-β signaling

doi: 10.3892/mmr.2019.10699

Figure Lengend Snippet: LINC01638 is significantly upregulated in tumor tissues than in adjacent healthy tissues in the majority of patients with PDAC (*P<0.05 tumor vs. healthy tissue). PDAC, pancreatic ductal adenocarcinoma.

Article Snippet: Human PDAC cell line PL45 (ATCC ® CRL-2558TM) and normal pancreas duct cell line hTERT-HPNE (ATCC ® CRL-4023TM) were purchased from the American Type Culture Collection (Manassas, VA, USA).

Techniques:

Journal: Molecular Medicine Reports

Article Title: Downregulation of LINC01638 lncRNA inhibits migration and invasion of pancreatic ductal adenocarcinoma cells by reducing TGF-β signaling

doi: 10.3892/mmr.2019.10699

Figure Lengend Snippet: Upregulation of plasma LINC01638 can distinguish patients with PDAC from healthy controls. (A) Plasma levels of LINC01638 were significantly higher in PDAC patients than in healthy controls and (B) upregulation of plasma LINC01638 distinguished PDAC patients from healthy controls in receiver operating characteristic (*P<0.05). PDAC, pancreatic ductal adenocarcinoma.

Article Snippet: Human PDAC cell line PL45 (ATCC ® CRL-2558TM) and normal pancreas duct cell line hTERT-HPNE (ATCC ® CRL-4023TM) were purchased from the American Type Culture Collection (Manassas, VA, USA).

Techniques: Clinical Proteomics

Journal: Molecular Medicine Reports

Article Title: Downregulation of LINC01638 lncRNA inhibits migration and invasion of pancreatic ductal adenocarcinoma cells by reducing TGF-β signaling

doi: 10.3892/mmr.2019.10699

Figure Lengend Snippet: Plasma levels of LINC01638 and TGF-β1 are positively correlated in patients with PDAC, and not in healthy controls. Pearson correlation analysis revealed a significant positive correlation between plasma levels of LINC01638 and TGF-β1 in (A) patients with PDAC and (B) healthy controls. PDAC, pancreatic ductal adenocarcinoma; TGF-β1, transforming growth factor-β1.

Article Snippet: Human PDAC cell line PL45 (ATCC ® CRL-2558TM) and normal pancreas duct cell line hTERT-HPNE (ATCC ® CRL-4023TM) were purchased from the American Type Culture Collection (Manassas, VA, USA).

Techniques: Clinical Proteomics

Journal: Molecular Medicine Reports

Article Title: Downregulation of LINC01638 lncRNA inhibits migration and invasion of pancreatic ductal adenocarcinoma cells by reducing TGF-β signaling

doi: 10.3892/mmr.2019.10699

Figure Lengend Snippet: LINC01638 regulates TGF-β1 expression in PDAC cells. (A) LINC01638 overexpression upregulated, (B) while LINC01638 shRNA downregulated the expression of TGF-β1 in cells of PDAC cell line, PL45, but not in the normal pancreas duct cell line hTERT-HPNE (*P<0.05). PDAC, pancreatic ductal adenocarcinoma; C, untransfected; NC, negative control (empty vector or NC shRNA transfection); TGF-β1, transforming growth factor-β1; shRNA, short hairpin RNA.

Article Snippet: Human PDAC cell line PL45 (ATCC ® CRL-2558TM) and normal pancreas duct cell line hTERT-HPNE (ATCC ® CRL-4023TM) were purchased from the American Type Culture Collection (Manassas, VA, USA).

Techniques: Expressing, Over Expression, shRNA, Negative Control, Plasmid Preparation, Transfection

Journal: Molecular Medicine Reports

Article Title: Downregulation of LINC01638 lncRNA inhibits migration and invasion of pancreatic ductal adenocarcinoma cells by reducing TGF-β signaling

doi: 10.3892/mmr.2019.10699

Figure Lengend Snippet: LINC01638 regulated PDAC cell migration and invasion through TGF-β1. Effects of LINC01638 overexpression, shRNA silencing and exogenous TGF-β1 treatment on (A) migration and (B) invasion of PL45 human PDAC cell line and hTERT-HPNE normal pancreas duct cell line. *P<0.05. Magnification, ×40. PDAC, pancreatic ductal adenocarcinoma; C, untransfected; NC, negative control (empty vector transfection); shRNA, short hairpin RNA; TGF-β1, transforming growth factor-β1.

Article Snippet: Human PDAC cell line PL45 (ATCC ® CRL-2558TM) and normal pancreas duct cell line hTERT-HPNE (ATCC ® CRL-4023TM) were purchased from the American Type Culture Collection (Manassas, VA, USA).

Techniques: Migration, Over Expression, shRNA, Negative Control, Plasmid Preparation, Transfection