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human pdac cell line capan  (ATCC)


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    ATCC human pdac cell line capan
    A Experimental procedure of the GEM-treated PDX <t>PDAC</t> model. B Immunoblotting assay to detect the expression of cyclin and cyclin-dependent kinases (Cyclin D1, Cyclin E, CDK2, CDK4) at the G1/S cell cycle checkpoint and cancer stem cell master genes (CD133, OCT4, NANOG, and Sox2) in tissues from the 3-generation PDX mice that treated with saline or gemcitabine. C Heatmap shows differentially expressed lncRNAs in GEM-treated and control PDX mice. D Comparison of expression of lncRNAs in tumor tissues from 36 PDAC patients with paired paracancerous tissues. E Correlation analysis of LINC01134 with cyclin and cyclin-dependent kinases and cancer stem cell master genes as described in ( B ). F Comparison of the expression of LINC01134 in tumor tissues and paired paraneoplastic tissues from 70 PDAC patients. G Kaplan–Meier analysis of the correlation between expression levels of LINC01134 and PDAC prognosis in 57 patients. Data are expressed as mean ± SD * p < 0.05, ** p < 0.01.
    Human Pdac Cell Line Capan, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1696 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+pdac+tissue+array/Capan-1/pmc10620239-229-8-21
    Average 97 stars, based on 1696 article reviews
    human pdac cell line capan - by Bioz Stars, 2026-10
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    Images

    1) Product Images from "FTO-mediated LINC01134 stabilization to promote chemoresistance through miR-140-3p/WNT5A/WNT pathway in PDAC"

    Article Title: FTO-mediated LINC01134 stabilization to promote chemoresistance through miR-140-3p/WNT5A/WNT pathway in PDAC

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-023-06244-7

    A Experimental procedure of the GEM-treated PDX PDAC model. B Immunoblotting assay to detect the expression of cyclin and cyclin-dependent kinases (Cyclin D1, Cyclin E, CDK2, CDK4) at the G1/S cell cycle checkpoint and cancer stem cell master genes (CD133, OCT4, NANOG, and Sox2) in tissues from the 3-generation PDX mice that treated with saline or gemcitabine. C Heatmap shows differentially expressed lncRNAs in GEM-treated and control PDX mice. D Comparison of expression of lncRNAs in tumor tissues from 36 PDAC patients with paired paracancerous tissues. E Correlation analysis of LINC01134 with cyclin and cyclin-dependent kinases and cancer stem cell master genes as described in ( B ). F Comparison of the expression of LINC01134 in tumor tissues and paired paraneoplastic tissues from 70 PDAC patients. G Kaplan–Meier analysis of the correlation between expression levels of LINC01134 and PDAC prognosis in 57 patients. Data are expressed as mean ± SD * p < 0.05, ** p < 0.01.
    Figure Legend Snippet: A Experimental procedure of the GEM-treated PDX PDAC model. B Immunoblotting assay to detect the expression of cyclin and cyclin-dependent kinases (Cyclin D1, Cyclin E, CDK2, CDK4) at the G1/S cell cycle checkpoint and cancer stem cell master genes (CD133, OCT4, NANOG, and Sox2) in tissues from the 3-generation PDX mice that treated with saline or gemcitabine. C Heatmap shows differentially expressed lncRNAs in GEM-treated and control PDX mice. D Comparison of expression of lncRNAs in tumor tissues from 36 PDAC patients with paired paracancerous tissues. E Correlation analysis of LINC01134 with cyclin and cyclin-dependent kinases and cancer stem cell master genes as described in ( B ). F Comparison of the expression of LINC01134 in tumor tissues and paired paraneoplastic tissues from 70 PDAC patients. G Kaplan–Meier analysis of the correlation between expression levels of LINC01134 and PDAC prognosis in 57 patients. Data are expressed as mean ± SD * p < 0.05, ** p < 0.01.

    Techniques Used: Western Blot, Expressing, Saline, Control, Comparison

    A Statistical analysis of the primary and secondary sphere formation ability of PDAC cells, and representative images show secondary sphere formation in these cells. B Western blot was performed to detect the effects of silencing or overexpression of LINC01134 on the expression of the stemness-related genes. C qRT-PCR detects the effect of silencing or overexpression of LINC01134 on the expression of the stemness-related genes. D Effects of silencing LINC01134 on transplanted tumors in nude mice. Data are expressed as mean, * p < 0.05, ** p < 0.01.
    Figure Legend Snippet: A Statistical analysis of the primary and secondary sphere formation ability of PDAC cells, and representative images show secondary sphere formation in these cells. B Western blot was performed to detect the effects of silencing or overexpression of LINC01134 on the expression of the stemness-related genes. C qRT-PCR detects the effect of silencing or overexpression of LINC01134 on the expression of the stemness-related genes. D Effects of silencing LINC01134 on transplanted tumors in nude mice. Data are expressed as mean, * p < 0.05, ** p < 0.01.

    Techniques Used: Western Blot, Over Expression, Expressing, Quantitative RT-PCR

    A Colony formation assay of cells containing silenced or overexpressed LINC01134 after GEM treatment. B Effects of different concentrations of GEM on the viability of PDAC cells. C Expression of Ki67 in xenograft tumors formed from PDAC cells transfected with Ctrl or shLINC01134 in GEM-treated nude mice. D Typical images of xenograft tumors formed from PDAC cells transfected with Ctrl or shLINC01134 in GEM-treated nude mice. Tumor growth curves of PDAC cells transfected with Ctrl or shLINC01134 in GEM-treated nude mice. E Expression of cyclin and cyclin-dependent kinases and and cancer stem cell master genes in xenograft tumor tissues formed from PDAC cells that transfected with Ctrl or shLINC01134 in GEM-treated nude mice. Data are expressed as mean, * p < 0.05, ** p < 0.01.
    Figure Legend Snippet: A Colony formation assay of cells containing silenced or overexpressed LINC01134 after GEM treatment. B Effects of different concentrations of GEM on the viability of PDAC cells. C Expression of Ki67 in xenograft tumors formed from PDAC cells transfected with Ctrl or shLINC01134 in GEM-treated nude mice. D Typical images of xenograft tumors formed from PDAC cells transfected with Ctrl or shLINC01134 in GEM-treated nude mice. Tumor growth curves of PDAC cells transfected with Ctrl or shLINC01134 in GEM-treated nude mice. E Expression of cyclin and cyclin-dependent kinases and and cancer stem cell master genes in xenograft tumor tissues formed from PDAC cells that transfected with Ctrl or shLINC01134 in GEM-treated nude mice. Data are expressed as mean, * p < 0.05, ** p < 0.01.

    Techniques Used: Colony Assay, Expressing, Transfection

    A FISH assay detects the localization of LINC01134 in PDAC cells. B qRT-PCR detects the distribution of LINC01134 in nuclear and cytoplasm in PDAC cells. C Wayne diagram shows microRNAs predicted by the bioinformatics databases Encyclopedia of RNA Interactomes and lncRNASNP2 to target bind to LINC01134. D RNA pull-down analysis shows that miR-140-3p was highly enriched in LINC01134 precipitates. E Correlation analysis shows a significant negative correlation between LINC01134 and miR-140-3p in PDAC. F Dual-luciferase reporter assay detects the relative activity of luciferase in transfected PDAC cells. G RIP assay detects the relative enrichment of LINC01134 and miR-140-3p in anti-IgG or anti-AGO2 specific immunoprecipitates. H RNA pull-down assay was used to detect the inter-relationship between LINC01134, miR-140-3p, and AGO2. I Effects of silencing or overexpression of LINC01134 on the expression of miR-140-3p. Data are expressed as mean, * p < 0.05, ** p < 0.01.
    Figure Legend Snippet: A FISH assay detects the localization of LINC01134 in PDAC cells. B qRT-PCR detects the distribution of LINC01134 in nuclear and cytoplasm in PDAC cells. C Wayne diagram shows microRNAs predicted by the bioinformatics databases Encyclopedia of RNA Interactomes and lncRNASNP2 to target bind to LINC01134. D RNA pull-down analysis shows that miR-140-3p was highly enriched in LINC01134 precipitates. E Correlation analysis shows a significant negative correlation between LINC01134 and miR-140-3p in PDAC. F Dual-luciferase reporter assay detects the relative activity of luciferase in transfected PDAC cells. G RIP assay detects the relative enrichment of LINC01134 and miR-140-3p in anti-IgG or anti-AGO2 specific immunoprecipitates. H RNA pull-down assay was used to detect the inter-relationship between LINC01134, miR-140-3p, and AGO2. I Effects of silencing or overexpression of LINC01134 on the expression of miR-140-3p. Data are expressed as mean, * p < 0.05, ** p < 0.01.

    Techniques Used: Quantitative RT-PCR, Luciferase, Reporter Assay, Activity Assay, Transfection, Pull Down Assay, Over Expression, Expressing

    A Heatmap and volcano map showing differentially expressed genes in PDAC after the overexpression of miR-140-3p. B KEGG pathway analysis of the major pathways associated with differentially expressed genes. C Correlation analysis shows that miR-140-3p was negatively correlated with WNT5A. D Dual-luciferase reporter analysis detects the relative activity of luciferase in post-transfected PDAC cells. E , F Effects of silencing or overexpression of miR-140-3p on the expression of WNT5A in PDAC cells. G Effects of co-transfection of LINC01134 and miR-140-3p on the expression of WNT5A in PDAC cells. Data are expressed as mean, * p < 0.05, ** p < 0.01.
    Figure Legend Snippet: A Heatmap and volcano map showing differentially expressed genes in PDAC after the overexpression of miR-140-3p. B KEGG pathway analysis of the major pathways associated with differentially expressed genes. C Correlation analysis shows that miR-140-3p was negatively correlated with WNT5A. D Dual-luciferase reporter analysis detects the relative activity of luciferase in post-transfected PDAC cells. E , F Effects of silencing or overexpression of miR-140-3p on the expression of WNT5A in PDAC cells. G Effects of co-transfection of LINC01134 and miR-140-3p on the expression of WNT5A in PDAC cells. Data are expressed as mean, * p < 0.05, ** p < 0.01.

    Techniques Used: Over Expression, Luciferase, Activity Assay, Transfection, Expressing, Cotransfection

    A Correlation analysis shows that the abundance of LINC01134 was positively correlated with WNT5A. B CCK-8 analysis of the effects of silencing or overexpressing LINC01134 and overexpressing or silencing WNT5A when co-transfected on the viability of PDAC cells. C Representative phase contrast images of tumorspheres formed by PDAC cells transduced with indicated constructs or a nontarget shRNA. D Statistical analysis of the primary and secondary sphere formation ability of PDAC cells as described in ( C ). E Effects of silencing or overexpression of LINC01134 and overexpression or silencing of WNT5A on the expression of the stemness-related genes when co-transfected. Data are expressed as mean, * p < 0.05, ** p < 0.01.
    Figure Legend Snippet: A Correlation analysis shows that the abundance of LINC01134 was positively correlated with WNT5A. B CCK-8 analysis of the effects of silencing or overexpressing LINC01134 and overexpressing or silencing WNT5A when co-transfected on the viability of PDAC cells. C Representative phase contrast images of tumorspheres formed by PDAC cells transduced with indicated constructs or a nontarget shRNA. D Statistical analysis of the primary and secondary sphere formation ability of PDAC cells as described in ( C ). E Effects of silencing or overexpression of LINC01134 and overexpression or silencing of WNT5A on the expression of the stemness-related genes when co-transfected. Data are expressed as mean, * p < 0.05, ** p < 0.01.

    Techniques Used: CCK-8 Assay, Transfection, Transduction, Construct, shRNA, Over Expression, Expressing

    A Silencing LINC01134 reduced the level of WNT5A and its downstream signaling activity in PDAC cells, and overexpression of LINC01134 enhanced the level of WNT5A and its downstream signaling activity in PDAC cells. B Overexpression of LINC01134 promoted the growth of transplanted tumors in PDAC nude mice and induced resistance to GEM. At the same time, the application of salinomycin effectively antagonized the pro-tumorigenic effect of LINC01134 and restored the sensitivity of transplanted tumors to GEM treatment. C IHC assays indicate the expression of Cyclin D1, Cyclin E, CDK2, CD133, Ki67, OCT4, NANOG and Sox2. Data are expressed as mean, * p < 0.05, ** p < 0.01.
    Figure Legend Snippet: A Silencing LINC01134 reduced the level of WNT5A and its downstream signaling activity in PDAC cells, and overexpression of LINC01134 enhanced the level of WNT5A and its downstream signaling activity in PDAC cells. B Overexpression of LINC01134 promoted the growth of transplanted tumors in PDAC nude mice and induced resistance to GEM. At the same time, the application of salinomycin effectively antagonized the pro-tumorigenic effect of LINC01134 and restored the sensitivity of transplanted tumors to GEM treatment. C IHC assays indicate the expression of Cyclin D1, Cyclin E, CDK2, CD133, Ki67, OCT4, NANOG and Sox2. Data are expressed as mean, * p < 0.05, ** p < 0.01.

    Techniques Used: Activity Assay, Over Expression, Expressing

    A The results of MeRIP-qPCR indicate an overall lower level of m6A in BxPC-3 and PANC-1 cells than in HPDE6-C7 cells. B Analysis of the expression of FTO in PDAC using the GEPIA database. C Correlation analysis shows that the expression of FTO was significantly and positively correlated with the abundance of LINC01134. D Effects of silencing FTO on the expression of LINC01134. E Effects of overexpression of FTO on the expression of LINC01134. F An online engine ( http://m6avar.renlab.org/ ) can be used to predict the m6A modification site of LINC01134 and the prediction was confirmed by a luciferase analysis report. G Effects of silencing or overexpression of FTO on the degree of m6A enrichment of LINC01134. H Effects of silencing or overexpression of FTO on the stability of LINC01134 in the presence of radio-luciferin D. I RIP assay confirms the binding between YTHDF2 and LINC01134. J Effects of silencing YTHDF2 on the expression of LINC01134. K Effects of silencing YTHDF2 on the stability of LINC01134 in the presence of radio-labeled D. L RIP experiments confirm the effects of silencing FTO on the expression of YTHDF2. Data are expressed as mean, * p < 0.05, ** p < 0.01.
    Figure Legend Snippet: A The results of MeRIP-qPCR indicate an overall lower level of m6A in BxPC-3 and PANC-1 cells than in HPDE6-C7 cells. B Analysis of the expression of FTO in PDAC using the GEPIA database. C Correlation analysis shows that the expression of FTO was significantly and positively correlated with the abundance of LINC01134. D Effects of silencing FTO on the expression of LINC01134. E Effects of overexpression of FTO on the expression of LINC01134. F An online engine ( http://m6avar.renlab.org/ ) can be used to predict the m6A modification site of LINC01134 and the prediction was confirmed by a luciferase analysis report. G Effects of silencing or overexpression of FTO on the degree of m6A enrichment of LINC01134. H Effects of silencing or overexpression of FTO on the stability of LINC01134 in the presence of radio-luciferin D. I RIP assay confirms the binding between YTHDF2 and LINC01134. J Effects of silencing YTHDF2 on the expression of LINC01134. K Effects of silencing YTHDF2 on the stability of LINC01134 in the presence of radio-labeled D. L RIP experiments confirm the effects of silencing FTO on the expression of YTHDF2. Data are expressed as mean, * p < 0.05, ** p < 0.01.

    Techniques Used: Expressing, Over Expression, Modification, Luciferase, Binding Assay, Labeling

    Related Articles

    Cell Culture:

    Article Title: Evaluating mesothelin as an immunotherapeutic target for endogenous T cells
    Article Snippet: A panel of human cancer cell lines, including pancreatic cancer (CFPAC-1, CAPAN-1), cervical carcinoma (MS751), colon adenocarcinoma (SK-CO-1), breast cancer (Hs578T, HCC1806), uterine adenocarcinoma (KLE), ovarian cancer (OVCAR3), prostate cancer (LNCaP), and mesothelioma (NCI-H2052, NCI-H2452, NCI-H28) were purchased from the American Type Culture Collection (ATCC, Manassas, VA). .. CFPAC-1 and CAPAN-1 cells were cultured in IMDM (Gibco, Waltham, MA); MS751 and SK-CO-1 in EMEM (ATCC); Hs578T and KLE in DMEM (HyClone Laboratories), with KLE additionally supplemented with Ham’s F-12 (Gibco); and OVCAR3, HCC1806, LNCaP, NCI-H2052, NCI-H2452, and NCI-H28 in RPMI-1640. .. All media were supplemented with 10% fetal bovine serum (FBS) (Gibco).

    other:


    Article Title: Olverembatinib, a novel BCR-ABL tyrosine kinase inhibitor, exhibits anti-tumor activity and synergizes with gemcitabine in pancreatic ductal adenocarcinoma.
    Article Snippet: Four PDAC cell lines, including PANC1, ASPC1, CAPAN1 and BXPC3, were acquired from American Type Culture Collection (ATCC, Manassas, USA) and verified through STR (shorttandem-repeat) profiling.

    Isolation:

    Article Title: Functional Rescue of CFTR-Dependent Transport in a Pancreatic Ductal Epithelial Cell Model: The Impact of Pharmacological Modulation and Inflammation
    Article Snippet: .. Human pancreatic ductal epithelial CAPAN-1 cells, originally isolated from the pancreas of a 40-year-old male with pancreatic adenocarcinoma [28,30,32], were commercially obtained from the American Type Culture Collection (ATCC, HTB-79, Manassas, VA, USA). https://doi.org/10.3390/ijms27114868 Immortalized human bronchial epithelial cells (16HBE14o−, HBE [28,29,63]) were kindly provided by the Biobank of the IRCCS Istituto Giannina Gaslini, Genova, Italy. ..



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    Image Search Results


    (A) Representative IHC staining of ITGB3 in PDAC tissue microarrays (TMA) showing varying expression levels in non-cancer and cancer tissue sections. (B). High magnification IHC images demonstrating the expression of ITGB3 on normal pancreas and cancer cells with stromal regions. (D-I) . Scatter plots depicting the correlation between ITGB3 and key tumor-associated markers such as HIF-1α (D) , GLUT-1 (E) , VEGFA (F) , Vimentin (G) , COL1A1 (H) , and PECAM1 (I) . Pearson correlation coefficients (R) and p -values indicate statistically significant positive correlation between ITGB3 and these markers. Statistical significance was assessed using a two-tailed unpaired Student’s t-test. All quantitative data represent the mean ± SEM. ∗∗∗∗p < 0.0001.

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    Article Title: ProAgio, a Novel Integrin αvβ3 Targeted Cytotoxin, Suppresses Tumor Growth and Reprograms the PDAC Microenvironment

    doi: 10.64898/2026.01.15.699725

    Figure Lengend Snippet: (A) Representative IHC staining of ITGB3 in PDAC tissue microarrays (TMA) showing varying expression levels in non-cancer and cancer tissue sections. (B). High magnification IHC images demonstrating the expression of ITGB3 on normal pancreas and cancer cells with stromal regions. (D-I) . Scatter plots depicting the correlation between ITGB3 and key tumor-associated markers such as HIF-1α (D) , GLUT-1 (E) , VEGFA (F) , Vimentin (G) , COL1A1 (H) , and PECAM1 (I) . Pearson correlation coefficients (R) and p -values indicate statistically significant positive correlation between ITGB3 and these markers. Statistical significance was assessed using a two-tailed unpaired Student’s t-test. All quantitative data represent the mean ± SEM. ∗∗∗∗p < 0.0001.

    Article Snippet: To evaluate the role of ITGB3 in PDAC, we analyzed its expression using IHC in a human PDAC tissue array (PA483-L97, Biomax) that contains 40 cancer and eight non-cancer tissues ( Supplementary Table 1 ).

    Techniques: Immunohistochemistry, Expressing, Two Tailed Test

    STING expression in human PDAC stroma and CAFs. ( a ) Groups categorized by positive, weakly positive, and negative STING expression in PDAC stroma. Representative IHC analysis of STING using a human PDAC tissue array (scale bar, 100 μm). ( b ) Percentages of the indicated groups in 40 PDAC samples. ( c ) Co-immunofluorescence staining for α-SMA (red) and STING (green) in STING positive or weakly positive or negative in stroma. ( d ) 5-AZA (0.1 nM) was administered to CAF1 and CAF2 derived from murine PDACs and incubated for 24 h.

    Journal: Scientific Reports

    Article Title: Activation of STING in pancreatic cancer-associated fibroblasts exerts an antitumor effect by enhancing tumor immunity

    doi: 10.1038/s41598-024-68061-y

    Figure Lengend Snippet: STING expression in human PDAC stroma and CAFs. ( a ) Groups categorized by positive, weakly positive, and negative STING expression in PDAC stroma. Representative IHC analysis of STING using a human PDAC tissue array (scale bar, 100 μm). ( b ) Percentages of the indicated groups in 40 PDAC samples. ( c ) Co-immunofluorescence staining for α-SMA (red) and STING (green) in STING positive or weakly positive or negative in stroma. ( d ) 5-AZA (0.1 nM) was administered to CAF1 and CAF2 derived from murine PDACs and incubated for 24 h.

    Article Snippet: The human PDAC tissue array was purchased commercially from TissueArray.com (No.PA482a).

    Techniques: Expressing, Immunofluorescence, Staining, Derivative Assay, Incubation

    a, Immunohistochemistry staining of LPAR4 in a PDAC tissue array consisted of 15 PDAC samples and 4 samples of normal pancreas. Scale bar is 50 μM. Representative images showing normal pancreas (n=4 biological samples), low-LPAR4 PDAC (n=9 biological samples), and high-LPAR4 PDAC (n=6 biological samples). Bar graph shows the relative percentage of LPAR4-low and LPAR4-high patients in the PDAC tissue array. b, Quantitative RT-PCR confirming the manipulation of LPAR4 expression in 2 pancreatic cancer cell lines (Colo-357, MIA PaCa-2) and 2 patient-derived cancer cells (79E, 34E). Data were shown as mean ± s.d. (n=4 independent experiments for Colo-357 and 79E cells with LPAR4 stable knockdown, n=3 for Colo-357, 79E, and MiaPaCa2 cells with LPAR4 ectopic expression, n=3 for 34E cells with LPAR4 stable knockdown, and n=4 for 34E with LPAR4 ectopic expression). c, Non-invasive Bioluminescence images showing tumors formed at day 10 for Colo-357+sh-CTRL+luciferase or Colo-357+sh-R4.1+luciferase of various number implanted in the pancreas of nu/nu mice. Right panel showing the luminescence intensity in a blue-to-red spectrum. d, f, Trypan blue exclusion assay showing the relative number of viable cells with or without LPAR4 expression manipulation grown in 10% serum and 2D at day 4 and day 7. e, Tumor growth rates for 1 million Colo-357 cells with or without LPAR4 expression manipulation in a subcutaneous tumor model. Data were presented as mean ± s.d. for n=8 independent samples for each group. g, Quantitative RT-PCR confirming the knockdown of LPAR1 in Colo-357 cells. h, Effects of LPAR1 knockdown using siRNA on 2D or 3D (methylcellulose sphere forming) cell growth. Data were presented as mean ± s.d. for n=3 independent experiments (d,f,g, and h). Statistical analyses were performed using two tailed unpaired one sample t-test (b,g, and h) and one-way ANOVA (d-f). Source numerical data are available in source data.

    Journal: Nature cell biology

    Article Title: Pancreatic cancer cells upregulate LPAR4 in response to isolation stress to promote an ECM-enriched niche and support tumor initiation

    doi: 10.1038/s41556-022-01055-y

    Figure Lengend Snippet: a, Immunohistochemistry staining of LPAR4 in a PDAC tissue array consisted of 15 PDAC samples and 4 samples of normal pancreas. Scale bar is 50 μM. Representative images showing normal pancreas (n=4 biological samples), low-LPAR4 PDAC (n=9 biological samples), and high-LPAR4 PDAC (n=6 biological samples). Bar graph shows the relative percentage of LPAR4-low and LPAR4-high patients in the PDAC tissue array. b, Quantitative RT-PCR confirming the manipulation of LPAR4 expression in 2 pancreatic cancer cell lines (Colo-357, MIA PaCa-2) and 2 patient-derived cancer cells (79E, 34E). Data were shown as mean ± s.d. (n=4 independent experiments for Colo-357 and 79E cells with LPAR4 stable knockdown, n=3 for Colo-357, 79E, and MiaPaCa2 cells with LPAR4 ectopic expression, n=3 for 34E cells with LPAR4 stable knockdown, and n=4 for 34E with LPAR4 ectopic expression). c, Non-invasive Bioluminescence images showing tumors formed at day 10 for Colo-357+sh-CTRL+luciferase or Colo-357+sh-R4.1+luciferase of various number implanted in the pancreas of nu/nu mice. Right panel showing the luminescence intensity in a blue-to-red spectrum. d, f, Trypan blue exclusion assay showing the relative number of viable cells with or without LPAR4 expression manipulation grown in 10% serum and 2D at day 4 and day 7. e, Tumor growth rates for 1 million Colo-357 cells with or without LPAR4 expression manipulation in a subcutaneous tumor model. Data were presented as mean ± s.d. for n=8 independent samples for each group. g, Quantitative RT-PCR confirming the knockdown of LPAR1 in Colo-357 cells. h, Effects of LPAR1 knockdown using siRNA on 2D or 3D (methylcellulose sphere forming) cell growth. Data were presented as mean ± s.d. for n=3 independent experiments (d,f,g, and h). Statistical analyses were performed using two tailed unpaired one sample t-test (b,g, and h) and one-way ANOVA (d-f). Source numerical data are available in source data.

    Article Snippet: Immunohistochemistry staining of LPAR4 or FN1 in human PDAC tissue array (US Biomax PA484a) or formalin-fixed, paraffin-embedded xenograft tumors were performed using the LPAR4 antibody (Thermo Fisher, #PA5–49727) or FN1 antibody (CST, #26836, E5H6X) following the manufacturer’s protocol.

    Techniques: Immunohistochemistry, Staining, Quantitative RT-PCR, Expressing, Derivative Assay, Luciferase, Trypan Blue Exclusion Assay, Two Tailed Test