lif inhibitor ec330 Search Results


lif inhibitor ec330  (MedChemExpress)
93
MedChemExpress lif inhibitor ec330
CTHRC1 in CAFs mediates the activation of STAT3 signaling pathway in pancreatic cancer cells by positively regulating LIF. (A) Western Blot was used to detect the activation of STAT3 signaling pathway in Panc‐1 after adding <t>EC330</t> in CAFs‐CM and protein gray scale analysis. (B) Western Blot was used to detect the activation of STAT3 signaling pathway in Aspc‐1 after adding EC330 in CAFs‐CM and protein gray scale analysis. (C) Effect of CAFs‐CM on the proliferation function of Panc‐1 after adding EC330. (D) Effect of CAFs‐CM on the colony‐forming function of Panc‐1 after adding EC330. (E) Effect of CAFs‐CM on the migration function of Panc‐1 after adding EC330. (F, G) Western Blot was used to detect the activation of STAT3 signaling pathway in Panc‐1 after adding EC330 in CAFs‐CM overexpressing CTHRC1 and protein gray scale analysis. (H) Effect of CAFs‐CM overexpressing CTHRC1 on the proliferation function of Panc‐1 after adding EC330. (I, J) Effect of CAFs‐CM overexpressing CTHRC1 on the colony‐forming function of Panc‐1 after adding EC330. (K) Effect of CAFs‐CM overexpressing CTHRC1 on the migration function of Panc‐1 after adding EC330. (L) Effect of CAFs‐CM on the proliferative function of Aspc‐1 after adding Stattic. (M) Effect of CAFs‐CM overexpressing CTHRC1 on the migration function of Aspc‐1 after adding Stattic. ** p < 0.01; *** p < 0.001.
Lif Inhibitor Ec330, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/lif+inhibitor+ec330/EC330/pmc12317280-29-0-6
Average 93 stars, based on 1 article reviews
lif inhibitor ec330 - by Bioz Stars, 2026-09
93/100 stars
  Buy from Supplier
first in class steroidal lif inhibitor ec330  (Selleck Chemicals)
92
Selleck Chemicals first in class steroidal lif inhibitor ec330
ADT induces LIF abundance and NE differentiation of prostate cancer cells. (A) Western blotting for LIFR, p-STAT3, STAT3, CgA, and NSE in LNCaP and C4–2 cells treated with LIF protein at various concentrations for 24 h. (B) Protein levels of LIF, LIFR, p-STAT3, STAT3, CgA, and NSE in LNCaP and C4–2 cells following stable expression of an LIF cDNA vector. (C) mRNA levels of LIF, LIFR, STAT3, CHGA, and ENO2 in PC3 and NCI-H660 cells following stable expression of an LIF shRNA vector. (D) Western blotting for LIF, LIFR, p-STAT3, STAT3, CgA, and NSE in PC3 and NCI-H660 cells stably expressing the LIF shRNA vector. (E) Western blotting for LIFR, p-STAT3, STAT3, CgA, and NSE in PC3 and NCI-H660 cells treated with <t>EC330</t> (35 nM) for 24 h. (F) GSEA of the TCGA prostate cancer dataset showing that higher LIF expression was associated with an androgen-inactivated gene signature. NES, normalized enrichment score; FDR, false discovery rate. (G) Effects of DHT and MDV3100 (MDV), relative to that of the vehicle (methanol or DMSO), on the expression of LIF, LIFR, p-STAT3, STAT3, CgA, and NSE proteins in LNCaP and C4–2 cells cultured with 10% CSS-containing medium. (H) LIF, LIFR, p-STAT3, STAT3, CgA, and NSE protein levels in control (Luc) and LIF-knockdown LNCaP or C4–2 cells and those treated with androgen withdrawal (CSS) for 1 week. (I and J) IHC staining (I) and analysis (J) of cytoplasmic LIF in prostate cancer tissue sections from patients before and after ADT treatment. The 18 samples were obtained from Taipei Medical University-Wan Fang Hospital. Scale bars, 100 μm. Statistical analysis by the two-tailed Student’s t-test. Data from the quantification of mRNA are presented as the mean ± SEM, n=3. * p<0.05, ** p<0.01, *** p<0.001.
First In Class Steroidal Lif Inhibitor Ec330, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/lif+inhibitor+ec330/EC330/pmc07168873-117-8-5
Average 92 stars, based on 1 article reviews
first in class steroidal lif inhibitor ec330 - by Bioz Stars, 2026-09
92/100 stars
  Buy from Supplier

Image Search Results


CTHRC1 in CAFs mediates the activation of STAT3 signaling pathway in pancreatic cancer cells by positively regulating LIF. (A) Western Blot was used to detect the activation of STAT3 signaling pathway in Panc‐1 after adding EC330 in CAFs‐CM and protein gray scale analysis. (B) Western Blot was used to detect the activation of STAT3 signaling pathway in Aspc‐1 after adding EC330 in CAFs‐CM and protein gray scale analysis. (C) Effect of CAFs‐CM on the proliferation function of Panc‐1 after adding EC330. (D) Effect of CAFs‐CM on the colony‐forming function of Panc‐1 after adding EC330. (E) Effect of CAFs‐CM on the migration function of Panc‐1 after adding EC330. (F, G) Western Blot was used to detect the activation of STAT3 signaling pathway in Panc‐1 after adding EC330 in CAFs‐CM overexpressing CTHRC1 and protein gray scale analysis. (H) Effect of CAFs‐CM overexpressing CTHRC1 on the proliferation function of Panc‐1 after adding EC330. (I, J) Effect of CAFs‐CM overexpressing CTHRC1 on the colony‐forming function of Panc‐1 after adding EC330. (K) Effect of CAFs‐CM overexpressing CTHRC1 on the migration function of Panc‐1 after adding EC330. (L) Effect of CAFs‐CM on the proliferative function of Aspc‐1 after adding Stattic. (M) Effect of CAFs‐CM overexpressing CTHRC1 on the migration function of Aspc‐1 after adding Stattic. ** p < 0.01; *** p < 0.001.

Journal: Cancer Medicine

Article Title: CTHRC 1 Derived From Cancer‐Associated Fibroblasts Promotes Pancreatic Cancer Progression and Metastasis via the LIF ‐ STAT 3 Pathway

doi: 10.1002/cam4.71126

Figure Lengend Snippet: CTHRC1 in CAFs mediates the activation of STAT3 signaling pathway in pancreatic cancer cells by positively regulating LIF. (A) Western Blot was used to detect the activation of STAT3 signaling pathway in Panc‐1 after adding EC330 in CAFs‐CM and protein gray scale analysis. (B) Western Blot was used to detect the activation of STAT3 signaling pathway in Aspc‐1 after adding EC330 in CAFs‐CM and protein gray scale analysis. (C) Effect of CAFs‐CM on the proliferation function of Panc‐1 after adding EC330. (D) Effect of CAFs‐CM on the colony‐forming function of Panc‐1 after adding EC330. (E) Effect of CAFs‐CM on the migration function of Panc‐1 after adding EC330. (F, G) Western Blot was used to detect the activation of STAT3 signaling pathway in Panc‐1 after adding EC330 in CAFs‐CM overexpressing CTHRC1 and protein gray scale analysis. (H) Effect of CAFs‐CM overexpressing CTHRC1 on the proliferation function of Panc‐1 after adding EC330. (I, J) Effect of CAFs‐CM overexpressing CTHRC1 on the colony‐forming function of Panc‐1 after adding EC330. (K) Effect of CAFs‐CM overexpressing CTHRC1 on the migration function of Panc‐1 after adding EC330. (L) Effect of CAFs‐CM on the proliferative function of Aspc‐1 after adding Stattic. (M) Effect of CAFs‐CM overexpressing CTHRC1 on the migration function of Aspc‐1 after adding Stattic. ** p < 0.01; *** p < 0.001.

Article Snippet: LIF inhibitor EC330 was purchased from MedChemExpress (MCE).

Techniques: Activation Assay, Western Blot, Migration

ADT induces LIF abundance and NE differentiation of prostate cancer cells. (A) Western blotting for LIFR, p-STAT3, STAT3, CgA, and NSE in LNCaP and C4–2 cells treated with LIF protein at various concentrations for 24 h. (B) Protein levels of LIF, LIFR, p-STAT3, STAT3, CgA, and NSE in LNCaP and C4–2 cells following stable expression of an LIF cDNA vector. (C) mRNA levels of LIF, LIFR, STAT3, CHGA, and ENO2 in PC3 and NCI-H660 cells following stable expression of an LIF shRNA vector. (D) Western blotting for LIF, LIFR, p-STAT3, STAT3, CgA, and NSE in PC3 and NCI-H660 cells stably expressing the LIF shRNA vector. (E) Western blotting for LIFR, p-STAT3, STAT3, CgA, and NSE in PC3 and NCI-H660 cells treated with EC330 (35 nM) for 24 h. (F) GSEA of the TCGA prostate cancer dataset showing that higher LIF expression was associated with an androgen-inactivated gene signature. NES, normalized enrichment score; FDR, false discovery rate. (G) Effects of DHT and MDV3100 (MDV), relative to that of the vehicle (methanol or DMSO), on the expression of LIF, LIFR, p-STAT3, STAT3, CgA, and NSE proteins in LNCaP and C4–2 cells cultured with 10% CSS-containing medium. (H) LIF, LIFR, p-STAT3, STAT3, CgA, and NSE protein levels in control (Luc) and LIF-knockdown LNCaP or C4–2 cells and those treated with androgen withdrawal (CSS) for 1 week. (I and J) IHC staining (I) and analysis (J) of cytoplasmic LIF in prostate cancer tissue sections from patients before and after ADT treatment. The 18 samples were obtained from Taipei Medical University-Wan Fang Hospital. Scale bars, 100 μm. Statistical analysis by the two-tailed Student’s t-test. Data from the quantification of mRNA are presented as the mean ± SEM, n=3. * p<0.05, ** p<0.01, *** p<0.001.

Journal: Clinical cancer research : an official journal of the American Association for Cancer Research

Article Title: Leukemia inhibitory factor promotes castration-resistant prostate cancer and neuroendocrine differentiation by activated ZBTB46

doi: 10.1158/1078-0432.CCR-18-3239

Figure Lengend Snippet: ADT induces LIF abundance and NE differentiation of prostate cancer cells. (A) Western blotting for LIFR, p-STAT3, STAT3, CgA, and NSE in LNCaP and C4–2 cells treated with LIF protein at various concentrations for 24 h. (B) Protein levels of LIF, LIFR, p-STAT3, STAT3, CgA, and NSE in LNCaP and C4–2 cells following stable expression of an LIF cDNA vector. (C) mRNA levels of LIF, LIFR, STAT3, CHGA, and ENO2 in PC3 and NCI-H660 cells following stable expression of an LIF shRNA vector. (D) Western blotting for LIF, LIFR, p-STAT3, STAT3, CgA, and NSE in PC3 and NCI-H660 cells stably expressing the LIF shRNA vector. (E) Western blotting for LIFR, p-STAT3, STAT3, CgA, and NSE in PC3 and NCI-H660 cells treated with EC330 (35 nM) for 24 h. (F) GSEA of the TCGA prostate cancer dataset showing that higher LIF expression was associated with an androgen-inactivated gene signature. NES, normalized enrichment score; FDR, false discovery rate. (G) Effects of DHT and MDV3100 (MDV), relative to that of the vehicle (methanol or DMSO), on the expression of LIF, LIFR, p-STAT3, STAT3, CgA, and NSE proteins in LNCaP and C4–2 cells cultured with 10% CSS-containing medium. (H) LIF, LIFR, p-STAT3, STAT3, CgA, and NSE protein levels in control (Luc) and LIF-knockdown LNCaP or C4–2 cells and those treated with androgen withdrawal (CSS) for 1 week. (I and J) IHC staining (I) and analysis (J) of cytoplasmic LIF in prostate cancer tissue sections from patients before and after ADT treatment. The 18 samples were obtained from Taipei Medical University-Wan Fang Hospital. Scale bars, 100 μm. Statistical analysis by the two-tailed Student’s t-test. Data from the quantification of mRNA are presented as the mean ± SEM, n=3. * p<0.05, ** p<0.01, *** p<0.001.

Article Snippet: The AR antagonist enzalutamide (MDV3100) (Selleck) and the first-in-class steroidal LIF inhibitor EC330 (MedChemExpress) were used to treat cells at concentrations of 10 μM and 35 nM, respectively, for 24 h in 10% FBS-containing medium.

Techniques: Western Blot, Expressing, Plasmid Preparation, shRNA, Stable Transfection, Cell Culture, Control, Knockdown, Immunohistochemistry, Two Tailed Test

LIF promotes tumor growth and enzalutamide resistance, and LIF inhibitor reduces NE marker expression. (A and B) Proliferation assay in C4–2 cells treated with androgen withdrawal (A, charcoal-stripped serum (CSS)) or the combination of androgen withdrawal and enzalutamide (10 μM) (B, CSS+MDV3100), n=8. (C) Quantification and images of the colony formation of C4–2 cells with androgen withdrawal (CSS) or combined androgen withdrawal with MDV3100 (10 μM) treatment (CSS+MDV) for 6 days following empty vector (EV) or LIF-expressing vector overexpression. (D) Proliferation assays in LNCaP, C4–2, PC3, and NCI-H660 cells treated with an LIF inhibitor (EC330) at the indicated concentrations for 24 h, n=8. (E) Colony formation of PC3 and NCI-H660 cells with EC330 (35 nM) treatment for 6 days. (F-H) Tumor growth analysis of NCI-H660 cells subcutaneously inoculated into male nude mice followed by treatment with EC330 (2.5 mg/kg). Tumor sizes were monitored twice a week (F), and images (G) and tumor weights (H) were also measured at the end of the experiment. n=6 mice per group. (I) IHC staining of subcutaneous tumors with antibodies specific for p-STAT3, CgA, NSE, Ki67, and cleaved caspase-3 in tumor-bearing mice from F. Scale bars represent 100 μm. Data from the proliferation and colony formation assays are presented as the mean ± SEM from three independent experiments. * p<0.05, ** p<0.01, *** p<0.001.

Journal: Clinical cancer research : an official journal of the American Association for Cancer Research

Article Title: Leukemia inhibitory factor promotes castration-resistant prostate cancer and neuroendocrine differentiation by activated ZBTB46

doi: 10.1158/1078-0432.CCR-18-3239

Figure Lengend Snippet: LIF promotes tumor growth and enzalutamide resistance, and LIF inhibitor reduces NE marker expression. (A and B) Proliferation assay in C4–2 cells treated with androgen withdrawal (A, charcoal-stripped serum (CSS)) or the combination of androgen withdrawal and enzalutamide (10 μM) (B, CSS+MDV3100), n=8. (C) Quantification and images of the colony formation of C4–2 cells with androgen withdrawal (CSS) or combined androgen withdrawal with MDV3100 (10 μM) treatment (CSS+MDV) for 6 days following empty vector (EV) or LIF-expressing vector overexpression. (D) Proliferation assays in LNCaP, C4–2, PC3, and NCI-H660 cells treated with an LIF inhibitor (EC330) at the indicated concentrations for 24 h, n=8. (E) Colony formation of PC3 and NCI-H660 cells with EC330 (35 nM) treatment for 6 days. (F-H) Tumor growth analysis of NCI-H660 cells subcutaneously inoculated into male nude mice followed by treatment with EC330 (2.5 mg/kg). Tumor sizes were monitored twice a week (F), and images (G) and tumor weights (H) were also measured at the end of the experiment. n=6 mice per group. (I) IHC staining of subcutaneous tumors with antibodies specific for p-STAT3, CgA, NSE, Ki67, and cleaved caspase-3 in tumor-bearing mice from F. Scale bars represent 100 μm. Data from the proliferation and colony formation assays are presented as the mean ± SEM from three independent experiments. * p<0.05, ** p<0.01, *** p<0.001.

Article Snippet: The AR antagonist enzalutamide (MDV3100) (Selleck) and the first-in-class steroidal LIF inhibitor EC330 (MedChemExpress) were used to treat cells at concentrations of 10 μM and 35 nM, respectively, for 24 h in 10% FBS-containing medium.

Techniques: Marker, Expressing, Proliferation Assay, Plasmid Preparation, Over Expression, Immunohistochemistry