Compounds > n--((1e)-(4-(diethylamino)phenyl)methylene)-4-hydroxybenzohydrazide

n--((1e)-(4-(diethylamino)phenyl)methylene)-4-hydroxybenzohydrazide and Stomach-Neoplasms

n--((1e)-(4-(diethylamino)phenyl)methylene)-4-hydroxybenzohydrazide has been researched along with Stomach-Neoplasms* in 1 studies

Other Studies

1 other study(ies) available for n--((1e)-(4-(diethylamino)phenyl)methylene)-4-hydroxybenzohydrazide and Stomach-Neoplasms

Article	Year
Inhibition of EZH2 and activation of ERRγ synergistically suppresses gastric cancer by inhibiting FOXM1 signaling pathway. Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2021, Volume: 24, Issue:1 Gastric cancer (GC) is a leading cause of cancer-related mortality worldwide, because of the low efficacy of current therapeutic strategies. Estrogen-related receptor γ (ERRγ) was previously showed as a suppressor of GC. However, the mechanism and effective therapeutic method based on ERRγ is yet to be developed.. The expression levels of ERRγ, EZH2, and FOXM1 were detected by immunohistochemistry, qRT-PCR, and western blot. The regulatory mechanisms of ERRγ and FOXM1 were analyzed by ChIP, EMSA, and siRNA. The effects of EZH2 inhibitor (GSK126) or/and ERRγ agonist (DY131) on the tumorigenesis of gastric cancer cell lines were examined by cell proliferation, transwell migration, wound healing, and colony formation assays. Meanwhile, the inhibitory effects of GSK126 or/and DY131 on tumor growth were analyzed by xenograft tumor growth assay.. The expression of ERRγ was suppressed in tumor tissues of GC patients and positively correlated with prognosis, as opposed to that of EZH2 and FOXM1. EZH2 transcriptionally suppressed ERRγ via H3K27me3, which subsequently activated the expression of master oncogene FOXM1. The combination of GSK126 and DY131 synergistically activated ERRγ expression, which subsequently inhibited the expression of FOXM1 and its regulated pathways. Synergistic combination of GSK126 and DY131 significantly inhibited the tumorigenesis of GC cell lines and suppressed the growth of GC xenograft.. The FOXM1 signaling pathway underlying the ERRγ-mediated gastric cancer suppression was identified. Furthermore, combined treatment with EZH2 inhibitor and ERRγ agonist synergistically suppressed GC progression by inhibiting this signaling pathway, suggesting its high potential in treating GC patients. Topics: Carcinogenesis; Cell Line, Tumor; Drug Therapy, Combination; Enhancer of Zeste Homolog 2 Protein; Forkhead Box Protein M1; Gene Expression Regulation, Neoplastic; Humans; Hydrazines; Indoles; Pyridones; Receptors, Estrogen; Signal Transduction; Stomach Neoplasms; Xenograft Model Antitumor Assays	2021

Article

Year

Inhibition of EZH2 and activation of ERRγ synergistically suppresses gastric cancer by inhibiting FOXM1 signaling pathway.

Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2021, Volume: 24, Issue:1

Gastric cancer (GC) is a leading cause of cancer-related mortality worldwide, because of the low efficacy of current therapeutic strategies. Estrogen-related receptor γ (ERRγ) was previously showed as a suppressor of GC. However, the mechanism and effective therapeutic method based on ERRγ is yet to be developed.. The expression levels of ERRγ, EZH2, and FOXM1 were detected by immunohistochemistry, qRT-PCR, and western blot. The regulatory mechanisms of ERRγ and FOXM1 were analyzed by ChIP, EMSA, and siRNA. The effects of EZH2 inhibitor (GSK126) or/and ERRγ agonist (DY131) on the tumorigenesis of gastric cancer cell lines were examined by cell proliferation, transwell migration, wound healing, and colony formation assays. Meanwhile, the inhibitory effects of GSK126 or/and DY131 on tumor growth were analyzed by xenograft tumor growth assay.. The expression of ERRγ was suppressed in tumor tissues of GC patients and positively correlated with prognosis, as opposed to that of EZH2 and FOXM1. EZH2 transcriptionally suppressed ERRγ via H3K27me3, which subsequently activated the expression of master oncogene FOXM1. The combination of GSK126 and DY131 synergistically activated ERRγ expression, which subsequently inhibited the expression of FOXM1 and its regulated pathways. Synergistic combination of GSK126 and DY131 significantly inhibited the tumorigenesis of GC cell lines and suppressed the growth of GC xenograft.. The FOXM1 signaling pathway underlying the ERRγ-mediated gastric cancer suppression was identified. Furthermore, combined treatment with EZH2 inhibitor and ERRγ agonist synergistically suppressed GC progression by inhibiting this signaling pathway, suggesting its high potential in treating GC patients.

Topics: Carcinogenesis; Cell Line, Tumor; Drug Therapy, Combination; Enhancer of Zeste Homolog 2 Protein; Forkhead Box Protein M1; Gene Expression Regulation, Neoplastic; Humans; Hydrazines; Indoles; Pyridones; Receptors, Estrogen; Signal Transduction; Stomach Neoplasms; Xenograft Model Antitumor Assays

2021