Dataset Information

Curcumin Inhibits ERK/c-Jun Expressions and Phosphorylation against Endometrial Carcinoma.

ABSTRACT: Curcumin has been shown to have anticancer effects in a variety of tumors. However, there are fewer studies on the role of curcumin in endometrial carcinoma (EC). The purpose of this experiment was to examine the inhibitory effect of curcumin on endometrial carcinoma cells and ERK/c-Jun signaling pathway. We first predicted the mechanism of action of curcumin on endometrial carcinoma by network pharmacology. Then, we found that curcumin can decrease the cell viability of Ishikawa cells, inhibit the migration of cancer cells, induce apoptosis, and cause cell cycle arrest in the S phase. For molecular mechanism, curcumin reduced the mRNA expression levels of ERK2 and JUN genes and inhibited the phosphorylation of ERK and c-Jun. This suggests that curcumin inhibits the proliferation of endometrial carcinoma cells by downregulating ERK/c-Jun signaling pathway activity.

SUBMITTER: Zhang Z

PROVIDER: S-EPMC7012278 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Curcumin Inhibits ERK/c-Jun Expressions and Phosphorylation against Endometrial Carcinoma.

Zhang Zhenxue Z Yi Pengfei P Tu Changchun C Zhan Jiejie J Jiang Liping L Zhang Fanglin F

BioMed research international 20191031

Curcumin has been shown to have anticancer effects in a variety of tumors. However, there are fewer studies on the role of curcumin in endometrial carcinoma (EC). The purpose of this experiment was to examine the inhibitory effect of curcumin on endometrial carcinoma cells and ERK/c-Jun signaling pathway. We first predicted the mechanism of action of curcumin on endometrial carcinoma by network pharmacology. Then, we found that curcumin can decrease the cell viability of Ishikawa cells, inhibit ...[more]

PMID: 32083122

Similar Datasets

Project description:BackgroundEndometrial carcinoma (EC) is one of the three major malignant tumors of the female reproductive system. In recent years, the incidence and mortality rate of EC have increased. B-cell translocation gene 1 (BTG1) is an anti-proliferation gene that regulates the occurrence and development of a variety of tumors, but there is no research regarding this gene in EC.MethodsBased on The Cancer Genome Atlas (TCGA) database, we used a variety of bioinformatics tools and databases to explore the expression and prognosis of BTG1. We verified expression and prognosis of BTG1 in EC using qRT-PCR and analyzed the relevant clinicopathological parameters. We functionally enriched BTG1 and related genes in EC patients through the bioinformatics website and analyzed miRNA targets of BTG1 and interacting protein networks. Cell proliferation, wound healing, transwell invasion, and cell apoptosis assays were used to detect the effects of BTG1 on the malignant biological behavior of endometrial carcinoma cells (ECCs). The effect of BTG1 on the epithelial-to-mesenchymal transition (EMT) process was detected using western blot.ResultsWe analyzed the expression and prognosis of BTG1 based on TCGA and found that low expression of BTG1 was associated with poor EC prognosis. The qRT-PCR suggested that BTG1 had low expression in EC. BTG1 expression was significantly correlated with overall survival (OS) shortening. Clinicopathological analysis suggested that expression of BTG1 was related to invasion depth and the International Federation of Gynecology and Obstetrics (FIGO) stage. EC pathological tissue type, fertility history, lymphatic metastasis, menopause, estrogen receptor (ER), progesterone receptor (PR), and age of diagnosis were not related. Functional enrichment analysis showed that BTG1 plays an important role in regulating embryonic development, tumorigenesis, apoptosis, and cell cycle. Biological behavior experiments suggest that BTG1 inhibits proliferation, migration, and invasion of ECCs, and promotes apoptosis of ECCs. Western blot indicated that BTG1 inhibited the EMT process of ECCs.ConclusionsBTG1, as a tumor suppressor gene, plays an important role in the occurrence and development of EC. We believe that BTG1 can be used as a potential prognostic biomarker for EC.

Project description:The enhanced migratory ability of endometrial stromal cells (ESCs) is a key factor in the formation of functional endometrium?like tissues outside the uterine cavity during endometriosis (EMS). Although accumulating evidence has suggested the importance of microRNAs (miRNAs) in the pathogenesis of EMS, the role of particular miRNAs in the invasiveness of ESCs remain poorly understood. In the present study, the function of miRNAs in the invasiveness of ESCs, along with the associated underlying mechanism involved, were investigated. Initially, the expression patterns of miRNAs in the ectopic and eutopic endometrium isolated from patients with EMS were analyzed using microarray. MicroRNA?202?5p (miR?202) was selected for further study due to its previously reported suppressive effects on the invasion in various types of cancers. The expression of miR?202 and K?Ras in eutopic and ectopic endometrioma tissues were detected using reverse transcription?quantitative PCR, immunohistochemistry and western blotting. The migration and invasion ability of ESCs was determined using wound healing and Transwell invasion assays, respectively. Compared with that from healthy individuals, miR?202 expression was demonstrated to be lower in the eutopic endometrium from patients with EMS, which was even lower in ectopic endometrium. Functional experiments in primary ESCs revealed that enhanced miR?202 expression suppressed the cell invasion and migration abilities, which was also accompanied with increased E?cadherin and reduced N?cadherin expression in ESCs, suggesting its potentially suppressive role in epithelial?mesenchymal transition. K?Ras is a well?known regulator of the ERK signaling pathway that was shown to be directly targeted and negatively regulated by miR?202. In addition, K?Ras expression was found to be upregulated in the ectopic endometrium, where it correlated negatively with that of miR?202. Knocking down K?Ras expression mimicked the anti?invasive effects of miR?202 overexpression on ESCs, whilst K?Ras overexpression attenuated the inhibitory role of miR?202 overexpression in ESC invasion. The K?Ras/Raf1/MEK/ERK signaling pathway was also blocked by miR?202 overexpression. These findings suggested that miR?202 inhibited ESC migration and invasion by inhibiting the K?Ras/Raf1/MEK/ERK signaling pathway, rendering miR?202 a candidate for being a therapeutic target for EMS.

Dataset Information

Curcumin Inhibits ERK/c-Jun Expressions and Phosphorylation against Endometrial Carcinoma.

Publications

Curcumin Inhibits ERK/c-Jun Expressions and Phosphorylation against Endometrial Carcinoma.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure