scholarly journals Isoliquiritigenin attenuates MiR-21 expression via induction of PIAS3 in breast cancer cells

RSC Advances ◽  
2017 ◽  
Vol 7 (29) ◽  
pp. 18085-18092 ◽  
Author(s):  
Shilong Ning ◽  
Xiao Ma ◽  
Dongmei Zhu ◽  
Zhaoxia Shen ◽  
Jiao Liu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Specific Inhibitor ◽  
Stat3 Signaling

Activated STAT3 triggered miR-21 transcription via binding to its promoter. ISL induced PIAS3 expression, a specific inhibitor of activated STAT3, leading to inhibition of STAT3 signaling and subsequent miR-21 transcription in breast cancer cells.

scholarly journals Arginine Methyltransferase PRMT1 Regulates p53 Activity in Breast Cancer

Life ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 789
Author(s):  
Li-Ming Liu ◽  
Qiang Tang ◽  
Xin Hu ◽  
Jing-Jing Zhao ◽  
Yuan Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Asymmetric Dimethylarginine ◽  
Human Cancer ◽  
Specific Inhibitor ◽  
Dependent Manner ◽  
Breast Tumorigenesis ◽  
Stress Signals

The protein p53 is one of the most important tumor suppressors, responding to a variety of stress signals. Mutations in p53 occur in about half of human cancer cases, and dysregulation of the p53 function by epigenetic modifiers and modifications is prevalent in a large proportion of the remainder. PRMT1 is the main enzyme responsible for the generation of asymmetric-dimethylarginine, whose upregulation or aberrant splicing has been observed in many types of malignancies. Here, we demonstrate that p53 function is regulated by PRMT1 in breast cancer cells. PRMT1 knockdown activated the p53 signal pathway and induced cell growth-arrest and senescence. PRMT1 could directly bind to p53 and inhibit the transcriptional activity of p53 in an enzymatically dependent manner, resulting in a decrease in the expression levels of several key downstream targets of the p53 pathway. We were able to detect p53 asymmetric-dimethylarginine signals in breast cancer cells and breast cancer tissues from patients, and the signals could be significantly weakened by silencing of PRMT1 with shRNA, or inhibiting PRMT1 activity with a specific inhibitor. Furthermore, PRMT1 inhibitors significantly impeded cell growth and promoted cellular senescence in breast cancer cells and primary tumor cells. These results indicate an important role of PRMT1 in the regulation of p53 function in breast tumorigenesis.

scholarly journals Surgery-induced wound response promotes stem-like and tumor-initiating features of breast cancer cells, via STAT3 signaling

Oncotarget ◽  
2014 ◽  
Vol 5 (15) ◽  
pp. 6267-6279 ◽  
Author(s):  
Ilenia Segatto ◽  
Stefania Berton ◽  
Maura Sonego ◽  
Samuele Massarut ◽  
Tiziana Perin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Wound Response ◽  
Stat3 Signaling

scholarly journals Evaluation of STAT3 Signaling in ALDH+ and ALDH+/CD44+/CD24− Subpopulations of Breast Cancer Cells

PLoS ONE ◽  
2013 ◽  
Vol 8 (12) ◽  
pp. e82821 ◽  
Author(s):  
Li Lin ◽  
Brian Hutzen ◽  
Hsiu-Fang Lee ◽  
Zhengang Peng ◽  
Wenlong Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Stat3 Signaling

Downregulation of DPF3 promotes the proliferation and motility of breast cancer cells through activating JAK2/STAT3 signaling

2019 ◽  
Vol 514 (3) ◽  
pp. 639-644 ◽  
Author(s):  
Wei-hao Lin ◽  
Wei-gang Dai ◽  
Xiang-dong Xu ◽  
Qiu-hua Yu ◽  
Bing Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Stat3 Signaling

RERG involvement in the RAS pathway and ER-dependent transcription in breast cancer.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e14638-e14638
Author(s):  
Pei-Chen Hsu ◽  
Jar-Yi Ho ◽  
Cheng-Ping Yu
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Breast Cancer Cells ◽  
Small Gtpases ◽  
Breast Cancer Cell Lines ◽  
Ras Pathway ◽  
Ras Genes ◽  
Stat3 Signaling ◽  
Luminal Type

e14638 Background: Breast cancer is the highest incidence malignancies in women worldwide. Luminal breast cancers are typically estrogen receptor–positive with better prognosis. However, the rapid disease progression and the high relapse rate of this subtype of breast cancer have become a puzzle in breast cancer treatment. It gave us the motivation to figure out the anomalous molecular mechanism which devoted in. It has been well-documented that the RAS pathway is overloadly activated in more than half of human breast tumors. RAS genes encode a superfamily of small GTPases that contribute to cell growth signals. Methods: Gene expression level were measured by qPCR and Western Blot.Biological effects of each condition were evaluated in cell viability and migration. Results: In this study, we investigated one member of the RAS family, RERG, which was related to the ER pathway and contributed to inhibit Ras activated pathway. Our results showed that knockdown of RERG concomitantly promoted two major oncogenic pathways, Ras and Stat3 signaling pathways, in luminal type breast cancer cell lines. Moreover, ectopic RERG expression significantly inhibited Ras expression. It implicated that RERG mediated in RAS-driven biological effects. Our findings indicated that knockdown of RERG enhanced mobility of the breast cancer cells and made cells more intractable under SERM treatment. Conclusions: We elucidated the tumor-suppressor role of RERG in breast cancer cells though inhibition of the Ras and Stat3 signaling pathways. Therefore, this study might shed light on the important mechanistic insight into the tumorigenesis of ER-positive luminal type cancer and provided the prognostic and therapeutic improved roles of RERG.

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