HSPA6 augments garlic extract-induced inhibition of proliferation, migration, and invasion of bladder cancer EJ cells; Implication for cell cycle dysregulation, signaling pathway alteration, and transcription factor-associated MMP-9 regulation
Published 2017 View Full Article
- Home
- Publications
- Publication Search
- Publication Details
Title
HSPA6 augments garlic extract-induced inhibition of proliferation, migration, and invasion of bladder cancer EJ cells; Implication for cell cycle dysregulation, signaling pathway alteration, and transcription factor-associated MMP-9 regulation
Authors
Keywords
DNA-binding proteins, Gene regulation, Transcription factors, Transcriptional control, Binding analysis, Apoptosis, Cell cycle and cell division, Heat shock response
Journal
PLoS One
Volume 12, Issue 2, Pages e0171860
Publisher
Public Library of Science (PLoS)
Online
2017-02-11
DOI
10.1371/journal.pone.0171860
References
Ask authors/readers for more resources
Related references
Note: Only part of the references are listed.- Diallyl disulfide inhibits growth and metastatic potential of human triple-negative breast cancer cells through inactivation of the β-catenin signaling pathway
- (2015) Jing Huang et al. MOLECULAR NUTRITION & FOOD RESEARCH
- Antimetastatic Therapies of the Polysulfide Diallyl Trisulfide against Triple-Negative Breast Cancer (TNBC) via Suppressing MMP2/9 by Blocking NF-κB and ERK/MAPK Signaling Pathways
- (2015) Yuping Liu et al. PLoS One
- Bladder Carcinoma Data with Clinical Risk Factors and Molecular Markers: A Cluster Analysis
- (2015) Enrique Redondo-Gonzalez et al. Biomed Research International
- Identification of molecular target of diallyl trisulfide in leukemic cells
- (2014) Shun Suda et al. BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY
- Basal and stress-inducible expression of HSPA6 in human keratinocytes is regulated by negative and positive promoter regions
- (2014) Vincent P. Ramirez et al. CELL STRESS & CHAPERONES
- Diallyl disulfide suppresses proliferation and induces apoptosis in human gastric cancer through Wnt-1 signaling pathway by up-regulation of miR-200b and miR-22
- (2013) Hailin Tang et al. CANCER LETTERS
- Stress-induced localization of HSPA6 (HSP70B′) and HSPA1A (HSP70-1) proteins to centrioles in human neuronal cells
- (2013) Sam Khalouei et al. CELL STRESS & CHAPERONES
- AKT signaling is involved in fucoidan-induced inhibition of growth and migration of human bladder cancer cells
- (2013) Tae-Min Cho et al. FOOD AND CHEMICAL TOXICOLOGY
- Interleukin-20 Promotes Migration of Bladder Cancer Cells through Extracellular Signal-regulated Kinase (ERK)-mediated MMP-9 Protein Expression Leading to Nuclear Factor (NF-κB) Activation by Inducing the Up-regulation of p21WAF1Protein Expression
- (2012) Se-Jung Lee et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- Identification of Pro-Inflammatory Cytokines Associated with Muscle Invasive Bladder Cancer; The Roles of IL-5, IL-20, and IL-28A
- (2012) Se-Jung Lee et al. PLoS One
- Increased expression of MMP-9 and IL-8 are correlated with poor prognosis of Bladder Cancer
- (2012) Sabrina Thalita Reis et al. BMC Urology
- Global cancer statistics
- (2011) Ahmedin Jemal et al. CA-A CANCER JOURNAL FOR CLINICIANS
- Diallyl sulfide, diallyl disulfide, and diallyl trisulfide inhibit migration and invasion in human colon cancer colo 205 cells through the inhibition of matrix metalloproteinase-2, -7, and -9 expressions
- (2011) Kuang-Chi Lai et al. ENVIRONMENTAL TOXICOLOGY
- MMP-2 and MMP-9 in lymph-node-positive bladder cancer
- (2011) R. Seiler et al. JOURNAL OF CLINICAL PATHOLOGY
- Exploring contrary trends in bladder cancer incidence, mortality and survival: implications for research and cancer control
- (2009) C. Luke et al. INTERNAL MEDICINE JOURNAL
- Centrosome-associated regulators of the G2/M checkpoint as targets for cancer therapy
- (2009) Yingmei Wang et al. Molecular Cancer
Become a Peeref-certified reviewer
The Peeref Institute provides free reviewer training that teaches the core competencies of the academic peer review process.
Get StartedAsk a Question. Answer a Question.
Quickly pose questions to the entire community. Debate answers and get clarity on the most important issues facing researchers.
Get Started