The initial steps of heat stress in A431 cells were previously characterized by ligand-independent EGFR transactivation via an unknown mechanism and concomitant secretion of Hsp70. In this work we demonstrate that the depletion of Hsp70 from the conditioned medium of heated cells abolishes EGFR transactivation indicating that secreted Hsp70 is essential for EGFR transactivation during heat shock. This notion is supported by the findings that purified Hsp70 can induce EGFR transactivation and the activation of EGFR-dependent signaling pathways. Both heat stress and pure Hsp70 stimulate activation of TLR2/4 and their association with EGFR. These results suggest that the secreted Hsp70 mediates the cross-communication of TLR and EGFR signaling systems in A431 cells.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.febslet.2006.11.024 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Amiloride sensitizes prostate cancer cells to the reversible tyrosine kinase inhibitor lapatinib by modulating Erbb3 subcellular localization.
Cell Mol Life Sci
December 2024
Research Service, VA Northern California Health Care System, Mather, CA, USA.
Neoadjuvant therapy (NAT) has been studied in clinically localized prostate cancer (PCa) to improve the outcomes from radical prostatectomy (RP) by 'debulking' of high-risk PCa; however, using androgen deprivation therapy (ADT) at this point risks castration resistant PCa (CRPC) clonal proliferation. Our goal is to identify alternative NAT that reduce hormone sensitive PCa (HSPC) without affecting androgen receptor (AR) transcriptional activity. PCa is associated with increased expression and activation of the epidermal growth factor receptor (EGFR) family, including HER2 and ErbB3.
View Article and Find Full Text PDFTFF3 drives Hippo dependent EGFR-TKI resistance in lung adenocarcinoma.
Oncogene
December 2024
Institute of Biopharmaceutical and Health Engineering, Tsinghua Shenzhen International Graduate School, Tsinghua University, Shenzhen, 518055, PR China.
Intrinsic and acquired resistance represent major obstacles to optimize outcomes in epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) targeted therapy in lung adenocarcinoma (LUAD). Hence, a deeper understanding of EGFR-TKI resistance mechanisms in LUAD will potentially assist in formulating strategies to delay or overcome such resistance. Herein, it was observed that trefoil factor 3 (TFF3) is a crucial mediator of the LUAD EGFR-TKI response.
View Article and Find Full Text PDFHypoxia Induced Lnc191 Upregulation Dictates the Progression of Esophageal Squamous Cell Carcinoma by Activating GRP78/ERK Pathway.
Adv Sci (Weinh)
December 2024
State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
Hypoxia is a typical hallmark of solid tumors and plays a crucial role in the progression of esophageal squamous cell carcinogenesis (ESCC). Nevertheless, the precise mechanisms underlying the involvement of hypoxia in tumor development remain unclear. In the present study, a novel hypoxia-induced long noncoding RNA (lncRNA) is identified first, lnc191, which is highly expressed in clinical ESCC tissues and is positively correlated with poor prognosis of ESCC patients.
View Article and Find Full Text PDFPotential of epithelial membrane protein 3 as a novel therapeutic target for human breast cancer.
Oncol Rep
January 2025
Department of Food Safety Hygiene and Risk Management, College of Medicine, National Cheng Kung University, Tainan 701401, Taiwan, R.O.C.
Article Synopsis
- Amplification of the HER2 receptor and overexpression of estrogen and progesterone receptors are crucial for planning breast cancer treatments, but resistance to drugs is common, highlighting the need for new advances.
- This study is the first to reveal that EMP3, a membrane protein, interacts with HER2 in breast cancer, promoting cell growth, invasion, and migration while increasing estrogen and progesterone receptor levels.
- Knocking down EMP3 reduced breast cancer cell growth and increased sensitivity to the drug trastuzumab, suggesting that targeting EMP3 could be a promising new treatment strategy for patients, especially in those with co-expression of EMP3 and HER2.
Nuclear epidermal growth factor receptor (nEGFR) in clinical treatment.
Heliyon
November 2024
Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Xuhui District, Shanghai, 200032, China.
The epidermal growth factor receptor (EGFR) is a recognized target in tumor treatment. While there is significant focus on inhibiting membrane EGFR and its downstream signaling activation, the ectopic accumulation of EGFR, particularly nuclear EGFR (nEGFR), has been implicated in tumor-associated activities and associated with poor prognosis. Within the nucleus, nEGFR functions as a transcriptional regulator to modulate transcriptional landscape and exerts tyrosine kinase activity to phosphorylate nuclear proteins and subsequently influences DNA repair, cell cycle, proliferation, and resistance to radiotherapy and chemotherapy.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!