IER5 is a p53-reguated activator of HSF1 that contributes to promotion of cancer

Date

Wednesday, March 14, 2018 - 14:00 to 15:00

Location

D014 (Lab1, Level D)

Description

Dear All,

Cell Signal Unit (Yamamoto Unit) would like to inform you of a seminar by Dr. Rieko Ohki, Laboratory Head of Fundamental Oncology, National Cancer Center Research Institute.

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Date: Wednesday, March 14, 2018

Time: 14:00-15:00

Venue: D014, Level D, Lab 1

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Speaker:

Dr. Rieko Ohki, National Cancer Center Research Institute


Title:
IER5 is a p53-reguated activator of HSF1 that contributes to promotion of cancer


Abstract:
The p53 gene is one of the most frequently mutated genes in human cancer and functions as a tumor suppressor and transcriptional factor that regulates various genes involved in cancer. One p53 target gene is IER5, whose function was initially unknown, but we have shown facilitates the activation of the transcriptional activator HSF1 by recruiting the PP2A phosphatase to HSF1, leading to its hypo-phosphorylation and activation. HSF1 is the master transcriptional regulator of the HSP genes, which encode molecular chaperones essential for cellular homeostasis. HSPs also exhibit anti-apoptotic functions by repressing pro-apoptotic factors, thereby protecting stressed cells from cell death. Although HSF1-HSP pathway is generally activated by cellular stress such as heat shock, this pathway is also hyperactivated in cancers independent of heat shock and contribute to promotion of cancer development and resistance to cancer treatments. We observed that IER5 is overexpressed in several cancers in a p53-independent manner and contributes to tumor malignancy via activation of the HSF1-HSP pathway. We propose a model in which IER5 activates HSF1 in cancer as part of the p53-IER5-HSF1-HSPs pathway, thereby providing stress resistance to cancer cells.


Host:
Prof. Tadashi Yamamoto

 

We hope to see many of you at the seminar.

 

Best regards,

Yuki Nakagawa

Research Unit Administrator

Cell Signal Unit

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