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Last Updated: 10 July 2022

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Abstract 1267: The senescence-associated secretory phenotype requires the histone variant macroH2A1 and is antagonized by ATM in a novel ER stress response

In addition, we found that macroH2A1 is a key positive regulator of both transcriptional upregulation of SASP genes and persistent ATM activation seen during senescence. SASP factors play a positive feedback loop to maintain senescence by autocrine signaling, and can also cause paracrine senescence in bystander cells. Cells depleted of macroH2A1 are resistant to senescence triggered by SASP genes, according to a research by SASP researchers, suggesting that macroH2A1 is a key regulator of SASP positive feedback. In addition, ectopic expression of macroH2A1. 1, the macroH2A1 splice variant that is normally absent in cancer cells, is sufficient to induce senescence in normal cells with a quick SASP response and persistent ATM activation. Stress in the workplace has been shown to result in the development of reactive oxygen species that can cause DNA damage and ATM activation. During OIS in cells depleted of macroH2A1, we found that ER stress, assayed by the announcement of the unfolded protein response, is reduced. In addition, an activated ATM contributes to a reduced SASP expression in reaction to ER stress by triggering the deletion of macroH2A1 from SASP genes. Overall, our findings reveal that SASP gene expression is limited by a combination of actions of a positive feedback loop that includes macroH2A1 and a negative feedback loop in which ER stress leads to ATM activation that is crucial for the removal of macroH2A1 from SASP genes and subsequent repression.

Source link: https://doi.org/10.1158/1538-7445.am2015-1267


Abstract 1595: HMGA2 induces EMT in prostate cancer cells and may be antagonized by camalexin

Abstract Prostate cancer is the most commonly diagnosed cancer in men and the second leading cause of death in the United States. African American male men have the highest incidence and mortality rates of prostate cancer in comparison to every other ethnic group. EMT has been found to be induced by increased HMGA2 levels in prostate cancer, according to Loss of Let-7 miRNA. Camalexin treatment of prostate cancer cells increased ROS levels, which led to reduced cell proliferation and increased apoptosis. We speculate that HMGA2 could regulate EMT in part by inducing ROS and camalexin may antagonize HMGA2 signaling. By western blot analysis, we determined HMGA2 and EMT marker expression in a panel of prostate cancer cell lines. In LNCaP cells, we also transiently and stably overexpressed wild-type HMGA2 and mutant HMGA2. To determine HMGA2 expression, We treated ARCaP-M cells with different amounts of camalexin. HMGA2 is highly expressed in aggressive prostate cancer cell lines, according to RWPE1 and LNCaP cells, according to our findings. The transient overexpression of HMGA2 in LNCaP cells reduced E-cadherin more notably than with mutant HMGA2, but no change in ROS was observed in LNCaP cells. In conclusion, HMGA2 promotes EMT even more if its Let-7 suppressor binding web site is decommissioned, and camalexin may target HMGA2 to reduce prostate cancer progression. EMT is present in prostate cancer cells, and it can be antagonized by camalexin.

Source link: https://doi.org/10.1158/1538-7445.am2016-1595


The Neuroprotection Exerted by Memantine, Minocycline and Lithium, against Neurotoxicity of CSF from Patients with Amyotrophic Lateral Sclerosis, Is Antagonized by Riluzole

In primary cultures of rat embryo motor cortex neurons, cerebrospinal fluids from amyotrophic lateral sclerosis patients caused 20-30 percent loss of cell viability. We have extended this research to the interactions of riluzole with three other well-known neuroprotective agents, including memantine, minocycline, and lithium. By itself riluzole delivered neurotoxic results at 3-30 M u00b5 M u00b5 M; this cell damage was similar to that elicited by 30 u00b5 M glutamate and a 10% dilution of ALS/CSF; memantine, minocycline, and lithium provided 10-30% shield against ALS/CSF-elicited neurotoxicity, and at 1-10 M u00b5 M rilu00b5 M u00b5 M u00b5 M u00b5 M u00b5 M u00b5 M ed ted a u00b5 M amy u00b5 M afu00b5 M a u00b5 M e u00b5 M av. e et induced neurotoxic induced neurotoxic induced neurotoxicity; and u00b5 M u00b5 M nolicitedilu00b5 M u00b In future clinical trials of ALS patients with novel neuroprotective compounds, the inclusion of a group of patients free of riluzole therapy may be desirable in light of the latest findings.

Source link: https://doi.org/10.1159/000357281

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions