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• W4283171745 endingPage "5115" @default.
• W4283171745 startingPage "5097" @default.
• W4283171745 abstract "Calreticulin (CRT) is located in the endoplasmic reticulum (ER), it helps proteins fold correctly inside the ER, and acts as a modulator of Ca2+ homeostasis. Aberrant expression of CRT is implicated in several cancer types, qualifying CRT as a potential therapeutic target. However, it remains unclear how CRT affects specific oncogenic pathways. In this study, we used histone deacetylase inhibitors (HDACis) to establish drug-resistant liver cancer cells and further analyzed the molecular mechanism of development of drug resistance in those cells. The 2D gel electrophoresis and RT-PCR data showed that CRT was downregulated in HDACis-resistant cells by comparing with HA22T parental cells. We previously elucidated the development of drug-resistance in HCC cells via activation of PP1-eIF2α pathway, but not via ER stress pathway. Here, we show that thapsigargin induced ER stress through mechanism other than ER stress downstream protein GRP78-PERK to regulate CRT expression in HDACis-R cells. Moreover, the expression level of CRT was not the main cause of apoptosis in HDACis-resistant cells. Mechanistic studies identified the apoptosis factors in the nucleus—the HDACis-mediated overexpression of CRT, CRT translocation to the cell nucleus, and reduced CaM/CaMKII/CREB pathway—that led to chemosensitivity in HDACis-R HCC cells." @default.
• W4283171745 created "2022-06-21" @default.
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• W4283171745 date "2022-06-20" @default.
• W4283171745 modified "2023-09-23" @default.
• W4283171745 title "Calreticulin nuclear translocalization alleviates CaM/CaMKII/CREB signaling pathway to enhance chemosensitivity in HDAC inhibitor-resistant hepatocellular carcinoma cells" @default.
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• W4283171745 doi "https://doi.org/10.18632/aging.204131" @default.
• W4283171745 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35724265" @default.
• W4283171745 hasPublicationYear "2022" @default.

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