<scp>ER</scp> stress‐related <scp>ATF</scp>6 upregulates <scp>CIP</scp>2A and contributes to poor prognosis of colon cancer

Liu, Chun Yu; Hsu, Chia Chi; Huang, Tzu Ting; Lee, Chia-Han; Chen, Ji Lin; Yang, Shung Haur; Jiang, Jeng Kai; Chen, Wei Shone; Lee, Kuan Der; Teng, Hao Wei

doi:10.1002/1878-0261.12365

Cited by 49 publications

(26 citation statements)

References 43 publications

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“…Due to the major pro-survival role of ATF6, its expression level has been shown to be significantly upregulated in various cancer types [63][64][65][66]. Higher expression level of ATF6 has been closely correlated with cancer metastasis and recurrence [67,68] and served as a prognostic indicator of cancer [69]. For instance, ER stress-related ATF6 upregulated cancerous inhibitor of protein phosphatase 2A (CIP2A), which contributes to colon cancer cell survival and indicates a trend toward poor prognosis [69].…”

Section: Atf6α Pathwaymentioning

confidence: 99%

Interplay between endoplasmic reticulum stress and non-coding RNAs in cancer

Zhao

Zeng

2020

J Hematol Oncol

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To survive, cancer cells are subjected to various internal and external adverse factors, including genetic mutations, hypoxia, nutritional deficiencies, and drug toxicity. All of these factors result in the accumulation of unfolded proteins in the endoplasmic reticulum, which leads to a condition termed endoplasmic reticulum stress (ER stress) and triggers the unfolded protein response (UPR). UPR downstream components strictly control transcription and translation reprogramming to ensure selective gene expression, including that of non-coding RNA (ncRNAs), to adapt to adverse environments. NcRNAs, including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), play important roles in regulating target gene expression and protein translation, and their aberrant expression is related to tumor development. Dysregulation of ncRNAs is involved in the regulation of various cellular characteristics of cancer cells, including growth, apoptosis, metastasis, angiogenesis, drug sensitivity, and tumor stem cell properties. Notably, ncRNAs and ER stress can regulate each other and collaborate to determine the fate of tumor cells. Therefore, investigating the interaction between ER stress and ncRNAs is crucial for developing effective cancer treatment and prevention strategies. In this review, we summarize the ER stress-triggered UPR signaling pathways involved in carcinogenesis followed by the mutual regulation of ER stress and ncRNAs in cancer, which provide further insights into the understanding of tumorigenesis and therapeutic strategies.

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Section: Atf6α Pathwaymentioning

confidence: 99%

Interplay between endoplasmic reticulum stress and non-coding RNAs in cancer

Zhao

Zeng

2020

J Hematol Oncol

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“…GP96 is also upregulated in primary lymphomas caused by Marek’s disease virus, a pathology found in chickens that is used as a model for lymphomas that express Hodgkin’s disease antigen CD30 [131,132,133]. ATF6 promotes Xbp-1 and GP96 [14,58] expression, and ATF6 expression correlates with poor prognosis in a number of cancers [134,135]. However, it remains to be determined if ATF6 can directly influence T cell function in tumor immunity.…”

Section: Upr T Cells and Diseasementioning

confidence: 99%

Stressed: The Unfolded Protein Response in T Cell Development, Activation, and Function

Kemp

Poe

2019

IJMS

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The unfolded protein response (UPR) is a highly conserved pathway that allows cells to respond to stress in the endoplasmic reticulum caused by an accumulation of misfolded and unfolded protein. This is of great importance to secretory cells because, in order for proteins to traffic from the endoplasmic reticulum (ER), they need to be folded appropriately. While a wealth of literature has implicated UPR in immune responses, less attention has been given to the role of UPR in T cell development and function. This review discusses the importance of UPR in T cell development, homeostasis, activation, and effector functions. We also speculate about how UPR may be manipulated in T cells to ameliorate pathologies.

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“…Some studies ascertained that ER stress was correction with CRC progression. ER stress-related ATF6 upregulated cancerous inhibitor of protein phosphatase 2A contributing to poor prognosis of colon cancer (20). ATF6 induced intestinal dysbiosis to promote colorectal tumorigenesis through innate immune response (21).…”

Section: Discussionmentioning

confidence: 99%

Thapsigargin promotes colorectal cancer cell migration through upregulation of lncRNA MALAT1

Jiang

Wang

et al. 2020

Oncol Rep

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Colorectal cancer (CRC) is the third most common tumor in the world; however, the role and mechanism of endoplasmic reticulum (ER) stress in CRC metastasis remains largely unclear. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA (lncRNA), which has previously been associated with CRC metastasis. It has been suggested that ER stress pathways regulate lncRNA expression; however, the effect of ER stress on MALAT1 expression in cancer is unknown. The present study aimed to investigate the relationship between ER stress pathways, MALAT1 expression and cell migration in CRC cells. ER stress was induced by thapsigargin (TG); low dose TG induced the migration of HT29 and HCT116 cells, but not SW1116 and SW620 cells. This effect was associated with increased expression levels of MALAT1, as the knockdown of MALAT1 prevented TG-induced cell migration. TG-induced MALAT1 expression was associated with inositol-requiring enzyme 1 (IRE1) expression and activation of the protein kinase R (PKR)-like ER kinase (PERK) signaling pathway. X-box-binding protein 1 (XBP1) and activating transcription factor 4 (ATF4) binding sites were predicted to be located in the MALAT1 gene promoter regions and the expression of MALAT1 was positively associated with XBP1 and ATF4 expression levels in CRC tissue samples. Thus, these findings indicated that ER stress may promote the migration of CRC cells and contribute to the progression of CRC through the activation of the IRE1/XBP1 and PERK/eIF2α/ATF4 signaling pathways. In conclusion, to the best of our knowledge, this study is the first report that lncRNA MALAT1 expression is regulated by the IRE1/XBP1 pathway in CRC.

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ER stress‐related ATF6 upregulates CIP2A and contributes to poor prognosis of colon cancer

Cited by 49 publications

References 43 publications

Interplay between endoplasmic reticulum stress and non-coding RNAs in cancer

Interplay between endoplasmic reticulum stress and non-coding RNAs in cancer

Stressed: The Unfolded Protein Response in T Cell Development, Activation, and Function

Thapsigargin promotes colorectal cancer cell migration through upregulation of lncRNA MALAT1

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