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Cited by 4 publications
(5 citation statements)
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References 6 publications
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“…Due to proteotoxic stress produced in cancer cells by ROS and mutations which hamper the correct folding of proteins, the mtUPR is activated. It was demonstrated that ATF5 was upregulated in a wide range of cancers [ 168 ], such as lung cancer [ 169 ], pancreatic cancer [ 170 ], and carcinomas [ 171 ], including ovarian cancer [ 172 ], rectal cancer [ 173 ], leukemia [ 174 ], neural tumors [ 175 , 176 ], esophageal cancer [ 177 ], or astrocytoma [ 178 ]. Furthermore, ATF5 activation produced resistance to radiotherapy [ 168 ] and increased the invasiveness of cancer cells [ 179 ].…”
Section: Mtupr In Primary and Secondary Mitochondrial Diseasesmentioning
confidence: 99%
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“…Due to proteotoxic stress produced in cancer cells by ROS and mutations which hamper the correct folding of proteins, the mtUPR is activated. It was demonstrated that ATF5 was upregulated in a wide range of cancers [ 168 ], such as lung cancer [ 169 ], pancreatic cancer [ 170 ], and carcinomas [ 171 ], including ovarian cancer [ 172 ], rectal cancer [ 173 ], leukemia [ 174 ], neural tumors [ 175 , 176 ], esophageal cancer [ 177 ], or astrocytoma [ 178 ]. Furthermore, ATF5 activation produced resistance to radiotherapy [ 168 ] and increased the invasiveness of cancer cells [ 179 ].…”
Section: Mtupr In Primary and Secondary Mitochondrial Diseasesmentioning
confidence: 99%
“…It was demonstrated that ATF5 was upregulated in a wide range of cancers [ 168 ], such as lung cancer [ 169 ], pancreatic cancer [ 170 ], and carcinomas [ 171 ], including ovarian cancer [ 172 ], rectal cancer [ 173 ], leukemia [ 174 ], neural tumors [ 175 , 176 ], esophageal cancer [ 177 ], or astrocytoma [ 178 ]. Furthermore, ATF5 activation produced resistance to radiotherapy [ 168 ] and increased the invasiveness of cancer cells [ 179 ]. In addition, Hsp60 was also upregulated in several types of cancers [ 180 ], including mammary [ 181 ] and ovarian [ 182 ] carcinoma, prostate cancer [ 183 ], glioblastoma [ 184 ] and neuroblastoma [ 185 ], and colorectal [ 186 ], gastric [ 187 ] and pancreatic cancer [ 188 ] and this phenomenon is associated with reduced patient survival.…”
Section: Mtupr In Primary and Secondary Mitochondrial Diseasesmentioning
confidence: 99%
“…ATF5 also regulates growth and metabolism coordination factors, such as EGR1, mTOR and FGF21, as well as mitochondrial protection genes. 134 , 135 , 136 In addition to the growth-promoting and antiapoptotic phenotype, ATF5 also enhances the resistance to radiotherapy 137 and the invasiveness of tumour cells by inducing integrin-α 2 and integrin-β 1 . 138 …”
Section: Atf5mentioning
confidence: 99%
“…However, to our knowledge, a specific role for the UPR mt in cancer biology has not been explicitly examined. In principle, the UPR mt could promote cell growth and survival by ensuring mitochondrial function in the presence of mitochondrial stress related to cancer cell physiology or mutation accumulation, or influencing cancer cell metabolism, growth and inflammatory signaling, or responses to therapeutic agents perceived by the cell as xenobiotics [81, 82]. In this section, we review recent findings that suggest functions for UPR mt regulatory components as well as transcriptional outputs in cancer cell growth and survival.…”
Section: The Uprmt and Cancermentioning
confidence: 99%
“…ATF5 also regulates growth and metabolism coordinating factors such as EGR1, mTOR and FGF21, as well as the mitochondrial-protective genes outlined above [59, 101103]. In addition to pro-growth and anti-apoptotic phenotypes, ATF5 contributes the resistance to radiotherapy [81] and the invasiveness of tumor cells by inducing integrin-α2 and integrin-β1 [96]. …”
Section: The Uprmt and Cancermentioning
confidence: 99%