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Fig. 5 | Journal of Hematology & Oncology

Fig. 5

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

Fig. 5

LncRNAs regulate the tumor characteristics apoptosis (a), invasion and metastasis (b), and metabolism (c) by regulating the UPR. a FOXD3-AS1 could competitively bind to let-7e-5p to regulate RCN1. Silencing FOXD3-AS1 or upregulating let-7e-5p increased the expression profiles of GRP78, CHOP, and ATF4, consequently promoting ER stress-induced apoptosis. MEG3 increased the expression of ER stress-related proteins, including GRP78, IRE1, PERK, ATF6, and CHOP, consequently inhibiting growth and induce the apoptosis of cancer cells. In addition, MEG3 competitively combines with miR-7-5p or miR-103a-3p to promote ER stress-mediated apoptosis. Ectopic expression of lincRNA-p21 activates ER stress by inducing the expression of IRE1, CHOP, and GRP78 and upregulating the PERK phosphorylation level. Sorafenib also could increase the expression of lincRNA-p21 to induce ER stress-mediated apoptosis. Overexpression of CASC2 increases the stability of PERK mRNA, which triggers the PERK/eIF2α/CHOP pathway and promotes radiation-induced apoptosis. b NORAD may act as a sponge for miR‐205 and reduce the transcriptional repression of the miR-205 target gene EGLN2. NORAD silencing can inhibit UPR-related gene expression including that of GRP78, CHOP, and eIF2α. Downregulation of NORAD also restrained malignant melanoma cell migration and invasion. Overexpression of NEAT1 promote expression of the UPR-related proteins IRE1, XBP-1, and CHOP. Resveratrol attenuates the effects of NEAT1 on inducing ER stress. LUCRC can regulate Bip expression and induce the splicing of XBP1 from XBP1u (unspliced) to XBP1s (spliced), resulting in activation of UPR to promote tumor progression. c OR3A4 functions as a sponge for miR-1207-5p, modulating the target gene glucose-6-phosphate dehydrogenase (G6PD). Knockdown of OR3A4 inhibits the expression of G6PD, blocks the pentose phosphate pathway, and significantly reduces the level of nicotinamide adenine dinucleotide phosphate (NADPH). This abnormal metabolic pathway upregulates the redox state content, which increases the expression of PERK and IRE1 in osteosarcoma cells

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