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Fig. 3 | Journal of Hematology & Oncology

Fig. 3

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

Fig. 3

MiRNAs regulate tumor characteristics including apoptosis, invasion, EMT, and metastasis by regulating the UPR. a MiR-657 mimics can attenuate the CHOP expression to reverse apoptosis. Anticancer compounds downregulate the expression of miR-211 in U937 and U266 cells. The downregulated miR-211 is associated with CHOP and triggers tumor cell apoptosis. MiR-34c overexpression significantly increased the levels of eIF2α and IRE1α by directly targeting the 3ʹUTR of HMGB1 and inhibiting HMGB1 translation, promoting apoptosis. The expression of miR-216b directly targets c-JUN and inhibition of c-JUN sensitizes cells to apoptosis. MiR-451a increases apoptosis by suppressing BAP31 to induce ER stress. MiR-233 downregulates the heat shock protein 70 (Hsp70) protein levels and downstream JNK/JUN signaling pathways, thereby enhancing apoptosis. JUN can bind to the promoter region of miR-223 to promote its transcription, forming a feedback loop. b Some chemotherapy drugs activate the PERK pathway by upregulating the expression levels of SNAI1 and ZEB1. LAMP3 is regulated by activation of the PERK/eIF2a/ATF4 arm of the UPR to promote lymph node metastasis. CHOP induced by PERK- eIF2α can bind to GDF15 and activate its transcription, regulating EMT and metastasis. MiR-410 directly targets ERLIN2 to up-regulate UPR components to inhibit the migration, invasion, and EMT of breast cancer cells. MiR-224/-520c-dependent TUSC3 deletion enhances NSCLC metastasis via increased ATF6α activity

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