Table 2 Non-coding RNAs implicated in endoplasmic reticulum stress in breast cancer

lncRNA MEG3

MEG3 overexpression increases the expression of endoplasmic reticulum stress-related proteins involved in the unfolded protein response, including GRP78, IRE1, PERK, and ATF6. It also upregulates proapoptotic proteins CHOP and caspase-3. Additionally, MEG3 overexpression enhances NF-κB expression, its translocation to the nucleus, and p53 expression

In vitro–In vivo

[7]

lncRNA MIAT

5-FU-induced endoplasmic reticulum stress increases the expression of GRP78 in MCF-7 cells. GRP78 could positively regulate the expression of MIAT and AKT through upregulating OCT4, thereby contributing to 5-FU resistance in BC cells. Additionally, the function of GRP78 silencing in promoting tumor cell sensitivity has been confirmed in vivo

In vitro–in vivo

[76]

lncRNAs CASC2, LINC00299, NEAT1

The association between the expression of lncRNAs CASC2, LINC00299, NEAT1, and the XBP1s/u ratio suggests that these lncRNAs have the potential to act as regulators of the unfolded protein response pathway in breast cancer

In vitro

[77]

miR-27a-3p

Endoplasmic reticulum stress promotes the secretion of exosomes, which contain elevated levels of miR-27a-3p. These exosomes are taken up by macrophages, leading to increased expression of miR-27a-3p and PD-L1 in macrophages. miR-27a-3p targets and negatively regulates MAGI2, while MAGI2 down-regulates PD-L1 by up-regulating PTEN, thereby inactivating the PI3K/AKT signaling pathway. The presence of exosomal miR-27a-3p reduces CD4+ and CD8+ T cells, IL-2 production, and promotes T cell apoptosis when macrophages and CD3+ T cells are co-cultured

In vitro

[78]

miR-3607, miR-374a, and miR-96

IRE1, a gene that frequently amplifies and overexpresses in aggressive luminal B breast cancer cells, is associated with worse overall survival. It mediates the degradation of tumor suppressor microRNAs including miR-3607, miR-374a, and miR-96 through Regulated IRE1-Dependent Decay (RIDD). Degradation of miR-3607 leads to elevated levels of RAB3B, a RAS oncogene GTPase, in breast cancer cells. Inhibiting IRE1 effectively suppresses proliferation and aggressive phenotypes in luminal breast cancer cells

In vitro

[79]

miR-153

Hypoxia-induced endoplasmic reticulum stress activates IRE1α and XBP1, leading to the upregulation of miR-153 expression. miR-153 is involved in fine-tuning the HIF1α/VEGFA axis in breast cancer angiogenesis. It directly binds to the promoter of the miR-153 host gene PTPRN, activating its transcription

In vitro–in vivo

[80]

miR-616-5p and miR-616-3p

In human breast cancer, the expression of miR-616 and its host gene CHOP is downregulated. During endoplasmic reticulum stress, both arms of miR-616 (miR-616-5p and miR-616-3p) are increased through the PERK pathway. Ectopic expression of miR-616 suppresses cell proliferation and colony formation, while knockout of miR-616 increases it. MiR-616 represses c-MYC expression by binding to its protein coding region. This repression of c-MYC by miR-616 leads to growth inhibition of cells

In vitro

[81]