Long noncoding RNA MEG3 inhibits breast cancer growth via upregulating endoplasmic reticulum stress and activating NF‐κB and p53

2018 ◽  
Vol 120 (4) ◽  
pp. 6789-6797 ◽  
Author(s):  
Yan Zhang ◽  
Jiang Wu ◽  
Hong Jing ◽  
Gui Huang ◽  
Zhulei Sun ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Cancer Growth ◽  
Breast Cancer Growth

Baicalein inhibits breast cancer growth via activating a novel isoform of the long noncoding RNA PAX8‐AS1‐N

2018 ◽  
Vol 119 (8) ◽  
pp. 6842-6856 ◽  
Author(s):  
Xiaolan Yu ◽  
Yong Cao ◽  
Li Tang ◽  
Yingcheng Yang ◽  
Feng Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Cancer Growth ◽  
Breast Cancer Growth

scholarly journals Long noncoding RNA SNHG1 promotes TERT expression by sponging miR-18b-5p in breast cancer

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yujuan Kang ◽  
Lin Wan ◽  
Qin Wang ◽  
Yanling Yin ◽  
Jiena Liu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Malignant Tumors ◽  
Inhibitory Effect ◽  
Positive Role ◽  
Breast Cancer Growth ◽  
Tert Expression

Abstract Background Long noncoding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) plays a positive role in the progression of human malignant tumors. However, the molecular mechanism of SNHG1 remains elusive in breast cancer. Results LncRNA SNHG1 was upregulated and had a positive relationship with poor prognosis according to bioinformatics analysis in pan-cancer including breast cancer. Silencing SNHG1 inhibited tumorigenesis in breast cancer both in vitro and in vivo. Mechanistically, SNHG1 functioned as a competing endogenous RNA (ceRNA) to promote TERT expression by sponging miR-18b-5p in breast cancer. miR-18b-5p acted as a tumor repressor in breast cancer. Moreover, the combination of SNHG1 knockdown and TERT inhibitor administration showed a synergistic inhibitory effect on breast cancer growth in vivo. Finally, E2F1 as a transcription factor, binding to SNHG1 promoter and enhanced SNHG1 transcription in breast cancer. Conclusions Our results provide a comprehensive understanding of the oncogenic mechanism of lncRNA SNHG1 in breast cancer. Importantly, we identified a novel E2F1–SNHG1–miR-18b-5p–TERT axis, which may be a potential therapeutic target for breast cancer. Our results also provided a potential treatment for breast cancer when knockdown SNHG1 and TERT inhibitor administration simultaneously.

scholarly journals L-Ascorbic Acid Inhibits Breast Cancer Growth by Inducing IRE/JNK/CHOP-Related Endoplasmic Reticulum Stress-Mediated p62/SQSTM1 Accumulation in the Nucleus

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1351 ◽  
Author(s):  
Youn Kyung Choi ◽  
Jung-Il Kang ◽  
Sanghoon Han ◽  
Young Ree Kim ◽  
Jaemin Jo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Ascorbic Acid ◽  
Er Stress ◽  
Cancer Cells ◽  
Cancer Growth ◽  
Autophagic Flux ◽  
Sequestosome 1 ◽  
Breast Cancer Growth

Anticancer effects of L-ascorbic acid (Vitamin C, L-AA) have been reported in various types of cancers. L-AA intake reduces breast cancer recurrence and mortality; however, the role of L-AA in the treatment of breast cancer remains poorly understood. In this study, we investigated the effect and mechanism action of L-AA on breast cancer growth. L-AA inhibited the growth of breast cancer cells by inducing apoptotic cell death at the evaluated treatment concentrations without affecting normal cells. Moreover, L-AA induces autophagosome formation via regulation of mammalian target of rapamycin (mTOR), Beclin1, and autophagy-related genes (ATGs) and increased autophagic flux. Notably, we observed that L-AA increased p62/SQSTM1 (sequestosome 1) protein levels. Accumulation of p62 protein in cancer cells in response to stress has been reported, but its role in cancer regulation remains controversial. Here, we demonstrated that L-AA-induced p62 accumulation is related to L-AA-induced breast cancer growth inhibition. Furthermore, L-AA induced endoplasmic reticulum (ER) stress via the IRE–JNK–CHOP (inositol-requiring endonuclease–c-Jun N-terminal kinase–C/EBP homologous protein) signaling pathways, which increased the nuclear levels of p62/SQSTM1. These findings provide evidence that L-AA-induced ER stress could be crucial for p62 accumulation-dependent cell death, and L-AA can be useful in breast cancer treatment.

Combined Treatment with Exendin-4 and Metformin Attenuates Breast Cancer Growth

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1227-P
Author(s):  
CHIKAYO IWAYA ◽  
TAKASHI NOMIYAMA ◽  
TAKAKO KAWANAMI ◽  
YURIKO HAMAGUCHI ◽  
TOMOKO TANAKA ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Combined Treatment ◽  
Cancer Growth ◽  
Breast Cancer Growth
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