Knockdown of REV7 Inhibits Breast Cancer Cell Migration and Invasion

REV7 (also known as MAD2L2) is a multifunctional protein involved in DNA damage tolerance, cell cycle regulation, gene expression, and carcinogenesis. Although its expression is reportedly associated with poor prognosis in several kinds of human cancers, the significance of REV7 expression in breast malignancies is unclear. In this study, REV7 was found to be increased in breast cancer. We found that knockdown of REV7 inhibited the migration, invasion, and epithelial‐mesenchymal transition (EMT) of breast cancer cells. Meanwhile, overexpression of REV7 promoted the migration, invasion, and EMT of breast cancer cells. As shown by Western blot, knockdown of REV7 can promote TGF-β1 expression. Western blot analysis indicated that TGF-β1 may play a role as a downstream factor of REV7. Moreover, interference of TGF-β1 can also inhibit the cell’s ability for migration, invasion, and EMT, as well as in a cell line whose REV7 is overexpressed. Taken together, these results contributed to a recognition of the oncogene functions of REV7 in breast cancer cells and provided a novel direction to treat breast cancer.

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Activation of NF-κB by TOPK upregulates Snail/Slug expression in TGF-β1 signaling to induce epithelial-mesenchymal transition and invasion of breast cancer cells

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2020.07.015 ◽

2020 ◽

Vol 530 (1) ◽

pp. 122-129 ◽

Cited By ~ 1

Author(s):

Young-Ju Lee ◽

Jung-Hwan Park ◽

Sang-Muk Oh

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Breast Cancer Cells ◽

Epithelial Mesenchymal Transition ◽

Mesenchymal Transition ◽

Slug Expression ◽

Tgf Β1

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STAT3 Targets ERR-α to Promote Epithelial–Mesenchymal Transition, Migration, and Invasion in Triple-Negative Breast Cancer Cells

Molecular Cancer Research ◽

10.1158/1541-7786.mcr-18-1194 ◽

2019 ◽

Vol 17 (11) ◽

pp. 2184-2195 ◽

Cited By ~ 6

Author(s):

Jia-Hui Ma ◽

Jie Qi ◽

Shi-Qi Lin ◽

Cai-Yun Zhang ◽

Fang-yuan Liu ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Triple Negative Breast Cancer ◽

Breast Cancer Cells ◽

Triple Negative ◽

Epithelial Mesenchymal Transition ◽

Migration And Invasion ◽

Mesenchymal Transition

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miR-29a contributes to breast cancer cells epithelial–mesenchymal transition, migration, and invasion via down-regulating histone H4K20 trimethylation through directly targeting SUV420H2

Cell Death and Disease ◽

10.1038/s41419-019-1437-0 ◽

2019 ◽

Vol 10 (3) ◽

Cited By ~ 15

Author(s):

You Wu ◽

Wanyue Shi ◽

Tingting Tang ◽

Yidong Wang ◽

Xin Yin ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Breast Cancer Cells ◽

Epithelial Mesenchymal Transition ◽

Migration And Invasion ◽

Mesenchymal Transition

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FL118, a novel camptothecin analogue, suppressed migration and invasion of human breast cancer cells by inhibiting epithelial-mesenchymal transition via the Wnt/β-catenin signaling pathway

BioScience Trends ◽

10.5582/bst.2017.01288 ◽

2018 ◽

Vol 12 (1) ◽

pp. 40-46 ◽

Cited By ~ 8

Author(s):

Zhihong Yang ◽

Lixia Ji ◽

Guohui Jiang ◽

Ranran Liu ◽

Zhantao Liu ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Human Breast Cancer ◽

Breast Cancer Cells ◽

Epithelial Mesenchymal Transition ◽

Migration And Invasion ◽

Human Breast Cancer Cells ◽

Human Breast ◽

Mesenchymal Transition ◽

Camptothecin Analogue

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RAGE-binding S100A8/A9 promotes the migration and invasion of human breast cancer cells through actin polymerization and epithelial–mesenchymal transition

Breast Cancer Research and Treatment ◽

10.1007/s10549-013-2737-1 ◽

2013 ◽

Vol 142 (2) ◽

pp. 297-309 ◽

Cited By ~ 52

Author(s):

Chonggao Yin ◽

Hongli Li ◽

Baogang Zhang ◽

Yuqing Liu ◽

Guohua Lu ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Human Breast Cancer ◽

Breast Cancer Cells ◽

Actin Polymerization ◽

Epithelial Mesenchymal Transition ◽

Migration And Invasion ◽

Human Breast Cancer Cells ◽

Human Breast ◽

Mesenchymal Transition

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Cancer-associated fibroblast-derived exosomal miR-18b promotes breast cancer invasion and metastasis by regulating TCEAL7

Cell Death and Disease ◽

10.1038/s41419-021-04409-w ◽

2021 ◽

Vol 12 (12) ◽

Author(s):

Ziqian Yan ◽

Zhimei Sheng ◽

Yuanhang Zheng ◽

Ruijun Feng ◽

Qinpei Xiao ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Cancer Progression ◽

Breast Cancer Cells ◽

Epithelial Mesenchymal Transition ◽

Xenograft Model ◽

Migration And Invasion ◽

Invasion And Metastasis ◽

Mesenchymal Transition ◽

Mouse Xenograft Model

AbstractStudies have shown that cancer-associated fibroblasts (CAFs) play an irreplaceable role in the occurrence and development of tumors. Therefore, exploring the action and mechanism of CAFs on tumor cells is particularly important. In this study, we compared the effects of CAFs-derived exosomes and normal fibroblasts (NFs)-derived exosomes on breast cancer cells migration and invasion. The results showed that exosomes from both CAFs and NFs could enter into breast cancer cells and CAFs-derived exosomes had a more enhancing effect on breast cancer cells migration and invasion than NFs-derived exosomes. Furthermore, microRNA (miR)-18b was upregulated in CAFs-derived exosomes, and CAFs-derived exosomes miR-18b can promote breast cancer cell migration and metastasis by specifically binding to the 3′UTR of Transcription Elongation Factor A Like 7 (TCEAL7). The miR-18b-TCEAL7 pathway promotes nuclear Snail ectopic activation by activating nuclear factor-kappa B (NF-κB), thereby inducing epithelial-mesenchymal transition (EMT) and promoting cell invasion and metastasis. Moreover, CAFs-derived exosomes miR-18b could promote mouse xenograft model tumor metastasis. Overall, our findings suggest that CAFs-derived exosomes miR-18b promote nuclear Snail ectopic by targeting TCEAL7 to activate the NF-κB pathway, thereby inducing EMT, invasion, and metastasis of breast cancer. Targeting CAFs-derived exosome miR-18b may be a potential treatment option to overcome breast cancer progression.

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