scholarly journals SIN1 promotes the proliferation and migration of breast cancer cells by Akt activation

2016 ◽  
Vol 36 (6) ◽  
Author(s):  
Deqiang Wang ◽  
Ping Wu ◽  
Hui Wang ◽  
Lei Zhu ◽  
Wei Zhao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Tumour Growth ◽  
Human Breast Cancer Cell ◽  
Human Breast ◽  
And Migration ◽  
Proliferation And Migration

Stress-activated protein kinase (SAPK) interacting protein 1 (SIN1) is an essential TORC2 component and a key regulator of Akt pathway that plays an important role in various pathological conditions including cancer. Whereas its functional role in breast cancer has not been well characterized. In the present study, SIN1 is associated with the progression and survival of breast cancer patients, as well as human breast cancer cell proliferation and migration. SIN1 mRNA level was significantly up-regulated in human breast cancer samples compared with their corresponding paracancerous histological normal tissues. Furthermore, the expression levels of SIN1 were also increased in three human breast cancer cell lines compared with human breast epithelial cell MCF10A. Overexpression of SIN1 promoted cell proliferation, colony formation and migration of breast cancer cells. Knockdown of SIN1 in MDA-MB-468 cells inhibited cell proliferation, colony formation and migration. In addition, SIN1 overexpression increased phosphorylation of Akt and knockdown of SIN1 inhibited phosphorylation of Akt in MDA-MB-468 cells. In a tumour xenograft model, overexpression of SIN1 promoted tumour growth of MDA-MB-468 cells in vivo, whereas SIN1 knockdown inhibits the tumour growth. Taken together, our results reveal that SIN1 plays an important role in breast cancer and SIN1 is a potential biomarker and a promising target in the treatment of breast cancer.

scholarly journals tRNA Queuosine Modification Enzyme Modulates the Growth and Microbiome Recruitment to Breast Tumors

Cancers ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 628
Author(s):  
Jilei Zhang ◽  
Rong Lu ◽  
Yongguo Zhang ◽  
Żaneta Matuszek ◽  
Wen Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
And Migration

Background: Transfer RNA (tRNA) queuosine (Q)-modifications occur specifically in 4 cellular tRNAs at the wobble anticodon position. tRNA Q-modification in human cells depends on the gut microbiome because the microbiome product queuine is required for its installation by the enzyme Q tRNA ribosyltransferase catalytic subunit 1 (QTRT1) encoded in the human genome. Queuine is a micronutrient from diet and microbiome. Although tRNA Q-modification has been studied for a long time regarding its properties in decoding and tRNA fragment generation, how QTRT1 affects tumorigenesis and the microbiome is still poorly understood. Results: We generated single clones of QTRT1-knockout breast cancer MCF7 cells using Double Nickase Plasmid. We also established a QTRT1-knockdown breast MDA-MB-231 cell line. The impacts of QTRT1 deletion or reduction on cell proliferation and migration in vitro were evaluated using cell culture, while the regulations on tumor growth in vivo were evaluated using a xenograft BALB/c nude mouse model. We found that QTRT1 deficiency in human breast cancer cells could change the functions of regulation genes, which are critical in cell proliferation, tight junction formation, and migration in human breast cancer cells in vitro and a breast tumor mouse model in vivo. We identified that several core bacteria, such as Lachnospiraceae, Lactobacillus, and Alistipes, were markedly changed in mice post injection with breast cancer cells. The relative abundance of bacteria in tumors induced from wildtype cells was significantly higher than those of QTRT1 deficiency cells. Conclusions: Our results demonstrate that the QTRT1 gene and tRNA Q-modification altered cell proliferation, junctions, and microbiome in tumors and the intestine, thus playing a critical role in breast cancer development.

scholarly journals Macrophage conditioned media promotes adipocyte cancer-association, which in turn stimulates breast cancer proliferation and migration

2020 ◽  
Author(s):  
Karin A. Vallega ◽  
Dale B. Bosco ◽  
Yi Ren ◽  
Qing-Xiang Sang
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Conditioned Media ◽  
Human Breast ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Breast cancer is the most common cancer in women and the leading cause of female cancer deaths worldwide. Obesity causes chronic inflammation and is a risk factor for post-menopausal breast cancer and poor prognosis. Obesity is known to trigger increased infiltration of macrophages into adipose tissue, yet little research has focused on the effects of macrophages in the early stages of breast tumor development in obese patients. In this study, the effects of pro-inflammatory macrophages on breast cancer-adipocyte crosstalk were investigated. Methods An innovative human cell co-culture system was used to model the paracrine interactions among adipocytes, macrophages, and breast cancer cells, and how they can facilitate tumor progression. The effects on human breast cancer cells were examined using cell counts and migration assays. Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) was used to measure the expression levels of several cytokines and proteases to analyze adipocyte cancer-association. Results Macrophage conditioned media intensified the effects of breast cancer-adipocyte crosstalk. More specifically, adipocytes became delipidated and increased production of pro-inflammatory cytokines, even in the absence of breast cancer cells, although the expression levels were highest with all three cell components. As a result, co-cultured breast cancer cells became more aggressive, with increased proliferation and migration potential when compared to adipocyte-breast cancer cell co-cultures treated with unconditioned media. Conclusions Macrophage conditioned media promotes adipocyte cancer-association and production of pro-inflammatory factors. These macrophage-adipocyte paracrine interactions promote human breast cancer cell proliferation and migration. Thus, macrophages may contribute to adipocyte inflammation and cancer-association and promote breast cancer progression.

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