scholarly journals Over expression of PTEN induces apoptosis and prevents cell proliferation in breast cancer cells

2020 ◽  
Author(s):  
Jinfeng Wu ◽  
Hong Gao ◽  
Wanyu Ge ◽  
Jie He
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Suppressive Effect ◽  
Logarithmic Growth Phase ◽  
Over Expression ◽  
Tensin Homolog ◽  
Apoptosis Pathways ◽  
And Migration

The phosphatase and tensin homolog (PTEN) is a tumor suppressor lipid phosphatase frequently mutated or deleted in breast cancer cells. Loss of PTEN is associated with aberrant activation of P13K/AKT signaling pathways, which are responsible for uncontrolled cell cycle, migration and prolonged survival. Therefore, stability and functional PTEN is essential for prevention of cancer growth and migration. In the present study, we have determined the effect of PTEN over expression in apoptosis induction and cell proliferation in breast cancer cells. We showed that PTEN over expression significantly declined the cell proliferation rate during logarithmic growth phase. Furthermore, the PTEN over expression leads to the activation of mitochondrial based intrinsic apoptosis pathways, which is confirmed by the activation and over expression of caspases 9 and caspases 3. In addition, the number of apoptotic cells are significantly more in PTEN over expressed cells, where they showed more apoptotic bodies in AO-EtBr and Hoechst 33344 staining. Finally, PTEN over expressed cells showed decreased chemo resistance as chemotherapeutic drugs kill them efficiently. Therefore, our findings suggest that tumor suppressive effect of PTEN is crucial for cancer prevention and thus PTEN might be a potential target for anti-cancer drugs.

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 MiR-92b-3p Inhibits Proliferation of HER2-Positive Breast Cancer Cell by Targeting circCDYL

2021 ◽  
Vol 9 ◽  
Author(s):  
Gehao Liang ◽  
Yun Ling ◽  
Qun Lin ◽  
Yu Shi ◽  
Qing Luo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Biological Function ◽  
Breast Cancer Tissue ◽  
Cancer Tissue ◽  
Breast Cancer Patients ◽  
Her2 Positive ◽  
Over Expression

ObjectivesCircular RNA (circRNA) is a novel class of RNA, which exhibits powerful biological function in regulating cellular fate of various tumors. Previously, we had demonstrated that over-expression of circRNA circCDYL promoted progression of HER2-negative (HER2–) breast cancer via miR-1275-ULK1/ATG7-autophagic axis. However, the role of circCDYL in HER2-positive (HER2+) breast cancer, in particular its role in modulating cell proliferation, one of the most important characteristics of cellular fate, is unclear.Materials and methodsqRT-PCR and in situ hybridization analyses were performed to examine the expression of circCDYL and miR-92b-3p in breast cancer tissues or cell lines. The biological function of circCDYL and miR-92b-3p were assessed by plate colony formation and cell viability assays and orthotopic animal models. In mechanistic study, circRNAs pull-down, RNA immunoprecipitation, dual luciferase report, western blot, immunohistochemical and immunofluorescence staining assays were performed.ResultsCircCDYL was high-expressed in HER2+ breast cancer tissue, similar with that in HER2– breast cancer tissue. Silencing HER2 gene had no effect on expression of circCDYL in HER2+ breast cancer cells. Over-expression of circCDYL promoted proliferation of HER2+ breast cancer cells but not through miR-1275-ULK1/ATG7-autophagic axis. CircRNA pull down and miRNA deep-sequencing demonstrated the binding of miR-92b-3p and circCDYL. Interestingly, circCDYL did not act as miR-92b-3p sponge, but was degraded in miR-92b-3p-dependent silencing manner. Clinically, expression of circCDYL and miR-92b-3p was associated with clinical outcome of HER2+ breast cancer patients.ConclusionMiR-92b-3p-dependent cleavage of circCDYL was an essential mechanism in regulating cell proliferation of HER2+ breast cancer cells. CircCDYL was proved to be a potential therapeutic target for HER2+ breast cancer, and both circCDYL and miR-92b-3p might be potential biomarkers in predicting clinical outcome of HER2+ breast cancer patients.

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 M2 macrophages contribute to cell proliferation and migration of breast cancer

2020 ◽  
Author(s):  
Daoyuan Tu ◽  
Jin Dou ◽  
Mingkao Wang ◽  
Haiwen Zhuang ◽  
Xiaoyu Xiaoyu
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Breast Cancer Cells ◽  
M2 Macrophage ◽  
M2 Macrophages ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background: Breast cancer is a kind of malignant tumor that severely threatens women’s health and life worldwide. Macrophages have been reported to mediate tumor progression, while the potential mechanism still needs further identification.Methods: Human monocytic cell line THP-1 was used to induce M2-macrophage. Real-time PCR and western blot were performed to determine gene expression in mRNA and protein level, respectively. Cell proliferation was determined using MTT assays, while cell migration was detected based on the scratch wound healing assays.Results: The supernatant medium of M2-macrophages incubated breast cancer cells showed increased cell proliferation and reduced expression of IRF-7. Overexpression of IRF-7 reversed the increased level of M2-macrophage induced cell proliferation and migration. The supernatant medium of M2-macrophages incubation promoted miR-1587 expression in breast cancer cells. miR-1587 overexpression promoted cell proliferation and migration of breast cancer. In addition, miR-1587 knockdown suppressed cell proliferation and migration that induced by M2-macrophages. miR-1587 targets IRF-7 to regulate its expression. Knockdown of IRF-7 reversed the effects of miR-1587 knockdown on cell proliferation and migration.Conclusion: Collectively, this study revealed that miR-1587/IRF-7 mediated the mechanism of M2-macrophages-induced breast cancer progression, and this would shed light on the further clinical therapy of breast cancer.

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