TRIM59 overexpression correlates with poor prognosis and contributes to breast cancer progression through AKT signaling pathway

2018 ◽  
Vol 57 (12) ◽  
pp. 1792-1802 ◽  
Author(s):  
Yunxiao Liu ◽  
Yanyan Dong ◽  
Liping Zhao ◽  
Lihong Su ◽  
Kexin Diao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Poor Prognosis ◽  
Akt Signaling ◽  
Breast Cancer Progression ◽  
Akt Signaling Pathway

Thidiazuron suppresses breast cancer progression via targeting miR-132 and miR-202-5p/PTEN axis mediated dysregulation of PI3K/AKT signaling pathway

2020 ◽  
Author(s):  
Hairul-Islam Ibrahim ◽  
Mohammad Bani Ismail ◽  
Rebai Ben Ammar ◽  
Emad Ahmed
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Cancer Metastasis ◽  
Metastatic Cancer ◽  
Akt Signaling ◽  
Breast Cancer Metastasis ◽  
Akt Signaling Pathway ◽  
Stressful Environment

Chemo-resistance and metastatic disease development are the most common causes of breast cancer recurrence and death. Thidiazuron (TDZ) is a plant growth regulator, its biological role on human and animals has not been yet clarified. In the present study, we investigated the anticancer activity of this plant phytohormone on the drug resistant-triple negative breast cancer MDA-MB-231 cell line. Treatment of the breast cancer cells with TDZ (1-50 μM) caused more stressful environment and induced a significant increase in percentages of active caspases positive cells. In addition, TDZ treatment (5 and 10 μM) significantly attenuated the migration and the invasion activities of these highly metastatic cancer cells. Mechanistically, TDZ reducesd cancer progression and invasive activity through targeting miR-202-5p, which stimulatesd the expression of the phosphatase and tensin homolog (PTEN), the tumor suppressor that downregulates PI3K/AKT signaling pathway. In the meantime, TDZ treatment statistically upregulatesd the suppressor of breast cancer proliferation, miRNA-132 that is also implicated in dysregulating the TEN-AKT/the nuclear factor NFκB signaling pathway. Interestingly, our molecular docking analysis revealed potential non-covalent interaction between TDZ with AKT, PTEN and PI3K. These findings suggest that TDZ may suppresses breast cancer metastasis through targeting miRNA-132, miR-202-5p/PTEN and PI3K/AKT downstream molecules.

scholarly journals Comprehensive Combined Proteomics and Genomics Analysis Identifies Prognostic Related Transcription Factors in Breast Cancer and Explores the Role of DMAP1 in Breast Cancer

2021 ◽  
Vol 11 (11) ◽  
pp. 1068
Author(s):  
Xuan Li ◽  
Hefen Sun ◽  
Yifeng Hou ◽  
Wei Jin
Keyword(s):  
Breast Cancer ◽  
Transcription Factors ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Immune Cell ◽  
Akt Signaling ◽  
High Expression ◽  
Akt Signaling Pathway ◽  
Normal Tissues

Transcription factors (TFs) are important for regulating gene transcription and are the hallmark of many cancers. The identification of breast cancer TFs will help in developing new diagnostic and individualized cancer treatment tools. In this study, we used quantitative proteomic analyses of nuclear proteins and massive transcriptome data to identify enriched potential TFs and explore the possible role of the transcription factor DMAP1 in breast cancer. We identified 13 prognostic-related TFs and constructed their regulated genes, alternative splicing (AS) events, and splicing factor (SF) regulation networks. DMAP1 was reported less in breast cancer. The expression of DMAP1 decreased in breast cancer tumors compared with normal tissues. The poor prognosis of patients with low DMAP1 expression may relate to the activated PI3K/Akt signaling pathway, as well as other cancer-relevant pathways. This may be due to the low methylation and high expression of these pathway genes and the fact that such patients show more sensitivity to some PI3K/Akt signaling pathway inhibitors. The high expression of DMAP1 was correlated with low immune cell infiltration, and the response to immune checkpoint inhibitor treatment in patients with high DMAP1 expression was low. Our study identifies some transcription factors that are significant for breast cancer progression, which can be used as potential personalized prognostic markers in the future.

scholarly journals WBP2 Downregulation Inhibits Proliferation by Blocking YAP Transcription and the EGFR/PI3K/Akt Signaling Pathway in Triple Negative Breast Cancer

2018 ◽  
Vol 48 (5) ◽  
pp. 1968-1982 ◽  
Author(s):  
Hongming Song ◽  
Tianqi Wu ◽  
Dan Xie ◽  
Dengfeng Li ◽  
Kaiyao Hua ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Signaling Pathway ◽  
Triple Negative Breast Cancer ◽  
Poor Prognosis ◽  
Triple Negative ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Qrt Pcr

Background/Aims: Dysregulated expression of WW domain-binding protein 2 (WBP2) is associated with poor prognosis in ER+ breast cancer patients. However, its role in triple negative breast cancer (TNBC) has not been previously assessed. Therefore, we aimed to elucidate the functional mechanism of WBP2 in TNBC cells. Methods: qRT-PCR, western blotting, and immunohistochemical staining were used to evaluate WBP2 expression in TNBC patient tumors and cell lines. HCC1937 and MDA-MB-231 cells transiently transfected with WBP2 small interfering RNA (siRNA), miR-613 mimics, or miR-613 inhibitors were subject to assays for cell viability, apoptosis and cell cycle distribution. Co-immunoprecipitation, western blotting or qRT-PCR were employed to monitor changes in signaling pathway-related genes and proteins. Luciferase assays were performed to assess whether WBP2 is a direct target of miR-613. The effect of miR-613 on tumor growth was assessed in vivo using mouse xenograft models. Results: The expression of WBP2 was upregulated in TNBC tissues and cells. Expression of WBP2 was significantly correlated with Ki67 in TNBC patients. Knockdown of WBP2 inhibited cellular proliferation, promoted apoptosis, and induced cell cycle arrest of TNBC cells. miR-613 directly bound to the 3’-untranslated region (3’-UTR) of WBP2 and regulated the expression of WBP2. Moreover, miR-613 reduced the expression of WBP2 and suppressed tumor growth of TNBC cells in vivo. Knockdown of WBP2 inhibited YAP transcription and the EGFR/PI3K/Akt signaling pathway in TNBC cells, and these effects were reversed by inhibition of miR-613. Conclusion: WBP2 overexpression is associated with the poor prognosis of TNBC patients and the miR-613-WBP2 axis represses TNBC cell growth by inactivating YAP-mediated gene expression and the EGFR/PI3K/Akt signaling pathway.

scholarly journals Hypermethylation of DLG3 Promoter Upregulates RAC1 and Activates the PI3K/AKT Signaling Pathway to Promote Breast Cancer Progression

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Bingbing Liu ◽  
Yanning Xu ◽  
Lin Zhang ◽  
Xue Yang ◽  
Ling Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Biological Activities ◽  
Akt Signaling ◽  
Akt Pathway ◽  
Akt Signaling Pathway ◽  
Mesenchymal Transition

Objective. This investigation aimed to figure out the relation between discs large homolog 3 (DLG3) expression and the progression and prognosis of breast cancer (BC). Methods. qRT-PCR was utilized for confirming DLG3 expression and RAC1 mRNA expression in BC tissues and cells. Subsequently, after overexpression or interference of DLG3, the changes of the biological activities of BC cells, including cell proliferation, migration, invasion, and apoptosis, were detected through CCK-8, colony formation assay, wound healing assay, transwell assay, and flow cytometry, respectively. Furthermore, western blotting was utilized to measure the protein expression of DLG3 and RAC1, as well as related proteins of epithelial-mesenchymal transition (EMT) and the PI3K/AKT signaling pathway. Results. At both cellular and tissue level in BC, DLG3 was downregulated and methylation level was upregulated; RAC1 showed an opposite change and was of a negative correlation with DLG3. In MCF-7 and HCC1937, we found that the upregulation of DLG3 could inhibit RAC1 expression as well as cell proliferation, invasion, migration, and EMT, while promoting apoptosis. Also, DLG3 inhibited the activation of the P13K/AKT pathway. Conclusion. Hypermethylation of DLG3 promoter upregulates RAC1 and activates the PI3K/AKT pathway, thus promoting BC progression. This conclusion provides ideas and experimental basis for improving and treating BC patients.

scholarly journals Huaier Suppresses Breast Cancer Progression via linc00339/miR-4656/CSNK2B Signaling Pathway

2019 ◽  
Vol 9 ◽  
Author(s):  
Wei Wang ◽  
Xiaolong Wang ◽  
Chen Li ◽  
Tong Chen ◽  
Ning Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Breast Cancer Progression

scholarly journals SU6668 modulates prostate cancer progression by downregulating MTDH/AKT signaling pathway

2017 ◽  
Vol 50 (5) ◽  
pp. 1601-1611 ◽  
Author(s):  
Benjiang Qian ◽  
Yi Yao ◽  
Changming Liu ◽  
Jiabing Zhang ◽  
Huihong Chen ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Akt Signaling ◽  
Prostate Cancer Progression ◽  
Akt Signaling Pathway

The phosphatidyl inositol 3-kinase/AKT signaling pathway in breast cancer

2010 ◽  
Vol 29 (4) ◽  
pp. 751-759 ◽  
Author(s):  
Carlos A. Castaneda ◽  
Hernán Cortes-Funes ◽  
Henry L. Gomez ◽  
Eva M. Ciruelos
Keyword(s):  
Breast Cancer ◽  
Signaling Pathway ◽  
Phosphatidyl Inositol ◽  
Akt Signaling ◽  
Akt Signaling Pathway
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