Carbonic anhydrase XII promotes invasion and migration ability of MDA-MB-231 breast cancer cells through the p38 MAPK signaling pathway

2010 ◽  
Vol 89 (8) ◽  
pp. 598-606 ◽  
Author(s):  
Ming-Ju Hsieh ◽  
Kuo-Shuen Chen ◽  
Hui-Ling Chiou ◽  
Yih-Shou Hsieh
Keyword(s):  
Breast Cancer ◽  
Carbonic Anhydrase ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Breast Cancer Cells ◽  
Mapk Signaling ◽  
Migration Ability ◽  
Invasion And Migration ◽  
And Migration

CCR10 activation stimulates the invasion and migration of breast cancer cells through the ERK1/2/MMP-7 signaling pathway

2017 ◽  
Vol 51 ◽  
pp. 124-130 ◽  
Author(s):  
Hao-yu Lin ◽  
Shu-ming Sun ◽  
Xiao-feng Lu ◽  
Ping-ying Chen ◽  
Chun-fa Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

Sevoflurane inhibits invasion and migration of lung cancer cells by inactivating the p38 MAPK signaling pathway

2012 ◽  
Vol 26 (3) ◽  
pp. 381-392 ◽  
Author(s):  
Hua Liang ◽  
Miaoning Gu ◽  
Chengxiang Yang ◽  
Hanbing Wang ◽  
Xianjie Wen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Lung Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals Knockdown of lncRNA FOXD2-AS1 Inhibits Proliferation, Migration, and Drug Resistance of Breast Cancer Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Qiaohong Nong ◽  
Shaokang Yu ◽  
Hui Hu ◽  
Xue Hu
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Invasion And Migration ◽  
And Migration ◽  
Mcf 7

Objective. In order to investigate the effect of lncRNA FOXD2-AS1 on breast cancer cells proliferation, migration, and drug resistance as well as its molecular mechanism. Methods. Real-time PCR was used to detect the expression of breast cancer tissues and cells from patients admitted to our hospital and the expression of lncRNA FOXD2-AS1 in MCF-7/ADR in adriamycin- (ADR-) resistant breast cancer cells. After interfering with or overexpressing lncRNA FOXD2-AS1 in MCF-7/ADR cells, cell proliferation, apoptosis, invasion, and migration were detected using CCK-8, flow cytometry, Transwell assay, and scratch test, respectively. The protein levels of PI3K, p-PI3K, AKT, and p-AKT in the PI3K/AKT signaling pathway were detected by Western blot. Results. lncRNA FOXD2-AS1 was upregulated in breast cancer tissues and cells and increased cell drug resistance to ADR. Downregulation of lncRNA FOXD2-AS1 inhibited invasion and migration of MCF-7/ADR cells, promoted apoptosis, increased chemosensitivity of MCF-7/ADR cells, and inhibited the activity of PI3K/AKT signaling pathway in MCF-7/ADR cells. Conclusions. lncRNA FOXD2-AS1 can promote the proliferation, invasion, migration, and drug resistance of breast cancer cells, inhibit apoptosis, and accelerate the development of breast cancer by positively regulating the PI3K/AKT signaling pathway.

scholarly journals Potassium Channel Protein KCNK6 Promotes Breast Cancer Cell Proliferation, Invasion, and Migration

2021 ◽  
Vol 9 ◽  
Author(s):  
Xiangchan Hou ◽  
Le Tang ◽  
Xiayu Li ◽  
Fang Xiong ◽  
Yongzhen Mo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Potassium Channel ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cancer Therapies ◽  
Migration Ability ◽  
Invasion And Migration ◽  
Therapy Targets ◽  
Novel Strategy ◽  
And Migration

Breast cancer is the most common malignant tumor in women, and its incidence is increasing each year. To effectively treat breast cancer, it is important to identify genes involved in its occurrence and development and to exploit them as potential drug therapy targets. Here, we found that potassium channel subfamily K member 6 (KCNK6) is significantly overexpressed in breast cancer, however, its function in tumors has not been reported. We further verified that KCNK6 expression is upregulated in breast cancer biopsies. Moreover, overexpressed KCNK6 was found to enhance the proliferation, invasion, and migration ability of breast cancer cells. These effects may occur by weakening cell adhesion and reducing cell hardness, thus affecting the malignant phenotype of breast cancer cells. Our study confirmed, for the first time, that increased KCNK6 expression in breast cancer cells may promote their proliferation, invasion, and migration. Moreover, considering that ion channels serve as therapeutic targets for many small molecular drugs in clinical treatment, targeting KCNK6 may represent a novel strategy for breast cancer therapies. Hence, the results of this study provide a theoretical basis for KCNK6 to become a potential molecular target for breast cancer treatment in the future.

scholarly journals FAM96A and FAM96B Suppress Breast Cancer Proliferation and Migration via the Wnt/β-Catenin Signaling Pathway

2021 ◽  
Author(s):  
Di-Di Zhang ◽  
Xiao-Lin Sun ◽  
Zhao-Yuan Liang ◽  
Li-Na Zhang
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Breast Cancer Cells ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation ◽  
Invasion And Migration ◽  
And Migration

Abstract Background: Family with sequence similarity 96 member A and B (FAM96A and FAM96B) are two highly conserved homologous proteins belonging to MIP18 family. Many studies have shown that FAM96A and FAM96B play many different functions mainly through interacting with other different proteins. Recently, several studies show that FAM96A and FAM96B are significantly down-regulated compared in human gastrointestinal stromal tumors, colon cancer, liver cancer and gastric cancer with corresponding normal tissues. However, the molecular regulatory mechanisms of FAM96A and FAM96B in breast cancer development and metastasis are still unclear. In this work, we aimed to explore the molecular mechanisms of FAM96A and FAM96B in breast cancer progression.Methods: We used specific siRNAs to down-regulate FAM96A and FAM96B expression, and used recombinant plasmids to up-regulate FAM96A and FAM96B expression in breast cancer cells. Cell proliferation was measured using MTT and colony formation assays. Cell cycle and apoptosis were detected by flow cytometry analysis. Wound healing and transwell assays were used to examine cell migration and invasion abilities. The relationships among FAM96A/B, EMT and Wnt/β-catenin signaling pathway were determined by analyzing the expression changes of classical markers and biological functional changes after XAV-939 inhibitor treatment. Results: We found that FAM96A and FAM96B expression in breast cancer was down-regulated. FAM96A/B overexpression suppressed breast cancer cell proliferation, invasion and migration, induced cell apoptosis and led to cell cycle arrested in G0/G1 phase. Conversely, FAM96A/B knockdown exhibited the opposite effects on breast cancer cells. Moreover, our data demonstrated that FAM96A/B overexpression suppressed EMT and Wnt/β-catenin signaling pathway, while FAM96A/B knockdown showed the promoting effects on EMT and Wnt/β-catenin signaling pathway in breast cancer cells. Furthermore, a Wnt pathway inhibitor, XAV-939 treatment reversed the promoting effects of FAM96A and FAM96B knockdown on breast cancer cell proliferation, invasion and migration.Conclusions: Our findings revealed that FAM96A and FAM96B may act as tumor suppressor genes and inhibit breast cancer progression via modulating the Wnt/β-catenin pathway, which can provide the potential markers for the diagnosis and treatment of breast cancer.

scholarly journals Oroxylin A Suppresses the Cell Proliferation, Migration, and EMT via NF-κB Signaling Pathway in Human Breast Cancer Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
XiaoHu Sun ◽  
Xinzhong Chang ◽  
Yunhua Wang ◽  
Boyang Xu ◽  
Xuchen Cao
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
Inflammatory Factors ◽  
Human Breast ◽  
Oroxylin A ◽  
Invasion And Migration ◽  
And Migration

Oroxylin A is a natural extract and has been reported to have a remarkable anticancer function. However, the mechanism of its anticancer activity remains not quite clear. In this study, we examined the inhibiting effects of Oroxylin A on breast cancer cell proliferation, migration, and epithelial-mesenchymal transition (EMT) and its possible molecular mechanism. The cytoactive and inflammatory factors were analyzed via Cell Counting Kit-8 assay and ELISA assay, respectively. Flow cytometry and western blotting were used to assess the cell proliferation. In addition, a wound healing assay and transwell assay were used to detect cell invasion and migration. qRT-PCR and western blot were employed to determine the effect of Oroxylin A on the EMT formation. Moreover, expression level of protein related to NF-κB signaling pathway was determined by western blot. The results revealed that Oroxylin A attenuated the cytoactivity of MDA-MB-231 cells in a dose- and a time-dependent manner. Moreover, cell proliferation, invasion, and migration of breast cancer cells were inhibited by Oroxylin A compared to the control. The mRNA and protein expression levels of E-cadherin were remarkably increased while N-cadherin and Vimentin remarkably decreased. Besides, Oroxylin A suppressed the expression of inflammatory factors and NF-κB activation. Furthermore, we also found that supplement of TNF-α reversed the effects of Oroxylin A on the cell proliferation, invasion, migration, and EMT in breast cancer cells. Taken together, our results suggested that Oroxylin A inhibited the cell proliferation, invasion, migration, and EMT through inactivating NF-κB signaling pathway in human breast cancer cells. These findings strongly suggest that Oroxylin A could be a therapeutic potential candidate for the treatment of breast cancer.

R-Spondin 2 Promoted Proliferation, Invasion and Migration of Triple Negative Breast Cancer Cells Through Activating Wnt/β-Catenin Signaling Pathway After Axin2 Inhibition

2020 ◽  
Vol 10 (1) ◽  
pp. 26-36
Author(s):  
XiaoHu Sun ◽  
Yue Yu ◽  
Jie Ge ◽  
Xin Wang ◽  
XuChen Cao
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Invasion And Migration ◽  
Tnbc Cell ◽  
And Migration ◽  
Related Proteins

Protein R-spondin 2, which is known as roof plate-specific spondin 2, is an extracellular matrix secreted protein that participates in a wide range of biological processes. However, the expression of R-spondin 2 in triple negative breast cancer (TNBC) and its specific mechanism have not been reported. In this study, RT-qPCR and western blot were used to detect the expression of R-spondin 2 and Axin2 in cells. Cell transfection techniques were used to overexpress Axin2 and interfere with the expression of R-spondin 2. CCk-8 and clone formation assay were used to detect cell viability. Wound healing and Traswell techniques were used to test the rate of invasion and migration of TNBC cells. Western blot was used to detect the expression of related proteins. The results showed that the expression of R-spondin 2 in TNBC cell lines was significantly increased compared with normal breast cancer cells. After interfering with the expression of R-spondin 2 in TNBC cell lines, the rate of cell viability, invasion and migration were decreased. It was also found that the expressions of Axin2 and β-catenin and Cyclin-D1, which are wnt/β-catenin pathway related proteins, were significantly decreased. Subsequently, the overexpression of Axin2 can inhibit the proliferation, invasion and migration that were ever promoted by R-spondin 2 of TNBC cells. Moreover, the overexpression of Axin2 inhibited the activation of wnt/β-catenin signaling pathway, which was also activated by R-spondin 2 in TNBC cells. In a word, R-spondin 2 promoted proliferation, invasion and migration of triple negative breast cancer cells through activating wnt/β-catenin signaling pathway after Axin2 inhibition.

scholarly journals Chemerin Promotes The Proliferation And Migration of Breast Cancer Cells Through JNK And ERK1/2 Signaling pathways

2021 ◽  
Author(s):  
Fanyu Zeng ◽  
Jie Zhang ◽  
Qianqian Liu ◽  
Shuya Yang ◽  
Xueqing Zhou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Abstract Breast cancer is the most common invasive malignancy. In 2020, the number of new cases of breast cancer worldwide has replaced lung cancer as the No.1 cancer in the global. Breast cancer is the leading cause of cancer death among women worldwide. Mammary tumorigenesis is severely linked to obesity, one potential connection is chemerin. Chemerin is a chemoattractant protein secreted by adipocytes, which contributes to the progression of breast cancer. Cell proliferation, migration, and invasion are cellular processes associated with various stages of metastasis. These processes are associated with mitogen-activated protein kinase (MAPK) signaling pathway. In this study, human breast cancer cell lines MCF-7 and MDA-MB-231were utilized to determine the effect of chemerin on cell proliferation, migration, and key proteins of MAPK signaling pathway. We found that chemerin promoted cell proliferation and migration in a concentration-dependent manner. Interestingly, these effects of chemerin were through promoting the proteins phosphorylation of ATF2 and ERK1/2 but not p38, in MAPK signaling pathway. Specific inhibitors of JNK and ERK1/2 pathway showed that the effect exerted by chemerin in cell proliferation and migration in breast cancer cells was dependent on these proteins. Our findings suggest that chemerin promotes the development of mammary cancer cells through JNK and ERK signaling pathways.

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