scholarly journals Long Noncoding RNA CAMTA1 Promotes Proliferation and Mobility of the Human Breast Cancer Cell Line MDA-MB-231 via Targeting miR-20b

2018 ◽  
Vol 26 (4) ◽  
pp. 625-635 ◽  
Author(s):  
Pengwei Lu ◽  
Yuanting Gu ◽  
Lin Li ◽  
Fang Wang ◽  
Xue Yang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cell Line ◽  
Long Noncoding Rna ◽  
Human Breast Cancer ◽  
Noncoding Rna ◽  
Breast Cancer Cells ◽  
Cancer Cell Line ◽  
Human Breast Cancer Cell ◽  
Human Breast

Breast cancer is a serious threat to women’s physical and psychological health. Long noncoding RNA CAMTA1 (lncCAMTA1) was believed to be related with tumor progression, but its role in breast cancer is not clear. The human breast cancer cell line MDA-MB-231 was used to investigate the effect of lncCAMTA1 on cell viability, migration/invasion, and apoptosis. The expression of lncCAMTA1, miR-20b, and VEGF in MDA-MB-231 were measured after corresponding transfections. Binding effects between lncCAMTA1 and miR-20b, miR-20b, and VEGF 3′-UTR were measured. The effects of miR-20b and VEGF on breast cancer cells were also assessed after transfections. The phosphorylation levels of the MAPK/ERK and JAK/STAT3 pathways were determined to assess the effect of VEGF. The results showed that lncCAMTA1 expression promoted cell viability and migration/invasion, while knockdown of lncCAMTA1 promoted cell apoptosis via binding with miR-20b. lncCAMTA1 negatively regulated miR-20b expression. VEGF was a target of miR-20b, leading to the modification of the phosphorylation levels of MAPK, ERK, JAK, STAT1, and STAT3. Our findings suggested that lncCAMTA1 might promote proliferation and mobility of human breast cancer cells via binding with miR-20b. VEGF was a direct target of miR-20b and regulated activation of the MAPK/ERK and JAK/STAT3 signaling pathways. Therefore lncCAMTA1 has potential as a novel cancer diagnostic marker and as a putative novel therapeutic target for breast cancer treatment.

A Novel Naphthotriazolyl-4-oxoquinoline Derivative that Selectively Controls Breast Cancer Cells Survival Through the Induction of Apoptosis

2018 ◽  
Vol 18 (17) ◽  
pp. 1465-1474 ◽  
Author(s):  
Jessica R. Branco ◽  
Vanessa G. Oliveira ◽  
Amanda M. Esteves ◽  
Ingrid C. Chipoline ◽  
Miriam F.O. Lima ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Line ◽  
Breast Cancer Cell Line ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Cancer Cell Line ◽  
Human Breast Cancer Cell ◽  
Human Breast ◽  
Mcf 7

Background: Breast cancer is a major cause of death among women worldwide. Treatment for breast cancer involves the surgical removal of cancer tissue, followed by chemotherapy. Although the treatment is efficient, especially when the cancer is detected early, recurrence is common and is often resistant to the previous treatment. Therefore, a constant search for efficient and novel drugs for the treatment of breast cancer is mandatory. Recently, triazole derivatives have shown promising effects against different types of cancer, revealing these molecules as putative anticancer drugs. Experimental: We have synthesized a series of naphthotriazolyl-4-oxoquinoline derivatives and tested their activity against a human breast cancer cell line. Among the compounds tested, we identified a molecule that killed the human breast cancer cell line MCF-7 with minimal effects on its noncancer counterpart, MCF10A. This effect was seen after 24 hours of treatment and persisted for additional 24 hours after treatment withdrawal. After 1 hour of treatment, the compound, here named 12c, promoted a decrease in cell glucose consumption and lactate production. Moreover, the cells treated with 12c for 1 hour showed diminished intracellular ATP levels with unaltered mitochondrial potential and increased reactive oxygen species production. Additionally, apoptosis was triggered after treatment with the drug for 1 hour. All of these effects are only observed with MCF-7 cells, and not MCF10A. These data show that 12c has selective activity against breast cancer cells and is a potential candidate for a novel anticancer drug. Results and Conclusion: The naphthotriazolyl-4-oxoquinoline derivatives were obtained in good to moderate yields, and one of them, 12c, exhibited strong and selective antitumor properties. The antitumor mechanism involves inhibition of glycolysis, diminished intracellular ATP levels, induction of ROS production and triggering of apoptosis. These effects are all selective for cancer cells, since noncancer cells are unaffected, and these effects can only be attributed to the whole molecule, as different pharmacophoric groups did not reproduce these effects.

scholarly journals DCLK1 Plays a Metastatic-Promoting Role in Human Breast Cancer Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Heshu Liu ◽  
Tao Wen ◽  
Ying Zhou ◽  
Xiaona Fan ◽  
Tan Du ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cell Line ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Cancer Metastasis ◽  
Cancer Cell Line ◽  
Breast Cancer Metastasis ◽  
Human Breast Cancer Cells ◽  
Human Breast

Background. Doublecortin-like kinase 1 (DCLK1) has been universally identified as a cancer stem cell (CSC) marker and is found to be overexpressed in many types of cancers including breast cancer. However, there is little data regarding the functional role of DCLK1 in breast cancer metastasis. In the present study, we sought to investigate whether and how DCLK1 plays a metastatic-promoting role in human breast cancer cells.Methods. We used Crispr/Cas9 technology to knock out DCLK1 in breast cancer cell line BT474, which basically possesses DCLK1 at a higher level, and stably overexpressed DCLK1 in another breast cancer cell line, T47D, that basically expresses DCLK1 at a lower level. We further analyzed the alterations of metastatic characteristics and the underlying mechanisms in these cells.Results. It was shown that, compared with the corresponding control cells, DCLK1 overexpression led to an increase in metastatic behaviors including enhanced migration and invasion of T47D cells. By contrast, forced depletion of DCLK1 drastically inhibited these metastatic characteristics in BT474 cells. Mechanistically, the epithelial-mesenchymal transition (EMT) program, which is critical for cancer metastasis, was prominently activated in DCLK1-overexpressing cancer cells, evidenced by a decrease in an epithelial marker ZO-1 and an enhancement in several mesenchymal markers including ZEB1 and Vimentin. In addition, DCLK1 overexpression induced the ERK MAPK pathway, which resultantly enhanced the expression of MT1-MMP that is also involved in cancer metastasis. Knockout of DCLK1 could reverse these events, further supporting a metastatic-promoting role for DCLK1.Conclusions. Collectively, our data suggested that DCLK1 overexpression may be responsible for the increased metastatic features in breast cancer cells. Targeting DCLK1 may become a therapeutic option for breast cancer metastasis.

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