scholarly journals The Janus Face of Lipids in Human Breast Cancer: How Polyunsaturated Fatty Acids Affect Tumor Cell Hallmarks

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Benoît Chénais ◽  
Vincent Blanckaert
Keyword(s):  
Breast Cancer ◽  
Fatty Acids ◽  
Cell Proliferation ◽  
Polyunsaturated Fatty Acids ◽  
Tumor Cell ◽  
Epidemiological Studies ◽  
Migration And Invasion ◽  
Cellular Mechanisms ◽  
Cancer Tissues ◽  
The Impact

For several years, lipids and especially and polyunsaturated fatty acids (PUFAs) receive much attention in human health. Epidemiological studies tend to correlate a PUFA-rich diet with a reduced incidence of cancer, including breast cancer. However, the molecular and cellular mechanisms supporting the effect of PUFAs in breast cancer cells remain relatively unknown. Here, we review some recent progress in understanding the impact that PUFA may have on breast cancer cell proliferation, apoptosis, migration, and invasion. While most of the results obtained with docosahexaenoic acid and/or eicosapentaenoic acid show a decrease of tumor cell proliferation and/or aggressivity, there is some evidence that other lipids, which accumulate in breast cancer tissues, such as arachidonic acid may have opposite effects. Finally, lipids and especially PUFAs appear as potential adjuvants to conventional cancer therapy.

ILF3-AS1 promotes cell proliferation and inhibits cell apoptosis of breast cancer by binding with miR-4429 to upregulate RAB14

2021 ◽  
pp. 096032712198942
Author(s):  
Xiaoxue Zhang ◽  
Xianxin Xie ◽  
Kuiran Gao ◽  
Xiaoming Wu ◽  
Yanwei Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Breast Cancer Cell ◽  
Cell Apoptosis ◽  
Breast Cancer Cells ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation ◽  
Cancer Tissues

As one of the leading causes of cancer-related deaths among women, breast cancer accounts for a 30% increase of incidence worldwide since 1970s. Recently, increasing studies have revealed that the long non-coding RNA ILF3-AS1 is involved in the progression of various cancers. Nevertheless, the role of ILF3-AS1 in breast cancer remains largely unknown. In the present study, we found that ILF3-AS1 was highly expressed in breast cancer tissues and cells. ILF3-AS1 silencing inhibited breast cancer cell proliferation, migration and invasion, and promoted cell apoptosis. ILF3-AS1 bound with miR-4429 in breast cancer cells. Moreover, RAB14 was a downstream target of miR-4429, and miR-4429 expression was negatively correlated with RAB14 or ILF3-AS1 expression in breast cancer tissues. The result of rescue experiments demonstrated that overexpression of RAB14 can reverse the inhibitory effect of ILF3-AS1 knockdown on breast cancer cell proliferation, migration and invasion. Overall, ILF3-AS1 promotes the malignant phenotypes of breast cancer cells by interacting with miR-4429 to regulate RAB14, which might offer a new insight into the underlying mechanism of breast cancer.

scholarly journals Knock Down of LINC00504 Represses Proliferation and Invasion via Regulation of miR-140-5p in Breast Cancer

2020 ◽  
Author(s):  
Tieying Hou ◽  
Long Ye ◽  
Qingsong Qin ◽  
Shulin Wu
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Breast Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation ◽  
Cancer Tissues ◽  
Proliferation And Invasion

Abstract Background: Breast cancer is one of the most common cancer in the world. Emerging evidence has demonstrated the critical role of long noncoding RNAs (lncRNAs) in the development of breast cancer. In this study, we aimed to investigate the role of LINC00504 in breast cancer progression. Methods: Quantification real-time PCR was used to analyzed the expression levels of LINC00504 and miR‐140-5p in breast cancer tissues and cell lines. Cell proliferation, migration and invasion were assessed by Cell Counting Kit‐8, transwell assay and Immunofluorescence. Dual-luciferase reporter assay and RNA Immunoprecipitation assay were performed to verify the interaction between LINC00504 and miR‐140-5p. The expression levels of VEGFA, CDH1 and VIM were demonstrated by western blot assays. Result: Here, we found that LINC00504 is up regulated in breast cancer tissues and cell lines. Down regulation of LINC00504 mediated by shRNA suppressed the proliferation, migration, and invasion of breast cancer cells in vitro and in vivo. Furthermore, LINC00504 was found to competitively regulate miR‐140-5p via targeting VEGFA. Inhibition of miR‐140-5p attenuated the knockdown-LINC00504 induced inhibition of breast cancer cell proliferation and invasion.Conclusion: Taken together, our results demonstrated the mechanism of the LINC00504–miR‐140-5p–VEGFA axis in breast cancer cell proliferation and invasion and may lead to new lncRNA-based diagnostics or therapeutics for breast cancer.

Upregulated PFTK1 promotes tumor cell proliferation, migration, and invasion in breast cancer

2015 ◽  
Vol 32 (7) ◽  
Author(s):  
Xiaoling Gu ◽  
Yingying Wang ◽  
Hua Wang ◽  
Qichao Ni ◽  
Chunhui Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Tumor Cell ◽  
Migration And Invasion ◽  
Tumor Cell Proliferation

scholarly journals A comparison of the effects of soya isoflavonoids and fish oil on cell proliferation, apoptosis and the expression of oestrogen receptors α and β in the mammary gland and colon of the rat

2008 ◽  
Vol 102 (1) ◽  
pp. 29-36 ◽  
Author(s):  
Franziska Kramer ◽  
Ian T. Johnson ◽  
Joanne F. Doleman ◽  
Elizabeth K. Lund
Keyword(s):  
Breast Cancer ◽  
Fatty Acids ◽  
Cell Proliferation ◽  
Mammary Gland ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Fish Oil ◽  
Female Rats ◽  
Colon Tissue ◽  
The Impact

Isoflavonoids and fish oil may be protective against colorectal cancer, but the evidence in relation to breast cancer risk is ambiguous. In the present study, we have investigated the impact of soya-derived isoflavonoids andn-3 fatty acids from fish oil, both individually and in combination, on apoptosis, cell proliferation and oestrogen receptor (ER) expression in the colon and mammary gland of the rat. Female rats were fed diets high inn-3 fatty acids (80 g/kg diet) or soya protein (765 mg/kg diet isoflavones) for 2 weeks, and then killed before the removal of the colon and mammary glands. Cell proliferation and apoptosis were quantified morphologically in whole crypts and terminal end buds. The expressions ofERαandERβwere measured in colon tissue scrapes and the mammary gland. Fish oil significantly increased apoptosis and decreased mitosis in both tissues, an effect associated with a decrease in the expressions ofERα andERβ. Soya had no effect on apoptosis in either tissue, but reduced mitosis in the colon (P < 0·001) while increasing it in the mammary gland (P = 0·001). The changes in proliferation were associated with contrasting changes in theERexpression such that fish oil significantly decreased bothERβandERα, while soya increasedERαand decreasedERβ. The results may provide a novel mechanism by whichn-3 fatty acids could reduce cancer risk, but the interpretation of the results in relation to soya consumption and breast cancer risk requires further investigation.

scholarly journals microRNA-98 inhibits the proliferation, invasion, migration and promotes apoptosis of breast cancer cells by binding to HMGA2

2018 ◽  
Vol 38 (5) ◽  
Author(s):  
Mi-Jia Wang ◽  
Hao Zhang ◽  
Jun Li ◽  
Hai-Dong Zhao
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
High Mobility ◽  
Phase Cell ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Normal Tissues ◽  
Cancer Breast ◽  
Cancer Tissues

Breast cancer is a major contributor leading to cancer death in females worldwide. The aim of the present study was to investigate the effects of microRNA-98 (miR-98) on the processes of cell proliferation, invasion, migration and apoptosis by binding to high-mobility group AT-hook 2 (HMGA2) in breast cancer. Breast cancer tissues and adjacent normal tissues were collected from 112 patients suffering from breast cancer. The target relationship between miR-98 and HMGA2 was verified by in connection with the bioinformatics website as well as a dual-luciferase reporter assay, both of which provided evidence indicating that HMGA2 was a target gene of miR-98. Human breast cancer MDA-MB-231 cells were treated with miR-98 mimics, miR-98 inhibitors, siRNA-HMGA2 or miR-98 inhibitors + siRNA-HMGA2. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry methods were performed to determine cell proliferation, cell cycle and apoptosis, respectively, while a Transwell assay was employed to detect cell migration and invasion. Breast cancer tissues exhibited decreased miR-98 expression, while increased expression levels of HMGA2 were recorded. The mRNA and protein expressions of HMGA2, cell proliferation, cells at the S phase, cell migration, invasion, expressions of matrix metalloproteinase (MMP)2 as well as MMP9 were all reduced in response to miR-98 mimics or siRNA-HMGA2, while a contradictory trend was observed in the miR-98 inhibitors group. In conclusion, the results of the study demonstrate that miR-98 inhibits cell proliferation, migration and invasion, while acting to promote apoptosis by negatively regulating HMGA2 in breast cancer.

scholarly journals CircRNA circ_0075796 is downregulated in breast cancer and suppresses cell proliferation, migration and invasion

2021 ◽  
Author(s):  
Yao Xu ◽  
Ya-Wen Wang ◽  
Xu Chen ◽  
Can Liu ◽  
Yan-Duo Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Bioinformatics Analysis ◽  
Diagnostic Value ◽  
Migration And Invasion ◽  
Normal Tissues ◽  
Qrt Pcr ◽  
Cancer Tissues ◽  
Normal Controls

Abstract Background Emerging evidence shows that circular RNAs (circRNAs) play crucial parts in tumorigenesis and progression. In this work, the expression, clinical significance, function and potential mechanism of circ_0075796 in breast cancer were explored. Methods The expression of circ_0075796 in 189 pairs of breast cancer tissues and adjacent normal tissues was detected by quantitative real-time PCR (qRT-PCR). Cell Counting Kit-8 (CCK-8) assay, methyl thiazolyl tetrazolium (MTT) assay and colony formation assay were conducted for cell proliferation. Transwell assay and wound healing assay were used for cell migration and invasion. Flow cytometry analysis was adopted for cell cycle and cell apoptosis. The cellular localization of circ_0075796 was determined by fluorescence in situ hybridization (FISH). The circ_0075796/miR-452-3p/SAMD5 axis was screened out by bioinformatics analysis and verified by qRT-PCR. Methylated RNA Immunoprecipitation (MeRIP) was used to detect the N6-methyladenosine (m6A) modification levels of circ_0075796. QRT-PCR was used to detect the expression of RNA binding protein Quaking (QKI) in breast cancer tissues and adjacent normal tissues. Results circ_0075796 was downregulated in breast cancer tissues compared with adjacent normal tissues. In addition, circ_0075796 showed satisfactory diagnostic value to discriminate breast cancer and normal controls. Downregulated circ_0075796 expression was correlated with lymph node metastasis, HER2 expression, larger tumor size, high Ki-67 expression, advanced histological grade, aggressive molecular subtypes and advanced clinical stages. Overexpression of circ_0075796 inhibited cell proliferation, migration and invasion in vitro. FISH showed that circ_0075796 was localized in the cytoplasm and nucleus of breast cancer cells. Bioinformatics analysis and qRT-PCR revealed the potential circ_0075796/miR-452-3p/SAMD5 axis. Moreover, circ_0075796 showed lower m6A modification levels in breast cancer tissues compared to adjacent normal tissues. QKI was predicted to contain binding sites of circ_0075796 and was downregulated in breast cancer tissues compared to adjacent normal controls. Conclusions circ_0075796 was downregulated in breast cancer compared to normal controls, and showed potential diagnostic value for breast cancer. Downregulation of circ_0075796 was correlated with aggressive clinical features of breast cancer and overexpression of circ_0075796 inhibited the progression of breast cancer in vitro, indicating that circ_0075796 may be related to tumorigenesis and development of breast cancer.

The roles of microRNA-328-3p on proliferation and radiotherapy in breast cancer

2021 ◽  
Author(s):  
Ying Shi ◽  
Pengli Jiang ◽  
Jinqiu Li ◽  
Shengnan Xu ◽  
Bin Liu
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Breast Carcinogenesis ◽  
Aberrant Expression ◽  
Induced Apoptosis ◽  
Cancer Tissues ◽  
The Impact

Abstract Objectives MicroRNAs regulates varieties of molecular pathways and involve in breast carcinogenesis. Here both breast cancer cell lines and human breast cancer tissues were used to investigate the roles of miR-328-3p in breast cancer. Methods The impact of miR-328-3p on proliferation of MDA-MB-231 and T47D cells was determined by MTT assay. transwell migration and matrigel invasion assays were performed to evaluate effects of miR-328-3p on migration and invasion of breast cancer cells. Caspase 3/7 activities were measured to examine the impact of miR-328-3p on radiotherapy-induced apoptosis in breast cancer cells. The possible binding site of miR-328-3p was verified by dual-luciferase reporter assay. Quantitative real-time polymerase chain reaction was performed to detect miR-328-3p expression level in breast cancer tissues. Western blot and immunohistochemical studies were used to examine protein expression in breast cancer cells and breast cancer tissue, respectively. Results miR-328-3p involved growth, migration and invasion in breast cancer cells and was associated with radiotherapy sensitivity. MiR-328-3p enhanced radiation-induced apoptosis in breast cancer cells by regulating BAX and Bcl-2 expression. Meanwhile, aberrant expression of miR-328-3p was associated with altered expression of PTEN and p-AKT in breast cancer cells. Further study showed miR-328-3p bound to 3’-UTR of PTEN. In addition, breast cancer tissues showed higher level of miR-328-3p than normal breast tissue and higher level of miR-328-3p was seen in lower stage in breast cancer. Conclusions miR-328-3p displayed essential functions in breast carcinogenesis and might be used to predict radiotherapy response and prognosis in breast cancer.

scholarly journals FXYD3 Protein Involved in Tumor Cell Proliferation Is Overproduced in Human Breast Cancer Tissues

2009 ◽  
Vol 32 (7) ◽  
pp. 1148-1154 ◽  
Author(s):  
Hiroto Yamamoto ◽  
Kenzo Okumura ◽  
Shotaro Toshima ◽  
Ken-ichi Mukaisho ◽  
Hiroyuki Sugihara ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Tumor Cell ◽  
Human Breast Cancer ◽  
Tumor Cell Proliferation ◽  
Human Breast ◽  
Cancer Tissues
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