scholarly journals KIF21A influences breast cancer metastasis and survival

2016 ◽  
Author(s):  
Anton J. Lucanus ◽  
Victoria King ◽  
George W. Yip
Keyword(s):  
Breast Cancer ◽  
Cancer Metastasis ◽  
Breast Cancer Metastasis ◽  
Breast Cancer Tissue ◽  
Clinicopathological Parameters ◽  
Cancer Tissue ◽  
Human Breast ◽  
Mcf 7

ABSTRACTBreast cancer pathogenesis is known to be propagated by the differential expression of a group of proteins called the Kinesin Superfamily (KIFs), which are instrumental in the intracellular transport of chromosomes along microtubules during mitosis. During mitosis, KIFs are strictly regulated through temporal synthesis so that they are only present when needed. However, their misregulation may contribute to uncontrolled cell growth due to premature sister chromatid separation, highlighting their involvement in tumorigenesis. One particular KIF, KIF21A, was recently found to promote the survival of human breast cancer cells in vitro. However, how KIF21A influences other cancerous phenotypes is currently unknown. This study therefore aimed to consolidate the in vitro role of KIF21A in breast cancer metastasis, while also analysing KIF21A expression in human breast cancer tissue to determine its prognostic value. This was achieved by silencing KIF21A in MCF-7 and MDA-MB-231 breast cancer cell lines via siRNA transfection. Migration, invasion, proliferation, and adhesion assays were then performed to measure the effects of KIF21A silencing on oncogenic behaviour. Immunohistochemistry was also conducted in 263 breast cancer tissue samples to compare KIF21A expression levels against various prognostic outcomes and clinicopathological parameters. KIF21A knockdown reduced cell migration (by 42.8% [MCF-7] and 69.7% [MDA-MB-231]) and invasion (by 72.5% [MCF-7] and 42.5% [MDA-MB-231]) in both cell lines, but had no effect on adhesion or proliferation, suggesting that KIF21A plays an important role in the early stages of breast cancer metastasis. Unexpectedly however, KIF21A was shown to negatively correlate with various pro-malignant clinicopathological parameters, including tumour size and histological grade, and high KIF21A expression predicted better breast cancer survival (hazard ratio = 0.45), suggesting that KIF21A is a tumour suppressor. The conflicting outcomes of in vitro and in vivo data may be due to the possible multi-functionality of KIF21A or study limitations, and means no definitive conclusions can be drawn about the role of KIF21A in breast cancer. This warrants further investigation, which may prove pivotal to the development of novel chemotherapeutic strategies to mediate KIF21A’s function and enhance prognostic outcomes.

Sam68 Promotes the Progression of Human Breast Cancer through inducing Activation of EphA3

2020 ◽  
Vol 20 (1) ◽  
pp. 76-83 ◽  
Author(s):  
Xinxin Chen ◽  
Lehong Zhang ◽  
Min Yuan ◽  
Ziqiao Kuang ◽  
Ying Zou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Metastasis ◽  
Breast Cancer Metastasis ◽  
Breast Cancer Tissue ◽  
Cancer Tissue ◽  
Poor Survival ◽  
Survival Prognosis ◽  
Positive Role ◽  
Well Assay

Background: Src associated with mitosis of 68 kDa (Sam68), is often highly expressed in human cancers. Overexpression of Sam68 has been shown to be correlated with poor survival prognosis in some cancer patients. However, little is known whether Sam68 plays a role in promoting metastasis in breast cancer. Materials and Methods: The expression of Sam68 protein in breast cancer tissue was detected by immunohistochemistry. Trans-well assay, wound-healing, real-time PCR and Western blotting analysis were used to detect the effect of Sam68 on promoting EMT or metastasis of breast cancer. Next-generation RNA sequencing was used to analyze genes that may be regulated by Sam68. Results: Sam68 plays a positive role in promoting breast cancer metastasis. Sam68 was found to be overexpressed in breast cancer along with lymph node metastasis. MMP-9 was also found to be overexpressed in breast cancer tissue and was correlated to the expression of Sam68 (P<0.01). Xenograft in NOD/SCID mice and in vitro experiments confirmed that the invasion and metastatic ability of breast cancer cells were regulated by Sam68. And EPHA3 could be up-regulated by Sam68 in breast cancer. Conclusion: High expression of Sam68 participates in breast cancer metastasis by up-regulating the EPHA3 gene.

scholarly journals Inhibitory Effects of PC-SPESII Herbal Extract on Human Breast Cancer Metastasis

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Xiu-Feng Wang ◽  
Jia Du ◽  
Tian-Ling Zhang ◽  
Qian-Mei Zhou ◽  
Yi-Yu Lu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Cancer Metastasis ◽  
Proteolytic Enzymes ◽  
Breast Cancer Metastasis ◽  
Herbal Extract ◽  
Dependent Manner ◽  
Matrix Degradation ◽  
Human Breast

Cancer metastasis is refractory to most forms of chemotherapy. Conventional and alternative drugs, such as Chinese herbal remedies, have been developed to target metastatic cancer cells. In this study, we investigated the effects of PC-SPESII, an herbal formulation, on the migration, invasion, and metastasis of an experimental human breast cancer cell linein vivoandin vitro. PC-SPESII suppressed pulmonary metastasis and tumor growth of MDA-MB-231 human breast cancer xenografts without affecting body weight, liver function, and kidney function. PC-SPESII also inhibited MDA-MB-231 cell migration and invasionin vitroin a dose-dependent manner. Based on ELISA analysis, secretion of MMP-2 and MMP-9, proteins associated with extracellular matrix degradation, was reduced in response to PC-SPESII treatment. Western blot analysis of whole-cell extracts revealed that the levels of proteolytic proteins associated with matrix and base membrane degradation (MMP-2, MMP-9, and uPA) were decreased and the levels of their endogenous inhibitors (TIMP1 and TIMP2) were increased. Moreover, the p38MAPK and SAPK/JNK signaling pathway, which stimulates proteolytic enzymes and matrix degradation, was inhibited by PC-PSESII. Remarkably, cotreatment with PC-PSESII and p38MAPK or SAPK/JNK inhibitors magnified the antimetastatic phenotype. Our results indicate that PC-PSESII impairs human breast cancer metastasis by regulating proteolytic enzymes and matrix dynamics through the p38MAPK and SAPK/JNK pathway.

Peroxidatic catecholestrogen production by human breast cancer tissue in vitro

1987 ◽  
Vol 28 (5) ◽  
pp. 513-520 ◽  
Author(s):  
Michael Levin ◽  
Judith Weisz ◽  
Quang D. Bui ◽  
Richard J. Santen
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Breast Cancer Tissue ◽  
Cancer Tissue ◽  
Human Breast ◽  
Human Breast Cancer Tissue

RESPONSE OF HUMAN BREAST-CANCER TISSUE TO STEROID HORMONES IN VITRO

The Lancet ◽  
1970 ◽  
Vol 295 (7652) ◽  
pp. 868-870 ◽  
Author(s):  
J. Chayen ◽  
F.P. Altmann ◽  
Lucille Bitensky ◽  
J.R. Daly
Keyword(s):  
Breast Cancer ◽  
Steroid Hormones ◽  
Human Breast Cancer ◽  
Breast Cancer Tissue ◽  
Cancer Tissue ◽  
Human Breast ◽  
Human Breast Cancer Tissue

scholarly journals Unravelling the Encapsulation of DNA and Other Biomolecules in HAp Microcalcifications of Human Breast Cancer Tissues by Raman Imaging

Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2658
Author(s):  
Monica Marro ◽  
Anna Maria Rodríguez-Rivero ◽  
Cuauhtémoc Araujo-Andrade ◽  
Maria Teresa Fernández-Figueras ◽  
Laia Pérez-Roca ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mammography Screening ◽  
Human Breast Cancer ◽  
Biochemical Analysis ◽  
Three Dimensional ◽  
Breast Cancer Tissue ◽  
Cancer Tissue ◽  
Human Breast ◽  
Cancer Tissues

Microcalcifications are detected through mammography screening and, depending on their morphology and distribution (BI-RADS classification), they can be considered one of the first indicators of suspicious cancer lesions. However, the formation of hydroxyapatite (HAp) calcifications and their relationship with malignancy remains unknown. In this work, we report the most detailed three-dimensional biochemical analysis of breast cancer microcalcifications to date, combining 3D Raman spectroscopy imaging and advanced multivariate analysis in order to investigate in depth the molecular composition of HAp calcifications found in 26 breast cancer tissue biopsies. We demonstrate that DNA has been naturally adsorbed and encapsulated inside HAp microcalcifications. Furthermore, we also show the encapsulation of other relevant biomolecules in HAp calcifications, such as lipids, proteins, cytochrome C and polysaccharides. The demonstration of natural DNA biomineralization, particularly in the tumor microenvironment, represents an unprecedented advance in the field, as it can pave the way to understanding the role of HAp in malignant tissues.

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