Skip to main content
Key Specialties
Cardiology Diabetology Endocrinology Gastroenterology Geriatrics and Gerontology Gynecology and Obstetrics Hematology Infectious Disease Internal Medicine Nephrology Neurology Oncology Pediatrics Respiratory Medicine Rheumatology Surgery
Congress Coverage
2024 ACC Congress 2023 ESMO Congress 2023 EASD Congress 2023 ERS Congress 2023 ESC Congress
Clinical Collections
Advances in Alzheimer’s

At a glance: The STEP trials

A round-up of the STEP phase 3 clinical trials evaluating semaglutide for weight loss in people with overweight or obesity.
ADVANCED SEARCH
Log in
Top
Breast Cancer
Published in: Breast Cancer 6/2019

01-11-2019 | Breast Cancer | Original Article

Knockdown of FAM64A suppresses proliferation and migration of breast cancer cells

Authors: Zhuocheng Yao, Xianchong Zheng, Sitong Lu, Zhanxin He, Yutian Miao, Hehai Huang, Xinwei Chu, Chunqing Cai, Fei Zou

Published in: Breast Cancer | Issue 6/2019

Login to get access

Abstract

Background

FAM64A is a mitotic regulator promoting cell metaphase–anaphase transition, and it is frequently reported to be highly expressed in cancer cells. However, the role of FAM64A in human breast cancer (BrC) is poorly studied.

Methods

The expression of FAM64A mRNA in BrC samples was determined by RT-qPCR assay and TCGA database mining. Kaplan–Meier plotter was used to analyze whether FAM64A expression impacted prognosis. Then, the expression of FAM64A was silenced using RNA interference. Cell-counting assay, colony formation assay and flow cytometry assay were conducted to detect proliferation; transwell migration assay, EMT-related proteins expression (E-cadherin, N-cadherin and vimentin), and EMT-related transcription factors mRNA expression (Snail, Twist, Slug) were conducted to evaluate the migration ability.

Results

FAM64A was highly expressed in human BrC samples, which was negatively associated with poor survival time. Analysis of FAM64A expression in BrC cell lines demonstrated that the expression of FAM64A was significantly correlated with the proliferation rate and migration ability of BrC cells. Indeed, knockdown of FAM64A suppressed the proliferation of MDA-MB-231 and MCF-7 cells. Importantly, we also found that silencing of FAM64A inhibited the migration of BrC cells via impeding epithelial–mesenchymal transition.

Conclusions

Our findings suggest that FAM64A plays an important role in the proliferation and migration of BrC cells, which might serve as a potential target for BrC treatment.
Literature
1.
2.
Bray F, et al. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin. 2018;68(6):394–424.CrossRefPubMed
3.
Yeo B, Turner NC, Jones A. An update on the medical management of breast cancer. BMJ. 2014;348(1):g3608.CrossRefPubMed
4.
Archangelo LF, et al. 2013) The CATS (FAM64A) protein is a substrate of the kinase interacting stathmin (KIS. Biochim Biophys Acta (BBA) (Molecular Cell Research). 1833;5:1269–79.
5.
Zhao W, et al. RCS1, a substrate of APC/C, controls the metaphase to anaphase transition. Proc Natl Acad Sci USA. 2008;105(36):1341–13420.CrossRef
6.
Archangelo LF, et al. The novel CALM interactor CATS influences the subcellular localization of the leukemogenic fusion protein CALM AF10. Oncogene. 2006;25(29):4099–109.CrossRefPubMed
7.
Zhang C, et al. Integrated analysis of expression profiling data identifies three genes in correlation with poor prognosis of triple-negative breast cancer. Int J Oncol. 2014;44(6):2025–33.CrossRefPubMed
8.
9.
10.
Hu S, et al. Transcriptional response profiles of paired tumor-normal samples offer novel perspectives in pan-cancer analysis. Oncotarget. 2017;8(25):41334.CrossRefPubMedPubMedCentral
11.
Liu J, et al. NKAP functions as an oncogene and its expression is induced by CoCl2 treatment in breast cancer via AKT/mTOR signaling pathway. Cancer Manag Res. 2018;10:5091–100.CrossRefPubMedPubMedCentral
12.
Sato K, Akimoto K. Expression levels of KMT2C and SLC20A1 identified by information-theoretical analysis are powerful prognostic biomarkers in estrogen receptor-positive breast cancer. Clin Breast Cancer. 2017;17(3):e135–42.CrossRefPubMed
13.
Wirapati P, et al. Meta-analysis of gene expression profiles in breast cancer: toward a unified understanding of breast cancer subtyping and prognosis signatures. Breast Cancer Res BCR. 2008;10(4):R65.CrossRefPubMed
14.
Chia SK, et al. A 50-gene intrinsic subtype classifier for prognosis and prediction of benefit from adjuvant tamoxifen. Clin Cancer Res. 2012;18(16):4465–72.CrossRefPubMedPubMedCentral
15.
Shibuta K, et al. The relevance of intrinsic subtype to clinicopathological features and prognosis in 4,266 Japanese women with breast cancer. Breast Cancer. 2011;18(4):292–8.CrossRefPubMed
16.
17.
Liu Y, Hu Z. Identification of collaborative driver pathways in breast cancer. BMC Genom. 2014;15(1):605.CrossRef
18.
Khaled N, Bidet Y. New insights into the implication of epigenetic alterations in the EMT of triple negative breast cancer. Cancers (Basel). 2019;11(4):559.CrossRef
19.
Diaz-Moralli S, et al. Targeting cell cycle regulation in cancer therapy. Pharmacol Ther. 2013;138(2):255–71.CrossRefPubMed
20.
Zhao TP, Wang XL, Han YM. Knockdown of p57 gene inhibits breast cancer cell proliferation. Oncol Lett. 2018;16(1):55–8.PubMedPubMedCentral
21.
Hanahan D, Weinberg RA. The hallmarks of cancer. Cell. 2000;1(100):57–70.CrossRef
22.
Kokkinos MI, et al. Vimentin and epithelial–mesenchymal transition in human breast cancer—observations in vitro and in vivo. Cells Tissues Organs. 2007;185(1–3):191–203.CrossRefPubMed
23.
Tsai PC, et al. Cardiotoxin III inhibits hepatocyte growth factor-induced epithelial–mesenchymal transition and suppresses invasion of MDA-MB-231 cells. J Biochem Mol Toxicol. 2016;30(1):12–21.CrossRefPubMed
24.
25.
26.
Vesuna F, et al. Twist is a transcriptional repressor of E-cadherin gene expression in breast cancer. Biochem Biophys Res Commun. 2008;367(2):235–41.CrossRefPubMed
27.
Voutsadakis I. Epithelial–mesenchymal transition (EMT) and regulation of EMT factors by steroid nuclear receptors in breast cancer: a review and in silico investigation. J Clin Med. 2016;5(1):11.CrossRefPubMedCentral
28.
Olea-Flores M, et al. Signaling pathways induced by leptin during epithelial–mesenchymal transition in breast cancer. Int J Mol Sci. 2018;19(11):3493.CrossRefPubMedCentral
Metadata
Title
Knockdown of FAM64A suppresses proliferation and migration of breast cancer cells
Authors
Zhuocheng Yao
Xianchong Zheng
Sitong Lu
Zhanxin He
Yutian Miao
Hehai Huang
Xinwei Chu
Chunqing Cai
Fei Zou
Publication date
01-11-2019
Publisher
Springer Japan
Published in
Breast Cancer / Issue 6/2019
Print ISSN: 1340-6868
Electronic ISSN: 1880-4233
DOI
https://doi.org/10.1007/s12282-019-00991-2

Other articles of this Issue 6/2019

Breast Cancer 6/2019 Go to the issue

Original Article

Reproductive history and breast cancer survival: a prospective patient cohort study in Japan

Original Article

Identification of differentially expressed genes between triple and non-triple-negative breast cancer using bioinformatics analysis

Original Article

Association between pre-diagnosis BMI, physical activity, pathologic complete response, and chemotherapy completion in women treated with neoadjuvant chemotherapy for breast cancer

Original Article

Pharmacotherapy decision-making among patients with breast cancer in Japan: results of an online survey

Original Article

Fatal events during clinical trials: an evaluation of deaths during breast cancer studies

Original Article

A novel nipple–areola complex involvement predictive index for indicating nipple-sparing mastectomy in breast cancer patients
Webinar | 19-02-2024 | 17:30 (CET)

Keynote webinar | Spotlight on antibody–drug conjugates in cancer

Watch now

Antibody–drug conjugates (ADCs) are novel agents that have shown promise across multiple tumor types. Explore the current landscape of ADCs in breast and lung cancer with our experts, and gain insights into the mechanism of action, key clinical trials data, existing challenges, and future directions.

Dr. Véronique Diéras
Prof. Fabrice Barlesi
Developed by: Springer Medicine
Image Credits