Expression of vimentin in serum of breast cancer patients and its clinical significance

doi:10.3877/cma.j.issn.1674-0807.2017.03.004

Abstract

Abstract:

Objective

To investigate the expression of vimentin in serum of breast cancer patients and its relationship with clinicopathological characteristics.

Methods

It was a prospective study. According to the inclusion and exclusion criteria, totally 52 breast cancer patients and 52 healthy women in the Lanzhou General Hospital of PLA from January 2016 to September 2016 were enrolled. In this study, the expression level of vimentin in serum was detected by ELISA. The difference of serum vimentin expression between two groups was analyzed by the t-test, the expression of serum vimentin among different molecular subtypes of breast cancer was analyzed by one-way ANOVA and the relationship between serum vimentin expression and clinicopathological characteristics was analyzed by Pearson χ² test.

Results

ELISA assay showed that serum vimentin expression in breast cancer patients was significantly higher than that in healthy women (0.608±0.019 vs 0.186±0.008,t=19.870, P＜0.001). Serum vimentin expression was significantly different among different molecular subtypes of breast cancer (luminal A subtype 0.487±0.017, luminal B subtype 0.557±0.018, HER-2 overexpression subtype 0.767±0.011, triple-negative subtype 0.823±0.022; F=58.390, P＜0.001). The pairwise comparison showed that serum vimentin expression in luminal B subtype, HER-2 overexpression subtype or triple-negative subtype was significantly higher than that in luminal A subtype (all P＜0.050), serum vimentin expression in HER-2 overexpression subtype or triple-negative subtype was significantly higher than that in luminal B subtype (both P＜0.050), while there was no significant difference in serum vimentin expression between HER-2 overexpression subtype and triple-negative subtype (both P ＞0.050). Pearson χ² test showed that serum vimentin expression was correlated with TNM stage (χ²=7.989,P=0.005), lymph node metastasis (χ²=5.142, P=0.023), but was not correlated with age (χ²=0.349,P=0.554), tumor size (χ² = 0.819, P = 0.366) and histological grading (χ² = 0.537, P = 0.765).

Conclusion

Vimentin is highly expressed in serum of breast cancer patients and is closely correlated with TNM stage and lymph node metastasis, with the potential as a new biological indicator of breast cancer.

Key words: Breast neoplasms, Serum, Vimentin

Ji Ma, Fengjun Zhang, Jing Wang, Qingli Zhang, Weiqiang Wu. Expression of vimentin in serum of breast cancer patients and its clinical significance[J]. Chinese Journal of Breast Disease(Electronic Edition), 2017, 11(03): 144-147.

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References 16

[1]	Liu CY, Lin HH, Tang MJ, et al. Vimentin contributes to epithelialmesenchymal transition cancer cell mechanics by mediating cytoskeletal organization and focal adhesion maturation[J]. Oncotarget, 2015,6(18):15 966-15 983.
[2]	Tadokoro A, Kanaji N, Liu D, et al. Vimentin regulates invasiveness and is a poor prognostic marker in non-small cell lung cancer[J].Anticancer Res,2016,36(4):1545-1551.
[3]	Lazarova DL, Bordonaro M. Vimentin, colon cancer progression and resistance to butyrate and other HDACis[J]. J Cell Mol Med, 2016,20(6):989-993.
[4]	Polioudaki H, Agelaki S, Chiotaki R, et al. Variable expression levels of keratin and vimentin reveal differential EMT status of circulating tumor cells and correlation with clinical characteristics and outcome of patients with metastatic breast cancer[J]. BMC Cancer, 2015, 15:399.
[5]	Zhang J, Liu D, Feng Z, et al. MicroRNA-138 modulates metastasis and EMT in breast cancer cells by targeting vimentin[J]. Biomed Pharmacother,2016,77:135-141.
[6]	Dine JL, O'Sullivan CC, Voeller D, et al. The TRAIL receptor agonist drozitumab targets basal B triple-negative breast cancer cells that express vimentin and Axl [J]. Breast Cancer Res Treat, 2016,155(2):235-251.
[7]	Tanaka K, Tokunaga E, Inoue Y, et al. Impact of expression of vimentin and axl in breast cancer[J]. Clin Breast Cancer, 2016,16(6):520-526.
[8]	Stewart TA, Azimi I, Brooks AJ, et al. Janus kinases and Src family kinases in the regulation of EGF-induced vimentin expression in MDAMB-468 breast cancer cells[J]. Int J Biochem Cell Biol, 2016, 76:64-74.
[9]	Liang S, Marti TM, Dorn P, et al. 18P Epithelial-to-mesenchymal transition (EMT) is required for resistance to anti-folate chemotherapy in lung cancer[J]. J Thorac Oncol,2016,11(4 Suppl): S63.
[10]	Zhang J, Chen XY, Huang KJ, et al. Expression of FoxM1 and the EMT-associated protein E-cadherin in gastric cancer and its clinical significance[J]. Oncol Lett,2016,12(4):2445-2450.
[11]	Gerecke C, Scholtka B, Löwenstein Y, et al. Hypermethylation of ITGA4,TFPI2 and VIMENTIN promoters is increased in inflamed colon tissue: putative risk markers for colitis-associated cancer[J]. J Cancer Res Clin Oncol,2015,141(12):2097-2107.
[12]	Fite K, Gomez-Cambronero J. Down-regulation of microRNAs (MiRs)203,887,3619 and 182 prevents vimentin-triggered, phospholipase D(PLD)-mediated cancer cell invasion [J]. J Biol Chem, 2016,291(2):719-730.
[13]	Li X, Yang J, Wang X, et al. Role of TWIST2, E-cadherin and vimentin in epithelial ovarian carcinogenesis and prognosis and their interaction in cancer progression [J]. Eur J Gynaecol Oncol, 2016,37(1):100-108.
[14]	Cong H, Yao RY, Sun ZQ, et al. DNA hypermethylation of the vimentin gene inversely correlates with vimentin expression in intestinaland diffuse-type gastric cancer [J]. Oncol Lett, 2016, 11 (1):842-848.
[15]	Lindsay CR, Le Moulec S, Billiot F, et al. Vimentin and Ki67 expression in circulating tumour cells derived from castrate-resistant prostate cancer[J]. BMC Cancer,2016,16:168.
[16]	Miyatake Y, Sheehy N, Ikeshita S, et al. Anchorage-dependent multicellular aggregate formation induces CD44 high cancer stem celllike ATL cells in an NF-kappaB and vimentin-dependent manner[J].Cancer Lett,2015,357(1):355-363.

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