Does vimentin help to delineate the so-called 'basal type breast cancer'?

Kusińska, Renata; Kordek, Radzisław; Płuciennik, Elżbieta; Piekarski, Janusz; Potemski, Piotr

doi:10.1186/1756-9966-28-118

Cited by 33 publications

(25 citation statements)

References 27 publications

(46 reference statements)

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“…[5] Eight of the patients with significant vimentin positivity were seen in females in their golden years (50 years) and one case in a 65 year old lady. An overall mean young age (45.6 years) has also been documented by Kusinska et al and Chen et al [11,17] Tumor grade is an important prognostic factor in carcinoma breast. The comparison of our findings with other studies is in Table 3.…”

Section: Discussionmentioning

confidence: 57%

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Expression of vimentin in breast carcinoma, its correlation with Ki67 and other histopathological parameters

Hemalatha¹,

Suresh²,

Kumar³

2013

Indian J Cancer

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Section: Discussionmentioning

confidence: 57%

“…Vimentin expression in tumor cells has been reported to be 7.7%, 21.1%, 14%, and 13.4% by various authors. [5,[11][12][13] . Our finding was lesser than Thomas et al who noted positivity in 25/53 (47.1%) cases.…”

Section: Discussionmentioning

confidence: 99%

Expression of vimentin in breast carcinoma, its correlation with Ki67 and other histopathological parameters

Hemalatha¹,

Suresh²,

Kumar³

2013

Indian J Cancer

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“…7,[9][10][11] Similar correlations between vimentin overexpression and invasion are observed in cancer cell lines and mouse models across most tumor types. 6,12 In breast cancer, in particular, vimentin positive tumors were observed in younger women, usually lacked estrogen and progesterone receptors, and correlated with high-grade cancer 13 and tumor size. 14 Studies done in vitro show that vimentin is essential for cell motility and migration, loss of vimentin expression nearly eliminates cell migration 5,[15][16][17] and increased expression enhances migration.…”

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confidence: 99%

Withaferin A inhibits breast cancer invasion and metastasis at sub‐cytotoxic doses by inducing vimentin disassembly and serine 56 phosphorylation

Thaiparambil

Bender

Ganesh

et al. 2011

Intl Journal of Cancer

229

208

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Withaferin A (WFA) is purified from the plant Withania somnifera and inhibits the vimentin cytoskeleton. Vimentin overexpression in cancer correlates with metastatic disease, induction of epithelial to mesenchymal transition and reduced patient survival. As vimentin functions in cell motility, we wanted to test the hypothesis that WFA inhibits cancer metastasis by disrupting vimentin function. These data showed that WFA had weak cytotoxic and apoptotic activity at concentrations less than or equal to 500 nM, but retained potent anti-invasive activity at these low doses. Imaging of breast cancer cell lines revealed that WFA induces perinuclear vimentin accumulation followed by rapid vimentin depolymerization. A concomitant induction of vimentin ser56 phosphorylation was observed, which is consistent with vimentin disassembly. Structure activity relationships were established using a set of chemically modified WFA analogs and showed that the predicted vimentin-binding region of WFA is necessary to induce vimentin ser56 phosphorylation and for its anti-invasive activity. Pharmacokinetic studies in mice revealed that WFA reaches peak concentrations up to 2 lM in plasma with a half-life of 1.36 hr following a single 4 mg/kg dose. In a breast cancer metastasis mouse model, WFA showed dose-dependent inhibition of metastatic lung nodules and induced vimentin ser56 phosphorylation, with minimal toxicity to lung tissue. Based upon these studies, we conclude that WFA is a potent breast cancer anti-metastatic agent and the anti-metastatic activity of WFA is, at least in part, mediated through its effects on vimentin and vimentin ser56 phosphorylation.Metastatic disease is the major cause of death in almost all cancer types; however, most treatments are developed to target the primary tumor and not the metastases. This is due to metastatic cells being difficult to detect, highly aggressive, chemoresistant and experimentally challenging to model. 1 At present, there is no agent in clinical use that effectively prevents metastasis and most patients ultimately succumb to metastatic disease.The metastatic process can be broadly categorized into three stages-tumor cell invasion into surrounding tissue, intravasation into blood or lymphatic vessels and extravasation into a new host environment. These events are triggered by genetic and epigenetic alterations that transform stationary epithelial cells into migratory cells, a process termed epithelialmesenchymal transition (EMT). 2,3 Recent data suggests that cancer cells can re-trigger EMT to migrate into surrounding tissue. 3,4 A classical EMT protein is vimentin; numerous reports show that vimentin is overexpressed in invasive human tumors but is nearly undetectable in non-invasive, stationary tumors. 3,[5][6][7] Vimentin is a Type III intermediate filament 8 and its overexpression correlates with metastatic disease, EMT induction, poor prognosis and reduced patient survival. 7,[9][10][11] Similar correlations between vimentin overexpression and invasion are observed in cancer ce...

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“…12,13 In the MCF-7 cells, vimentin gene transfection caused increased invasiveness. 13 A previous study demonstrated that invasive breast cancer cell lines expressed more vimentin, suggesting its important role in identifying cases with worse prognosis.…”

Section: -11mentioning

confidence: 99%

“…13 A previous study demonstrated that invasive breast cancer cell lines expressed more vimentin, suggesting its important role in identifying cases with worse prognosis. 12 Our study was aimed to investigate the effect of repeated exposure of endoxifen with or without β-estradiol to MCF-7 breast cancer cell line on cell viability, morphology and EMT progression through the analysis of vimentin mRNA expression.…”

Section: -11mentioning

confidence: 99%

Increased vimentin mRNA expression in MCF-7 breast cancer cell line after repeated endoxifen-treatment

2017

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ABSTRAK ABSTRACTBackground: Epithelial mesenchymal transition (EMT) plays a significant role in the development of cancer cell resistance to drugs. Vimentin, a type III intermediate filament protein, is a marker of EMT. Vimentin's overexpression in cancer correlates well with increased tumor growth, change in cell shape and poor prognosis. Endoxifen is an active metabolite of tamoxifen and has become a new potent agent in the treatment of breast cancer. This is a study that aimed to investigate the effect of endoxifen exposure with or without estradiol on cell viability, cell morphology and EMT progression through the analysis of vimentin mRNA expression after 4-week treatment.

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Does vimentin help to delineate the so-called 'basal type breast cancer'?

Cited by 33 publications

References 27 publications

Expression of vimentin in breast carcinoma, its correlation with Ki67 and other histopathological parameters

Expression of vimentin in breast carcinoma, its correlation with Ki67 and other histopathological parameters

Withaferin A inhibits breast cancer invasion and metastasis at sub‐cytotoxic doses by inducing vimentin disassembly and serine 56 phosphorylation

Increased vimentin mRNA expression in MCF-7 breast cancer cell line after repeated endoxifen-treatment

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