β3‐Tubulin is induced by estradiol in human breast carcinoma cells through an estrogen‐receptor dependent pathway

Saussede-Aim, Jennifer; Matera, Eva–Laure; Ferlini, Cristiano; Dumontet, Charles

doi:10.1002/cm.20377

Cited by 22 publications

(20 citation statements)

References 30 publications

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“…3B). β-estradiol increased the expression of TUBB3 in MCF-7 cells [23]. TUBB3 also was expressed in MDA-MB-231, TMX2-28, and ZR-75 breast cancer cells (Fig.…”

Section: Resultsmentioning

confidence: 99%

Guanylate-Binding Protein-1 protects ovarian cancer cell lines but not breast cancer cell lines from killing by paclitaxel

Tipton

Nyabuto

Trendel

et al. 2016

Biochemical and Biophysical Research Communications

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Forced expression of the cytokine-induced large GTPase, human Guanylate-Binding Protein-1 (hGBP-1), in ovarian cancer cell lines increases resistance to paclitaxel. Elevated hGBP-1 RNA in ovarian tumors correlates with shorter recurrence-free survival. In contract, hGBP-1 is part of a gene signature predicting improved prognosis in all subtypes of breast cancers. hGBP-1 does not confer paclitaxel resistance on MCF-7 and TMX2-28 breast cancer cells. Expression of the isotype of the hGBP-1-interacting protein, PIM1, which may contribute to paclitaxel resistance when associated with hGBP-1, is different in breast and ovarian cancer cell lines. Breast cancer cell lines express the 44 kDa isoform of PIM-1, and ovarian cancer cell lines express the 33 kDa isoform.

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“…3B). β-estradiol increased the expression of TUBB3 in MCF-7 cells [23]. TUBB3 also was expressed in MDA-MB-231, TMX2-28, and ZR-75 breast cancer cells (Fig.…”

Section: Resultsmentioning

confidence: 99%

Guanylate-Binding Protein-1 protects ovarian cancer cell lines but not breast cancer cell lines from killing by paclitaxel

Tipton

Nyabuto

Trendel

et al. 2016

Biochemical and Biophysical Research Communications

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“…In Drosophila, 3-tubulin expression is enhanced by an exposure to ecdysone, a steroid hormone, through a transcriptional mechanism [80]. Recently, Saussede-Aim J et al found that exposure of ER + MCF-7 cells to estradiol induced 3-tubulin expression in both mRNA and protein levels, while estradiol had no effect on the expression of 3-tubulin in ER -MDA-MB-231 cells [81]. They further showed that co-administration of antiestrogens including tamoxifen or fulvestrant, completely abolished the increase of 3-tubulin mRNA levels due to estradiol in MCF-7 cells, implying that estradiol regulates 3-tubulin expression, and thereby induces resistance of ER + breast tumors to antimicrotubule drugs through an ER -dependent pathway.…”

Section: Enhanced 3-tubulin Expression By E2/ermentioning

confidence: 99%

The Role of Estrogen and Estrogen Receptors in Chemoresistance

Sui¹,

Zhang²,

Fan³

2011

CMC

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Drug resistance is one of the major obstacles limiting the success of cancer chemotherapy. Biological mechanisms contributing to drug resistance may be present de novo and related to inherent features or may be raised after exposure to anticancer drugs. In recent years, both clinical observations and experimental studies suggested that steroid hormones and their receptors might also affect the therapeutic efficacy of antineoplastic drugs. Estrogens and estrogen receptors (ER) are well-known for their critical roles in the development and progression of breast tumors. It has long been known that breast tumors expressing ERα protein (ERα+) behave in a fundamentally different fashion than ERα-negative (ERα-) tumors with regard to their responses to hormonal therapy. Data obtained from both laboratory and clinical investigations suggested that some chemotherapeutic agents are clearly less effective in ERα+ tumors than ERα- tumors, although the mechanisms of ERα-mediated chemoresistance are not entirely clear. Moreover, recent studies from our laboratory and others demonstrated that the combination of antiestrogenic agents with chemotherapeutic drugs is of significant therapeutic benefit in ERα+ breast cancer over chemotherapy alone. In addition, the ERα-derived peptides, microRNAs specifically targeting ERα, as well as agents targeting estrogen-related receptors (ERRs) may hold promise to sensitize ERα+ breast tumors to chemotherapy. Considering that ERs are expressed in ˜ 65% of human breast cancer, the ERα-mediated chemoresistance has become a big challenge for clinical treatment. The hope to overcome this drug resistance relies on further clarification of specific pathways or molecules contributing to the resistance. More exhaustive and systematic studies are essential to reach deeper understandings on the underlying mechanisms and to develop novel approaches to sensitize ERα+ breast tumors to chemotherapy.

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“…This information further supports androgen regulation and the increased expression of β III-tubulin in castration-resistant tumours. Interestingly, one recent study provided evidence for a potential role of oestradiol and oestrogen receptor (ER) in regulating β III-tubulin in breast cancer cells (Saussede-Aim et al , 2009). Although it remains to be determined as to whether this regulation implies a genomic or a non-genomic effect of ER, this observation could be of interest in PCa as oestrogen-dependent signature has been linked to aggressive characteristics in this tissue (Bonkhoff et al , 2001; Setlur et al , 2008).…”

Section: Discussionmentioning

confidence: 99%

Increased expression of class III β-tubulin in castration-resistant human prostate cancer

et al. 2009

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Background:Class III β-tubulin (βIII-tubulin) is expressed in tissues of neuronal lineage and also in several human malignancies, including non-small-cell lung carcinoma, breast and ovarian cancer. Overexpression of βIII-tubulin in these tumours is associated with an unfavourable outcome and resistance to taxane-based therapies. At present, βIII-tubulin expression remains largely uncharacterised in prostate cancer.Methods:In this report, we evaluated the expression of βIII-tubulin in 138 different human prostate tumour specimens by immunohistochemistry from patients with hormone-treated or hormone-untreated prostate cancer. βIII-tubulin expression was also examined in various prostatic cancer cell lines including in androgen-sensitive human prostate cancer cells, LNCaP, grown in androgen-depleted medium in 2D cultures or as tumour xenografts when the host mouse was castrated.Results:Whereas moderate-to-strong βIII-tubulin expression was detected in only 3 out of 74 (4%) hormone-naive tumour specimens obtained from patients who never received hormone therapy, 6 out of 24 tumour specimens (25%) from patients treated for 3 months with neoadjuvant hormone therapy and 24 out of 40 (60%) castration-resistant tumour specimens from chronic hormone-treated patients were found to express significant levels of βIII-tubulin. These findings were supported by in vitro and in vivo settings.Conclusion:Our data indicate that βIII-tubulin expression is augmented in prostate cancer by androgen ablation and that the expression of this β-tubulin isoform is associated with the progression of prostate cancer to the castration-resistant state, a stage largely responsible for mortality from prostate cancer.

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β3‐Tubulin is induced by estradiol in human breast carcinoma cells through an estrogen‐receptor dependent pathway

Cited by 22 publications

References 30 publications

Guanylate-Binding Protein-1 protects ovarian cancer cell lines but not breast cancer cell lines from killing by paclitaxel

Guanylate-Binding Protein-1 protects ovarian cancer cell lines but not breast cancer cell lines from killing by paclitaxel

The Role of Estrogen and Estrogen Receptors in Chemoresistance

Increased expression of class III β-tubulin in castration-resistant human prostate cancer

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