Aberrations of TACC1 and TACC3 are associated with ovarian cancer

Lauffart, Brenda; Vaughan, Mary M.; Eddy, Roger; Chervinsky, David S.; DiCioccio, Richard A.; Black, Jennifer D.; Still, Ivan H.

doi:10.1186/1472-6874-5-8

Cited by 90 publications

(79 citation statements)

References 44 publications

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“…Disturbances of centrosome function have also been implicated in tumorigenesis (Zyss and Gergely, 2009). Intriguingly, aberrations of TACC3 expression are associated with the etiology of ovarian, bladder and non-small-cell lung cancer (Lauffart et al, 2005;Jung et al, 2006;Kiemeney et al, 2010). Moreover, we have recently shown that the cellular outcome of mitotic stress induced by TACC3 depletion is decisively determined by the status of the post-mitotic G 1 checkpoint.…”

Section: Introductionmentioning

confidence: 99%

The centrosomal protein TACC3 controls paclitaxel sensitivity by modulating a premature senescence program

et al. 2010

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Microtubule-interfering cancer drugs such as paclitaxel (PTX) often cause chemoresistance and severe side effects, including neurotoxicity. To explore potentially novel antineoplastic molecular targets, we investigated the cellular response of breast carcinoma cells to short hairpin(sh)RNA-mediated depletion of the centrosomal protein transforming acidic coiled coil (TACC) 3, an Aurora A kinase target expressed during mitosis. Unlike PTX, knockdown of TACC3 did not trigger a cell death response, but instead resulted in a progressive loss of the pro-apoptotic Bcl-2 protein Bim that links microtubule integrity to spindle poison-induced cell death. Interestingly, TACC3-depleted cells arrested in G 1 through a cellular senescence program characterized by the upregulation of nuclear p21 WAF , downregulation of the retinoblastoma protein and extracellular signal-regulated kinase 1/2, formation of HP1c (phospho-Ser83)-positive senescence-associated heterochromatic foci and increased senescence-associated b-galactosidase activity. Remarkably, the onset of senescence following TACC3 knockdown was strongly accelerated in the presence of non-toxic PTX concentrations. Thus, we conclude that mitotic spindle stress is a major trigger of premature senescence and propose that the combined targeting of the centrosomal Aurora A-TACC3 axis together with drugs interfering with microtubule dynamics may efficiently improve the chemosensitivity of cancer cells.

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Section: Introductionmentioning

confidence: 99%

The centrosomal protein TACC3 controls paclitaxel sensitivity by modulating a premature senescence program

et al. 2010

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“…5F-H). We had previously noted that TACC1 is expressed in the surface epithelium of the ovary (Lauffart et al, 2005) (Fig. 5F).…”

Section: Tacc1 Protein Expression In the Normal Human Reproductive Symentioning

confidence: 74%

“…1). We used a well-characterized specific antibody to TACC1 that identifies the mouse and human TACC1 proteins (Cully et al, 2005) and has been previously used for immunohistochemical procedures (Lauffart et al, 2005). Concentration matched rabbit IgG on a duplicate set of slides exhibited negative immunostaining (data available on request).…”

Section: Tacc1 Protein Expression During Mouse Embryogenesismentioning

confidence: 99%

“…Because of the well documented association between TACC1 and breast cancer and malignancies of the genitourinary system (Still et al, 1999a;Conte et al, 2003;Lauffart et al, 2005), we next examined the precise localization of TACC1 in these tissues. Notably, similar to TACC3, TACC1 is highly expressed in the human reproductive system (Fig.…”

Section: Tacc1 Protein Expression In the Normal Human Reproductive Symentioning

confidence: 99%

“…Immunohistochemical procedures were performed as previously described (Lauffart et al, 2005). Mouse embryo sections (no.…”

Section: Immunohistochemical Analysismentioning

confidence: 99%

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Temporal and spatial expression of TACC1 in the mouse and human

Lauffart¹,

DiMatteo²,

Vaughan³

et al. 2006

Dev. Dyn.

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TACC1 is the founding member of the evolutionarily conserved transforming acidic coiled coil genes. These genes play a role in normal development and tumorigenesis through interactions with multiple complexes involved in transcription, translation, and centrosomal dynamics. Despite its importance, detailed examination of the expression of TACC1 and splice variants has not previously been performed. In this study, the spatiotemporal distribution of the Tacc1 protein was examined immunohistochemically in cross-sections of mouse embryonic tissues. We also report the distribution of currently known/predicted TACC1 splice variants in adult humans. These results indicate that Tacc1 is regulated in a dynamic manner during embryogenesis. In adult humans, ubiquitous expression of at least one TACC1 splice variant is noted, although specific combinations of variants are evident in individual differentiated tissues. An important observation is that in the in vivo three-dimensional tissue architecture of the growing organism, both the human and mouse TACC1 protein can be localized to different subcellular compartments in a cell-and tissue-specific manner. This indicates that exploration of TACC1 function must take into account the temporal expression of specific splice variants that may perform different cell-type and tissue-specific functions. Furthermore, this analysis will provide the groundwork from which future Tacc1 knockout strategies can be designed and properly interpreted.

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LINC01140 inhibits nonsmall cell lung cancer progression and cisplatin resistance through the miR‐4742‐5p/TACC1 axis

Wang

Li²,

Zhang

et al. 2022

J Biochem & Molecular Tox

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Recent studies show that lncRNAs participate in drug resistance and nonsmall cell lung cancer (NSCLC) progression. This study aimed to study the roles and mechanisms of long intergenic nonprotein coding RNA 01140 (LINC01140) in regulating NSCLC progression and drug resistance. Real‐time quantitative polymerase chain reaction and western blot analysis were used to detect LINC01140, miR‐4742‐5p, and transforming acidic coiled‐coil 1 (TACC1) expression in NSCLC cells. The interaction between two molecules was examined by luciferase reporter and/or RNA immunoprecipitation assays. Cell invasion, apoptosis, and cisplatin cytotoxicity were assessed by transwell invasion assay, flow cytometry analysis, and CCK‐8 assay, respectively. LINC01140 was downregulated and miR‐4742‐5p was upregulated in NSCLC. LINC01140 inhibited miR‐4742‐5p expression by competitively binding to miR‐4742‐5p, while miR‐4742‐5p targeted TACC1 to inhibit TACC1 expression in NSCLC cells. LINC01140 enrichment repressed the invasive potential and cisplatin resistance and triggered apoptosis, which was reversed by miR‐4742‐5p overexpression. miR‐4742‐5p inhibition suppressed cell invasion and cisplatin resistance and accelerated apoptosis in NSCLC cells, while TACC1 silencing abolished these effects. Mechanistically, LINC01140 positively regulated TACC1 expression by sponging miR‐4742‐5p. In conclusion, LINC01140 inhibited NSCLC progression and cisplatin resistance via functioning as a ceRNA for miR‐4742‐5p to modulate TACC1.

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Aberrations of TACC1 and TACC3 are associated with ovarian cancer

Cited by 90 publications

References 44 publications

The centrosomal protein TACC3 controls paclitaxel sensitivity by modulating a premature senescence program

The centrosomal protein TACC3 controls paclitaxel sensitivity by modulating a premature senescence program

Temporal and spatial expression of TACC1 in the mouse and human

LINC01140 inhibits nonsmall cell lung cancer progression and cisplatin resistance through the miR‐4742‐5p/TACC1 axis

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