Induction of stathmin expression during liver regeneration

Koppel, Juraj; Loyer, Pascal; Maucuer, Alexandre; Rehák, P; Manceau, Valérie; Guguen‐Guillouzo, Christiane; Sobel, André

doi:10.1016/0014-5793(93)80298-9

Cited by 45 publications

(27 citation statements)

References 52 publications

(25 reference statements)

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“…Stathmin expression, in that case, is likely being up-regulated, in relation to the limitation of cell overgrowth at the stage preceding cell differentiation (Balogh et al, 1996). This cell culture result is in good agreement with the induction of stathmin expression during liver regeneration, stathmin displaying a delayed expression peak following the mitotic peak and correlating with the slowdown in cell proliferation (Koppel et al, 1993). Stimulated expression of stathmin may thus be part of a regulatory programme aimed at limiting cell overproliferation, and also activated, although inefficiently, in transformed tumoral cells.…”

Section: Discussionsupporting

confidence: 75%

“…Stathmin expression and phosphorylation are probably linked to the control of cell differentiation (Doye et al, 1992;Di Paolo et al, 1996) and proliferation (Braverman et al, 1986;Cooper et al, 1990;Koppel et al, 1993;Balogh et al, 1996) (for a review see Sobel, 1991). The state of stathmin phosphorylation changes markedly during the cell cycle (Strahler et al, 1992;Brattsand et al, 1994), and cell division also appears to require multisite phosphorylation of this protein (Larsson et al, 1995;Lawler et al, 1997).…”

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confidence: 99%

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Overexpression of the stathmin gene in a subset of human breast cancer

Bièche

Lachkar²,

Becette³

et al. 1998

Br J Cancer

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Summary Stathmin is a highly conserved cytosolic phosphoprotein that destabilizes microtubules. Stathmin, which has been proposed as a relay protein integrating diverse cell signalling pathways, acts in vitro as a tubulin-sequestering protein, and its activity is dramatically reduced by phosphorylation. Interestingly, stathmin expression and phosphorylation are regulated during the control of cell growth and differentiation, and there is much evidence suggesting that in vivo stathmin plays a role in the control of microtubule dynamics during mitosis. Stathmin may thus be considered as one of the key regulators of cell division. We examined 50 human primary breast tumours for stathmin mRNA

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Section: Discussionsupporting

confidence: 75%

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confidence: 99%

Overexpression of the stathmin gene in a subset of human breast cancer

Bièche

Lachkar²,

Becette³

et al. 1998

Br J Cancer

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“…30 There is considerable evidence that stathmin overexpression is relevant to proliferation, cell growth and carcinogenesis. [31][32][33] Stathmin is known to be upregulated in a subset of human breast cancers [34][35][36] and has been detected in ductal carcinoma in situ. 37 In the present study, we observed a close association between stathmin expression and Ki-67 immunostaining supporting the notion that stathmin overexpression is specific to proliferating cells.…”

Section: Discussionmentioning

confidence: 99%

Gene expression profiling in the mammary gland of rats treated with 7,12‐dimethylbenz[a]anthracene

Papaconstantinou

Shanmugam

Shan

et al. 2005

Intl Journal of Cancer

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Identification of molecular markers of early‐stage breast cancer development is important for the diagnosis and prevention of the disease. In the present study, we used microarray analysis to examine the differential expression of genes in the rat mammary gland soon after treatment with a known chemical carcinogen, 7,12‐dimethylbenz[a]anthracene (DMBA), and prior to tumor development. Six weeks after DMBA, differential expression of multiple genes involved in cell growth, differentiation and microtubule dynamics were observed. Gene expression changes were further validated by a combination of techniques, including real‐time PCR, RT‐PCR, Western blotting and immunohistochemistry. An inhibition of differentiation in this early stage was suggested by the lower expression of β‐casein and transferrin and higher expression of hsp27 in glands from DMBA‐treated rats. Possible cell cycle deregulation was indicated by an increased expression of cyclin D1 and hsp86, a heat shock protein associated with cyclin D1. Prior to tumor development, DMBA increased cellular proliferation as detected by Ki‐67 and stathmin immunostaining in histologically normal mammary gland. Genes regulating microtubule function, including stathmin, Ran, α‐tubulin and hsp27, were all overexpressed in the mammary gland of DMBA‐treated rats, raising the possibility that disruption of microtubule dynamics and abnormal mitosis may be critical events preceding breast cancer development. Several of the altered proteins, including hsp27, hsp86 and stathmin, may ultimately serve as markers of early breast cancer development. Published 2005 Wiley‐Liss, Inc.

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“…The murine coiled-coil domain has been shown to interact with a regulator of cell growth and di erentiation called stathmin (Li and Cohen, 1996;Dipaolo et al, 1996;Marklund et al, 1993). Stathmin, also known as oncoprotein 18 or metablastin, is an evolutionarily conserved protein which is phosphorylated in response to growth and di erentiation factors (Dipaolo et al, 1996;Marklund et al, 1993), T-cell activation (Gratiot-Deans et al, 1992), embryonic development (Doye et al, 1992) and tissue regeneration (Koppel et al, 1993). Stathmin levels have been reported as elevated in acute leukemias/aggressive lymphomas (Roos et al, 1993), and neuroblastomas (Hallat et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

TSG101 is not mutated in lung cancer but a shortened transcript is frequently expressed in small cell lung cancer

Proctor

Fan

et al. 1998

Oncogene

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TSG101 is a candidate tumor suppressor gene whose deletion in NIH3T3 cells leads to spontaneous lung metastases in nude mice. Aberrant transcripts of TSG101 have been identi®ed in 47% of primary breast carcinomas, without evidence of intragenic deletions at the TSG101 locus on 11p15. To investigate the possible role of TSG101 in lung cancer, which often shows 11p allele loss, we performed transcript analysis and mutational analysis of TSG101 in lung cancer cell lines. Reverse transcriptase RT ± PCR and Northern analysis detected a common TSG101 transcript, shortened because of an internal deletion, which was expressed simultaneously with the wild-type transcript in 89% of small cell lung cancer (SCLC) lines. In contrast, the wild-type transcript was expressed alone in normal tissues, primary non-small cell lung cancer (NSCLC) specimens, and the majority of NSCLC cell lines. Sequence of the shortened SCLC transcript was identical to that of the most common aberrant transcript identi®ed in breast cancer, consisting of a deletion of exons 2 ± 4 and part of 1 and 5. Southern analysis of SCLC lines expressing the shortened transcript did not detect any intragenic deletions. Single strand conformational polymorphism (SSCP) analysis and direct sequencing of TSG101 cDNAs also identi®ed no mutations or deletions. These results suggest that TSG101 is not mutated in lung cancer but that aberrant splicing of TSG101 occurs in SCLC.

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Induction of stathmin expression during liver regeneration

Cited by 45 publications

References 52 publications

Overexpression of the stathmin gene in a subset of human breast cancer

Overexpression of the stathmin gene in a subset of human breast cancer

Gene expression profiling in the mammary gland of rats treated with 7,12‐dimethylbenz[a]anthracene

TSG101 is not mutated in lung cancer but a shortened transcript is frequently expressed in small cell lung cancer

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