Down‐regulation but not phosphorylation of stathmin is associated with induction of HL60 cell growth arrest and differentiation by physiological agents

Johnson, William E.; Jones, Nick D.; Rowlands, David; Williams, Ann C.; Guest, Simon S.; Brown, Geoffrey

doi:10.1016/0014-5793(95)00416-7

Cited by 19 publications

(12 citation statements)

References 34 publications

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“…A previous report showing that TSG101 may interact with stathmin provides a clue as to the mechanism through which this protein may function as a tumor suppressor (Johnson et al, 1995). Stathmin, also termed Oncoprotein 18, phosphoprotein 18, and p19, is a highly conserved 19 kDa cytoplasmic protein which is phosphorylated in response to a wide variety of signals (Beretta et al, 1993;Chneiweiss et al, 1989;Duraj et al, 1995;Leighton et al, 1993;Nakamura et al, 1995;Sobel, 1991).…”

Section: T T1 T2 T T T T T T T Tmentioning

confidence: 99%

Frequent abnormalities of TSG101 transcripts in human prostate cancer

et al. 1997

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TSG101 has been identi®ed as a candidate tumor suppressor gene and abnormal transcripts have been identi®ed in a substantial fraction of breast cancers. To determine whether TSG101 expression is commonly altered in other tumors, a series of 15 primary and metastatic prostate cancers were analysed by reverse transcriptase-PCR ampli®cation. Abnormal transcripts with extensive deletions in the coding region were found in nine of these tumors, while only the normal transcript was found in control and benign prostatic hypertrophy tissues. More than one abnormal transcript was found in four of these nine cases and distinct abnormal TSG101 transcripts were found in separate biopsies taken from one tumor. Importantly, the normal TSG101 transcript was undetectable in two metastatic prostate cancers, indicating the absence of TSG101 protein. Sequence analysis demonstrated that there were at least six distinct deletions, with four of these deletions found in more than one tumor sample. The most commonly identi®ed deletion, from bp 153 to 1055, was identical to a deletion reported previously in breast cancer. These results demonstrate that TSG101 transcripts are frequently abnormal in prostate cancer and suggest that loss of TSG101 protein contributes to disease development or progression.

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Section: T T1 T2 T T T T T T T Tmentioning

confidence: 99%

Frequent abnormalities of TSG101 transcripts in human prostate cancer

et al. 1997

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“…Other studies show that stathmin functions as a primary factor in various biological contexts including human disease and development of the nervous system (Friedrich et al, 1995;Johnson et al, 1995;Di Paolo et al, 1996;Lewis et al, 2000;Cheon et al, 2001;Liedtke et al, 2002). Present models show stathmin expression to be regulated by p53 or p21 WAF1 (Johnsen et al, 2000).…”

Section: Introductionmentioning

confidence: 61%

Altered levels and regulation of stathmin in paclitaxel-resistant ovarian cancer cells

2003

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Two paclitaxel(Ptx)-resistant ovarian cancer cell lines, 1A9/Ptx-10 and 1A9/Ptx-22, isolated from the 1A9 cell line (a clone of the A2780 line) by continuous exposure to Ptx and verapamil, have point mutations in their major b-tubulin gene and in one or both alleles of their TP53 gene. These cells were examined for alterations in cell cycle regulators and the tubulin-binding protein stathmin. Unlike parental cells, neither 1A9/Ptx-10 nor 1A9/Ptx-22 expressed detectable levels of p21 WAF1/Cip1 , a putative transcriptional regulator of stathmin, but did overexpress stathmin and Bcl2. No differences were noted in the expression levels of proliferative cell nuclear antigen or tyrosine-phosphorylated p34 Cdc2 . Ptx treatment altered little the expression of stathmin in the parental cell line, although it increased p21 WAF1/Cip1 levels several-fold. Infection of Ptx-resistant lines with a wild-type TP53-bearing adenovirus (AdWTp53) changed cell cycle distribution and increased the levels of p21 WAF1/Cip1 , but caused no changes in stathmin levels. Microtubule drug resistance in ovarian carcinoma may be associated with altered p53/21 WAF1/Cip1 regulatory pathways for stathmin expression and function.

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“…It needs to be deactivated via phosphorylation of its serine residues in order for the cells to progress through mitosis. Overexpression of WT or nonphosphorylatable stathmin leads to reduced growth rate and in case of the latter to G 2 to M blockage (14,15,18,19). Paradoxically, a reduction in stathmin levels also leads to abnormal formation of the mitotic spindle and accumulation of cells in the G 2 to M phase (12,23,32).…”

Section: Discussionmentioning

confidence: 97%

“…Based on our previous studies (46), evidence showing that stathmin is involved in the regulation of mitosis (14,15,18,19,32) and the established role of coordinated regulation of cell cycle in recovery from renal injury (10,36,37,42), we hypothesized that the absence of stathmin adversely affects the tubular repair and recovery process subsequent to renal IRI. To test our hypothesis, WT and OP18Ϫ/Ϫ mice were subjected to kidney IRI.…”

Section: Discussionmentioning

confidence: 99%

“…These results indicate that stathmin is a marker of cells that have dedifferentiated, reentered the cell cycle and may be involved in the recovery process. Stathmin is a tubulin-binding phosphoprotein that plays an important role in the regulation of spindle formation and mitosis (14,15,18,19,32). It needs to be deactivated via phosphorylation of its serine residues in order for the cells to progress through mitosis.…”

Section: Discussionmentioning

confidence: 99%

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Stathmin-deficient mice develop fibrosis and show delayed recovery from ischemic-reperfusion injury

Zahedi

Revelo

Barone

et al. 2006

American Journal of Physiology-Renal Physiology

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In kidneys subjected to ischemic reperfusion injury (IRI) stathmin, a tubulin-binding protein involved in the regulation of mitosis, is expressed in dedifferentiated and proliferating renal tubule cells during the recovery phase. To ascertain the role of stathmin in the recovery from ischemic kidney injury, stathmin-deficient (OP18-/-) and wild-type (WT) animals were subjected to experimental IRI. At 3, 7, and 14 days after reperfusion serum samples and kidneys were collected for the examination of parameters of renal function, morphology, and recovery. Our studies indicate that on day 14 after reperfusion OP18-/- mice have significant renal failure, whereas the creatinine levels of WT animals have returned to baseline. Compared with WT animals OP18-/- mice had more extensive tubular fibrosis. The examination of proliferating cell nuclear antigen expression indicated that OP18-/- animals have increased proliferative or DNA repair activity for a more prolonged duration. The OP18-/- animals also had an increased number of tubules with apoptotic cells. These results suggest that in stathmin-deficient mice subjected to IRI, the aberrant regulation of cell cycle progression, not observed under normal conditions, impairs or at least delays the process of tubular repair and recovery after acute renal injury.

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Down‐regulation but not phosphorylation of stathmin is associated with induction of HL60 cell growth arrest and differentiation by physiological agents

Cited by 19 publications

References 34 publications

Frequent abnormalities of TSG101 transcripts in human prostate cancer

Frequent abnormalities of TSG101 transcripts in human prostate cancer

Altered levels and regulation of stathmin in paclitaxel-resistant ovarian cancer cells

Stathmin-deficient mice develop fibrosis and show delayed recovery from ischemic-reperfusion injury

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