Cell cycle arrest and cellular differentiation mediated by a cell surface sialoglycopeptide

Edson, Gregory D.; Fattaey, Heideh K.; Johnson, Terry C.

doi:10.1016/0024-3205(91)90236-5

Cited by 7 publications

(5 citation statements)

References 17 publications

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“…With the three prostate cancer cell lines examined here ( Fig. 1A-C), the kinetics of cell cycle inhibition, which allowed a degree of cell doubling prior to the cessation of cell proliferation, were consistent with a sitespecific cell cycle block that was previously observed with CeReS-18 and other cell lines [15,16]. Based on these observations, we conclude that CeReS-18 does not appear to exhibit differential effects on androgen receptor-positive or -negative cell lines, unlike other previously studied agents such as beta transforming growth factor (␤TGF), that elicit their inhibitory effect only on androgen receptor-positive cells [21].…”

Section: Discussionsupporting

confidence: 86%

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CeReS-18 inhibits growth and induces apoptosis in human prostatic cancer cells

et al. 1999

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BACKGROUND Polypeptide growth factors are positive and negative regulators of prostatic growth and function, and many positive regulators of growth in the prostate have been extensively studied. However, very few inhibitors of prostate cell proliferation have been identified. We have isolated a unique 18‐kDa sialoglycopeptide (CeReS‐18) which inhibits cell proliferation of three separate lines of human prostate cancer cells, as well as inducing cellular cytotoxicity via an apoptotic pathway unrelated to the Bcl‐2 family of proteins. METHODS Cell cycle inhibition was analyzed by direct cell counts with a Coulter (Miami, FL) cell counter. Apoptotic cells were analyzed by electron microscopy, annexin V‐fluorescein isothiocyanate (FITC) staining, fluorescence microscopy, and propidium iodide uptake measured with a fluorescence‐activated cell sorter. Expression of the proteins of the Bcl‐2 family was detected by Western blot analysis. RESULTS We found that CeReS‐18 inhibits cell proliferation of androgen‐responsive, LNCaP.FGC human prostate cancer cells, as well as of androgen‐nonresponsive DU‐145 and PC3 human prostate cancer cells. Furthermore a, fivefold increase over the inhibitory concentration of CeReS‐18 elicited a cytotoxic response by all three cell lines. We thus characterized the cytotoxic mechanism as apoptotic in nature, and we measured the expression of several members of the Bcl‐2 family in PC3 cells upon treatment with CeReS‐18. CONCLUSIONS The data indicate that CeReS‐18 is a potent inhibitor of cellular progression through the cell cycle by both androgen‐responsive and androgen‐nonresponsive human prostate cancer cells. In addition, treatment of both types of cells with increased concentrations of CeReS‐18 induces cellular cytotoxicity, characterized as apoptosis. Prostate 38:285–295, 1999. © 1999 Wiley‐Liss, Inc.

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Section: Discussionsupporting

confidence: 86%

“…1). The kinetics of inhibition, which allowed a degree of cell doubling prior to cessation of cell proliferation, were consistent with a site-specific block that previously was observed with mouse fibroblast Swiss 3T3 and other cell lines [15,16].…”

Section: Effect Of Ceres-18 On Prostate Cancer Cell Proliferationsupporting

confidence: 86%

CeReS-18 inhibits growth and induces apoptosis in human prostatic cancer cells

et al. 1999

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“…removal (Fattaey et al, 1989Edson et al, 1991). CeReS-18 binds to a specific cell surface receptor (Sharifi and Johnson, 1987), and binding to this receptor correlates with protein synthesis inhibition (Bascom et al, 1986).…”

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“…Our laboratory has purified an 18 kDa cell surface sialoglycopeptide (CeReS-18) from intact bovine cerebral cortex cells which can reversibly inhibit the proliferation of a wide array of fibroblasts and epithelial cells, both nontransformed and transformed, from a range of species including humans, mice, and insects (reviewed by Johnson, 1994). CeReS-18 appears to block most cell types in the late GI phase of the cell cycle, and results in cell cycle synchronization upon 0 1995 WILEY-LISS, INC. removal (Fattaey et al, 1989Edson et al, 1991). CeReS-18 binds to a specific cell surface receptor (Sharifi and Johnson, 1987), and binding to this receptor correlates with protein synthesis inhibition (Bascom et al, 1986).…”

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Role of calcium in growth inhibition induced by a novel cell surface sialoglycopeptide

Betz

Westhoff

Johnson

1995

Journal Cellular Physiology

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Our laboratory has purified an 18 kDa cell surface sialoglycopeptide growth inhibitor (CeReS-18) from intact bovine cerebral cortex cells. Evidence presented here demonstrates that sensitivity to CeReS-18-induced growth inhibition in BALB-c 3T3 cells is influenced by calcium, such that a decrease in the calcium concentration in the growth medium results in an increase in sensitivity to CeReS-18. Calcium did not alter CeReS-18 binding to its cell surface receptor and CeReS-18 does not bind calcium directly. Addition of calcium, but not magnesium, to CeReS-18-inhibited 3T3 cells results in reentry into the cell cycle. A greater than 3-hour exposure to increased calcium is required for escape from CeReS-18-induced growth inhibition. The calcium ionophore ionomycin could partially mimic the effect of increasing extracellular calcium, but thapsigargin was ineffective in inducing escape from growth inhibition. Increasing extracellular calcium 10-fold resulted in an approximately 7-fold increase in total cell-associated 45Ca+2, while free intracellular calcium only increased approximately 30%. However, addition of CeReS-18 did not affect total cell-associated calcium or the increase in total cell-associated calcium observed with an increase in extracellular calcium. Serum addition induced mobilization of intracellular calcium and influx across the plasma membrane in 3T3 cells, and pretreatment of 3T3 cells with CeReS-18 appeared to inhibit these calcium mobilization events. These results suggest that a calcium-sensitive step exists in the recovery from CeReS-18-induced growth inhibition. CeReS-18 may inhibit cell proliferation through a novel mechanism involving altering the intracellular calcium mobilization/regulation necessary for cell cycle progression.

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“…However, we have previously reported the isolation and purification of a unique 18-kDa sialoglycopeptide (SGP) from intact bovine cerebral cortex cells [Sharifi et al, 19861. The SGP was liberated from the cell surface by mild proteolysis, and shown to be a potent and reversible inhibitor of DNA synthesis, protein synthesis, and cell proliferation Chou et al, 1987;Edson et al, 1991;Fattaey et al, 1989, 19911. The SGP binds to a specific cell surface receptor and its inhibitory action is directly related to receptor occupancy [Bascom et al, 1986;Sharifi et al, 19871. We recently identified a 66-kDa protein on the surface of mouse Swiss 3T3 cells that was structurally related to the 18-kDa bovine cerebral cortex SGP inhibitor [Lakshmanarao et al, 19911.…”

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The identification of a naturally occurring cell surface growth inhibitor related to a previously described bovine sialoglycopeptide

Fattaey

Enebo

Moos

et al. 1993

J of Cellular Biochemistry

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A 66-kDa sialoglycoprotein has been identified as the parental membrane molecule of an earlier described sialoglycopeptide (SGP), an 18-kDa molecule released by protease treatment of intact bovine cerebral cortex cells that was shown to be a potent inhibitor of cellular proliferation. The 66-kDa parental sialoglycoprotein (p-SGP) was purified approximately 2,400-fold, to apparent homogeneity, from bovine cerebral cortex cell membranes by its release during incubation with 3 M NaCl, preparative isoelectric focusing and lectin affinity chromatography. Although a membrane-associated molecule, the p-SGP appeared to be tightly bound to the cell membrane, since it was not released during incubations in the absence of 3 M NaCl. Incubation of the membrane preparations with 3 M urea proved to be too harsh, and the antigenicity required to follow the purification of the p-SGP was abolished. Analyses by SDS-PAGE, under reducing and nonreducing conditions, suggested that the p-SGP membrane component was a single polypeptide without subunit structure. The p-SGP was shown to be structurally related to the SGP fragment by immunoblots with IgG raised to the SGP inhibitor, and functionally related to the SGP by its ability to inhibit Swiss 3T3 proliferation at concentrations strikingly similar to that previous measured with the SGP fragment.

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Cell cycle arrest and cellular differentiation mediated by a cell surface sialoglycopeptide

Cited by 7 publications

References 17 publications

CeReS-18 inhibits growth and induces apoptosis in human prostatic cancer cells

CeReS-18 inhibits growth and induces apoptosis in human prostatic cancer cells

Role of calcium in growth inhibition induced by a novel cell surface sialoglycopeptide

The identification of a naturally occurring cell surface growth inhibitor related to a previously described bovine sialoglycopeptide

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