Replacement of Fhit in cancer cells suppresses tumorigenicity

Zurab Siprashvili; Gabriella Sozzi; Larry D. Barnes; Peter Mccue; Angela K. Robinson; Vladimir Eryomin; Laura Sard; Elda Tagliabue; Angela Greco; Lisa Fusetti; Gary Schwartz; Marco A. Pierotti; Carlo M. Croce; Kay Huebner

doi:10.1073/pnas.94.25.13771

Replacement of Fhit in cancer cells suppresses tumorigenicity

Zurab Siprashvili
, Gabriella Sozzi
, Larry D. Barnes
, Peter Mccue
, Angela K. Robinson
, Vladimir Eryomin
, Laura Sard
, Elda Tagliabue
, Angela Greco
, Lisa Fusetti
, Gary Schwartz
, Marco A. Pierotti
, Carlo M. Croce
, Kay Huebner

Research output: Contribution to journal › Article › peer-review

367 Scopus citations

Abstract

The candidate tumor suppressor gene, FHIT, encompasses the common human chromosomal fragile site at 3p14.2, the hereditary renal caller translocation breakpoint, and cancer cell homozygous deletions. Fhit hydrolyzes dinucleotide 5',5^m-P¹,P³-triphosphate in vitro and mutation of a central histidine abolishes hydrolase activity. To study Fhit function, wild-type and mutant FHIT genes were transfected into cancer cell lines that lacked endogenous Fhit. No consistent effect of exogenous Fhit on growth in culture was observed, but Fhit and hydrolase 'dead' Fhit mutant proteins suppressed tumorigenicity in nude mice, indicating that 5',5^m-P¹,P³-triphosphate hydrolysis is not required for tumor suppression.

Original language	English
Pages (from-to)	13771-13776
Number of pages	6
Journal	Proceedings of the National Academy of Sciences of the United States of America
Volume	94
Issue number	25
DOIs	https://doi.org/10.1073/pnas.94.25.13771
State	Published - 9 Dec 1997
Externally published	Yes

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Siprashvili, Z., Sozzi, G., Barnes, L. D., Mccue, P., Robinson, A. K., Eryomin, V., Sard, L., Tagliabue, E., Greco, A., Fusetti, L., Schwartz, G., Pierotti, M. A., Croce, C. M., & Huebner, K. (1997). Replacement of Fhit in cancer cells suppresses tumorigenicity. Proceedings of the National Academy of Sciences of the United States of America, 94(25), 13771-13776. https://doi.org/10.1073/pnas.94.25.13771

@article{ab17a6b28bb94966b73c6650283a5bfa,

title = "Replacement of Fhit in cancer cells suppresses tumorigenicity",

abstract = "The candidate tumor suppressor gene, FHIT, encompasses the common human chromosomal fragile site at 3p14.2, the hereditary renal caller translocation breakpoint, and cancer cell homozygous deletions. Fhit hydrolyzes dinucleotide 5',5m-P1,P3-triphosphate in vitro and mutation of a central histidine abolishes hydrolase activity. To study Fhit function, wild-type and mutant FHIT genes were transfected into cancer cell lines that lacked endogenous Fhit. No consistent effect of exogenous Fhit on growth in culture was observed, but Fhit and hydrolase 'dead' Fhit mutant proteins suppressed tumorigenicity in nude mice, indicating that 5',5m-P1,P3-triphosphate hydrolysis is not required for tumor suppression.",

author = "Zurab Siprashvili and Gabriella Sozzi and Barnes, \{Larry D.\} and Peter Mccue and Robinson, \{Angela K.\} and Vladimir Eryomin and Laura Sard and Elda Tagliabue and Angela Greco and Lisa Fusetti and Gary Schwartz and Pierotti, \{Marco A.\} and Croce, \{Carlo M.\} and Kay Huebner",

year = "1997",

month = dec,

day = "9",

doi = "10.1073/pnas.94.25.13771",

language = "English",

volume = "94",

pages = "13771--13776",

journal = "Proceedings of the National Academy of Sciences of the United States of America",

issn = "0027-8424",

publisher = "National Academy of Sciences",

number = "25",

}

Siprashvili, Z, Sozzi, G, Barnes, LD, Mccue, P, Robinson, AK, Eryomin, V, Sard, L, Tagliabue, E, Greco, A, Fusetti, L, Schwartz, G, Pierotti, MA, Croce, CM & Huebner, K 1997, 'Replacement of Fhit in cancer cells suppresses tumorigenicity', Proceedings of the National Academy of Sciences of the United States of America, vol. 94, no. 25, pp. 13771-13776. https://doi.org/10.1073/pnas.94.25.13771

TY - JOUR

T1 - Replacement of Fhit in cancer cells suppresses tumorigenicity

AU - Siprashvili, Zurab

AU - Sozzi, Gabriella

AU - Barnes, Larry D.

AU - Mccue, Peter

AU - Robinson, Angela K.

AU - Eryomin, Vladimir

AU - Sard, Laura

AU - Tagliabue, Elda

AU - Greco, Angela

AU - Fusetti, Lisa

AU - Schwartz, Gary

AU - Pierotti, Marco A.

AU - Croce, Carlo M.

AU - Huebner, Kay

PY - 1997/12/9

Y1 - 1997/12/9

N2 - The candidate tumor suppressor gene, FHIT, encompasses the common human chromosomal fragile site at 3p14.2, the hereditary renal caller translocation breakpoint, and cancer cell homozygous deletions. Fhit hydrolyzes dinucleotide 5',5m-P1,P3-triphosphate in vitro and mutation of a central histidine abolishes hydrolase activity. To study Fhit function, wild-type and mutant FHIT genes were transfected into cancer cell lines that lacked endogenous Fhit. No consistent effect of exogenous Fhit on growth in culture was observed, but Fhit and hydrolase 'dead' Fhit mutant proteins suppressed tumorigenicity in nude mice, indicating that 5',5m-P1,P3-triphosphate hydrolysis is not required for tumor suppression.

AB - The candidate tumor suppressor gene, FHIT, encompasses the common human chromosomal fragile site at 3p14.2, the hereditary renal caller translocation breakpoint, and cancer cell homozygous deletions. Fhit hydrolyzes dinucleotide 5',5m-P1,P3-triphosphate in vitro and mutation of a central histidine abolishes hydrolase activity. To study Fhit function, wild-type and mutant FHIT genes were transfected into cancer cell lines that lacked endogenous Fhit. No consistent effect of exogenous Fhit on growth in culture was observed, but Fhit and hydrolase 'dead' Fhit mutant proteins suppressed tumorigenicity in nude mice, indicating that 5',5m-P1,P3-triphosphate hydrolysis is not required for tumor suppression.

UR - https://www.scopus.com/pages/publications/13144262880

U2 - 10.1073/pnas.94.25.13771

DO - 10.1073/pnas.94.25.13771

M3 - Article

C2 - 9391102

AN - SCOPUS:13144262880

SN - 0027-8424

VL - 94

SP - 13771

EP - 13776

JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

IS - 25

ER -

Replacement of Fhit in cancer cells suppresses tumorigenicity

Abstract

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