RNAi technology and lentiviral delivery as a powerful tool to suppress Tpr-Met-mediated tumorigenesis

Riccardo Taulli; Paolo Accornero; Antonia Follenzi; Tony Mangano; Alessandro Morotti; Claudio Scuoppo; Paolo E. Forni; Francesca Bersani; Tiziana Crepaldi; Roberto Chiarle; Luigi Naldini; Carola Ponzetto

doi:10.1038/sj.cgt.7700815

RNAi technology and lentiviral delivery as a powerful tool to suppress Tpr-Met-mediated tumorigenesis

Riccardo Taulli, Paolo Accornero, Antonia Follenzi, Tony Mangano, Alessandro Morotti, Claudio Scuoppo, Paolo E. Forni, Francesca Bersani, Tiziana Crepaldi, Roberto Chiarle, Luigi Naldini, Carola Ponzetto

Risultato della ricerca: Contributo su rivista › Articolo in rivista › peer review

Abstract

Tpr-Met, the oncogenic counterpart of the Met receptor, has been detected in gastric cancers, as well as in precursor lesions and in the adjacent normal gastric mucosa. This has prompted the suggestion that Tpr-Met may predispose to the development of gastric tumors. Given the sequence specificity of RNA interference, oncogenes activated by point mutation or rearrangements can be targeted while spearing the product of the wild-type allele. In this work, we report specific suppression of Tpr-Met expression and inhibition of Tpr-Met-mediated transformation and tumorigenesis by means of a short interfering RNA (siRNA) directed toward the Tpr-Met junction (anti-TM2). When delivered by a lentiviral vector, anti-TM2 siRNA was effective also in mouse embryonal fibroblasts or epithelial cells expressing high levels of Tpr-Met. Our results suggest that lentiviral-mediated delivery of anti-TM2 siRNA may be developed into a powerful tool to treat Tpr-Met-positive cancers.

Lingua originale	Inglese
pagine (da-a)	456-463
Numero di pagine	8
Rivista	Cancer Gene Therapy
Volume	12
Numero di pubblicazione	5
DOI	https://doi.org/10.1038/sj.cgt.7700815
Stato di pubblicazione	Pubblicato - mag 2005
Pubblicato esternamente	Sì

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title = "RNAi technology and lentiviral delivery as a powerful tool to suppress Tpr-Met-mediated tumorigenesis",

abstract = "Tpr-Met, the oncogenic counterpart of the Met receptor, has been detected in gastric cancers, as well as in precursor lesions and in the adjacent normal gastric mucosa. This has prompted the suggestion that Tpr-Met may predispose to the development of gastric tumors. Given the sequence specificity of RNA interference, oncogenes activated by point mutation or rearrangements can be targeted while spearing the product of the wild-type allele. In this work, we report specific suppression of Tpr-Met expression and inhibition of Tpr-Met-mediated transformation and tumorigenesis by means of a short interfering RNA (siRNA) directed toward the Tpr-Met junction (anti-TM2). When delivered by a lentiviral vector, anti-TM2 siRNA was effective also in mouse embryonal fibroblasts or epithelial cells expressing high levels of Tpr-Met. Our results suggest that lentiviral-mediated delivery of anti-TM2 siRNA may be developed into a powerful tool to treat Tpr-Met-positive cancers.",

keywords = "Gastric cancer, Lentiviral vector, Novel cancer therapies, ShRNA, Tpr-Met",

author = "Riccardo Taulli and Paolo Accornero and Antonia Follenzi and Tony Mangano and Alessandro Morotti and Claudio Scuoppo and Forni, \{Paolo E.\} and Francesca Bersani and Tiziana Crepaldi and Roberto Chiarle and Luigi Naldini and Carola Ponzetto",

note = "Funding Information: We are grateful to Roberto Piva, Andrea Manazza and Chiara Ambrogio for technical help. This work was supported by funds from the Italian Association for Cancer Research (AIRC, CP), the Oncology Project Compagnia di San Paolo/FIRMS (CeRMS) and PRIN 2003 (CP, LN). Paolo Accornero is a FIRC fellow. The continuing support of the Compagnia di San Paolo and Fondazione CRT to C Ponzetto{\textquoteright}s laboratory is gratefully acknowledged.",

year = "2005",

month = may,

doi = "10.1038/sj.cgt.7700815",

language = "English",

volume = "12",

pages = "456--463",

journal = "Cancer Gene Therapy",

issn = "0929-1903",

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number = "5",

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TY - JOUR

T1 - RNAi technology and lentiviral delivery as a powerful tool to suppress Tpr-Met-mediated tumorigenesis

AU - Taulli, Riccardo

AU - Accornero, Paolo

AU - Follenzi, Antonia

AU - Mangano, Tony

AU - Morotti, Alessandro

AU - Scuoppo, Claudio

AU - Forni, Paolo E.

AU - Bersani, Francesca

AU - Crepaldi, Tiziana

AU - Chiarle, Roberto

AU - Naldini, Luigi

AU - Ponzetto, Carola

N1 - Funding Information: We are grateful to Roberto Piva, Andrea Manazza and Chiara Ambrogio for technical help. This work was supported by funds from the Italian Association for Cancer Research (AIRC, CP), the Oncology Project Compagnia di San Paolo/FIRMS (CeRMS) and PRIN 2003 (CP, LN). Paolo Accornero is a FIRC fellow. The continuing support of the Compagnia di San Paolo and Fondazione CRT to C Ponzetto’s laboratory is gratefully acknowledged.

PY - 2005/5

Y1 - 2005/5

N2 - Tpr-Met, the oncogenic counterpart of the Met receptor, has been detected in gastric cancers, as well as in precursor lesions and in the adjacent normal gastric mucosa. This has prompted the suggestion that Tpr-Met may predispose to the development of gastric tumors. Given the sequence specificity of RNA interference, oncogenes activated by point mutation or rearrangements can be targeted while spearing the product of the wild-type allele. In this work, we report specific suppression of Tpr-Met expression and inhibition of Tpr-Met-mediated transformation and tumorigenesis by means of a short interfering RNA (siRNA) directed toward the Tpr-Met junction (anti-TM2). When delivered by a lentiviral vector, anti-TM2 siRNA was effective also in mouse embryonal fibroblasts or epithelial cells expressing high levels of Tpr-Met. Our results suggest that lentiviral-mediated delivery of anti-TM2 siRNA may be developed into a powerful tool to treat Tpr-Met-positive cancers.

AB - Tpr-Met, the oncogenic counterpart of the Met receptor, has been detected in gastric cancers, as well as in precursor lesions and in the adjacent normal gastric mucosa. This has prompted the suggestion that Tpr-Met may predispose to the development of gastric tumors. Given the sequence specificity of RNA interference, oncogenes activated by point mutation or rearrangements can be targeted while spearing the product of the wild-type allele. In this work, we report specific suppression of Tpr-Met expression and inhibition of Tpr-Met-mediated transformation and tumorigenesis by means of a short interfering RNA (siRNA) directed toward the Tpr-Met junction (anti-TM2). When delivered by a lentiviral vector, anti-TM2 siRNA was effective also in mouse embryonal fibroblasts or epithelial cells expressing high levels of Tpr-Met. Our results suggest that lentiviral-mediated delivery of anti-TM2 siRNA may be developed into a powerful tool to treat Tpr-Met-positive cancers.

KW - Gastric cancer

KW - Lentiviral vector

KW - Novel cancer therapies

KW - ShRNA

KW - Tpr-Met

UR - https://www.scopus.com/pages/publications/20944448996

U2 - 10.1038/sj.cgt.7700815

DO - 10.1038/sj.cgt.7700815

M3 - Article

SN - 0929-1903

VL - 12

SP - 456

EP - 463

JO - Cancer Gene Therapy

JF - Cancer Gene Therapy

IS - 5

ER -

RNAi technology and lentiviral delivery as a powerful tool to suppress Tpr-Met-mediated tumorigenesis

Abstract

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