Literature DB >> 10359076

Suppression of the neoplastic phenotype by transfection of phospholipase C beta 3 to neuroendocrine tumor cells.

P Stålberg1, S Wang, C Larsson, G Weber, K Oberg, A Gobl, B Skogseid.   

Abstract

The expression of phospholipase C beta 3 (PLCB3) is low or absent in several neuroendocrine neoplasias. To investigate the role of PLCB3 in the neuroendocrine tumorigenesis, we transfected a PLCB3 construct to three neuroendocrine tumor cell lines with a low PLCB3 expression. The growth rate and tumorigenicity were assessed in vitro by [3H]thymidine incorporation and cell counting, in vivo, by xenografting to nude mice. In vitro, PLCB3 expressing clones showed a significant growth inhibition. The tumor weight was reduced for one of the two xenografted PLCB3-transfected cell lines and in both, a reduced number of proliferating (Ki-67 positive) cells was observed. This study implies an essential role for PLCB3 in the neuroendocrine tumorigenesis.

Entities:  

Mesh:

Substances:

Year:  1999        PMID: 10359076     DOI: 10.1016/s0014-5793(99)00457-3

Source DB:  PubMed          Journal:  FEBS Lett        ISSN: 0014-5793            Impact factor:   4.124


  2 in total

1.  Calmodulin potentiates G beta gamma activation of phospholipase C-beta3.

Authors:  Jennifer S McCullar; Dean A Malencik; Walter K Vogel; Kristi M Crofoot; Sonia R Anderson; Theresa M Filtz
Journal:  Biochem Pharmacol       Date:  2006-10-13       Impact factor: 5.858

2.  Autophagy is a major regulator of beta cell insulin homeostasis.

Authors:  Yael Riahi; Jakob D Wikstrom; Etty Bachar-Wikstrom; Nava Polin; Hava Zucker; Myung-Shik Lee; Wenying Quan; Leena Haataja; Ming Liu; Peter Arvan; Erol Cerasi; Gil Leibowitz
Journal:  Diabetologia       Date:  2016-01-30       Impact factor: 10.122

  2 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.