BACKGROUND: SALL4 is a novel oncogene mediating tumorigenesis in multiple carcinomas. However, its actual role and mechanisms participating in the development of colorectal cancer remains unclear. METHODS: Immunohistochemical staining and Western blot were conducted to detect the expression of SALL4 and other molecules. siRNA of SALL4 was transfected to silence SALL4 expression in Caco-2 cell line. Flow cytometry was used for cell cycle and apoptosis analysis. Wound healing and transwell assay were used for invasion test. CCK-8 test was employed for cell proliferation and drug sensitivity assessment. RESULTS: By inhibition of SALL4 expression, the proliferation, invasiveness and drug resistance were dramatically reduced while apoptosis rate was up-regulated. Gli1 was found to decrease its expression in SALL4 silencing cells. Moreover, the inhibition on tumorigenesis of Caco-2 by SALL4 silencing was antagonized by Gli1 up-regulation, suggesting Gli1 as a downstream target of SALL4 in cancer development. CONCLUSION: SALL4 inhibition limited oncogenesis on colorectal cancer by reducing Gli1 expression.
BACKGROUND:SALL4 is a novel oncogene mediating tumorigenesis in multiple carcinomas. However, its actual role and mechanisms participating in the development of colorectal cancer remains unclear. METHODS: Immunohistochemical staining and Western blot were conducted to detect the expression of SALL4 and other molecules. siRNA of SALL4 was transfected to silence SALL4 expression in Caco-2 cell line. Flow cytometry was used for cell cycle and apoptosis analysis. Wound healing and transwell assay were used for invasion test. CCK-8 test was employed for cell proliferation and drug sensitivity assessment. RESULTS: By inhibition of SALL4 expression, the proliferation, invasiveness and drug resistance were dramatically reduced while apoptosis rate was up-regulated. Gli1 was found to decrease its expression in SALL4 silencing cells. Moreover, the inhibition on tumorigenesis of Caco-2 by SALL4 silencing was antagonized by Gli1 up-regulation, suggesting Gli1 as a downstream target of SALL4 in cancer development. CONCLUSION:SALL4 inhibition limited oncogenesis on colorectal cancer by reducing Gli1 expression.
Entities:
Keywords:
Gli1; SALL4; carcinogenesis; colorectal cancer
Authors: L Zhang; Z Xu; X Xu; B Zhang; H Wu; M Wang; X Zhang; T Yang; J Cai; Y Yan; F Mao; W Zhu; Q Shao; H Qian; W Xu Journal: Oncogene Date: 2013-11-25 Impact factor: 9.867
Authors: Kjell Magne Tveit; Tormod Guren; Bengt Glimelius; Per Pfeiffer; Halfdan Sorbye; Seppo Pyrhonen; Fridbjorn Sigurdsson; Elin Kure; Tone Ikdahl; Eva Skovlund; Tone Fokstuen; Flemming Hansen; Eva Hofsli; Elke Birkemeyer; Anders Johnsson; Hans Starkhammar; Mette Karen Yilmaz; Nina Keldsen; Anne Berit Erdal; Olav Dajani; Olav Dahl; Thoralf Christoffersen Journal: J Clin Oncol Date: 2012-04-02 Impact factor: 44.544
Authors: X Yuan; X Zhang; W Zhang; W Liang; P Zhang; H Shi; B Zhang; M Shao; Y Yan; H Qian; W Xu Journal: Oncogenesis Date: 2016-11-07 Impact factor: 7.485
Authors: Alba Rodriguez; Luís Antonio Corchete; José Antonio Alcazar; Juan Carlos Montero; Marta Rodriguez; Luis Miguel Chinchilla-Tábora; Rosario Vidal Tocino; Carlos Moyano; Saray Muñoz-Bravo; José María Sayagués; Mar Abad Journal: Cancers (Basel) Date: 2022-08-23 Impact factor: 6.575