title: All-trans retinoic acid enhances bystander effect of suicide gene therapy in the treatment of breast cancer.
abstract: All-trans retinoic acid (ATRA) has been shown to enhance the expression of connexin 43 (Cx43) and the bystander effect (BSE) in suicide gene therapy. These in turn improve effects of suicide gene therapies for several tumor types. However, whether ATRA can improve BSE remains unclear in suicide gene therapy for breast cancer. In the present study, MCF-7, human breast cancer cells were treated with ATRA in combination with a VEGFP-TK/CD gene suicide system developed by our group. We found that this combination enhances the efficiency of cell killing and apoptosis of breast cancer by strengthening the BSE in vitro. ATRA also promotes gap junction intercellular communication (GJIC) in MCF-7 cells by upregulation of the connexin 43 mRNA and protein in MCF-7 cells. These results indicate that enhancement of GJIC by ATRA in suicide gene system might serve as an attractive and cost-effective strategy of therapy for breast cancer cells.
authors.affiliation: Department of Thyroid and Breast Surgery, Shenzhen Key Laboratory for Endogenous Infection, Shenzhen Nanshan District People's Hospital (The Sixth People's Hospital of Shenzhen), Shenzhen, Guangdong 518052, P.R. China.
authors.forename: Heng
authors.initials: H
authors.lastname: Kong
authors.affiliation: Department of Human Resource, Shenzhen Nanshan District People's Hospital, Shenzhen, Guangdong 518052, P.R. China.
authors.forename: Xia
authors.initials: X
authors.lastname: Liu
authors.affiliation: Department of General Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.
authors.forename: Liucheng
authors.initials: L
authors.lastname: Yang
authors.affiliation: Department of Thyroid and Breast Surgery, Shenzhen Key Laboratory for Endogenous Infection, Shenzhen Nanshan District People's Hospital (The Sixth People's Hospital of Shenzhen), Shenzhen, Guangdong 518052, P.R. China.
authors.forename: Ke
authors.initials: K
authors.lastname: Qi
authors.affiliation: Department of Thyroid and Breast Surgery, Shenzhen Key Laboratory for Endogenous Infection, Shenzhen Nanshan District People's Hospital (The Sixth People's Hospital of Shenzhen), Shenzhen, Guangdong 518052, P.R. China.
authors.forename: Haoyun
authors.initials: H
authors.lastname: Zhang
authors.affiliation: Clinical Laboratory, Shenzhen Nanshan District People's Hospital, Shenzhen, Guangdong 518052, P.R. China.
authors.forename: Jingwen
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of General Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.
authors.forename: Zonghai
authors.initials: Z
authors.lastname: Huang
authors.affiliation: Department of Thyroid and Breast Surgery, Shenzhen Key Laboratory for Endogenous Infection, Shenzhen Nanshan District People's Hospital (The Sixth People's Hospital of Shenzhen), Shenzhen, Guangdong 518052, P.R. China.
authors.forename: Hongxian
authors.initials: H
authors.lastname: Wang
mesh_terms: D017209:Apoptosis / Q000235:genetics; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D024201:Bystander Effect; D018031:Connexin 43 / Q000096:biosynthesis* / Q000235:genetics; D005260:Female; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D041722:Genes, Transgenic, Suicide; D015316:Genetic Therapy; D006801:Humans; D061986:MCF-7 Cells; D014212:Tretinoin / Q000008:administration & dosage
chemical_list: D018031:Connexin 43; C500216:GJA1 protein, human; D014212:Tretinoin