All-trans retinoic acid restores gap junctional intercellular communication between oral cancer cells with upregulation of Cx32 and Cx43 expressions in vitro

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RESEARCH PRODUCT

All-trans retinoic acid restores gap junctional intercellular communication between oral cancer cells with upregulation of Cx32 and Cx43 expressions in vitro

Yun Hong Bin Cheng Xiaohua Chen Yaohui Dai Yulei Huang Juan Xia Hong Wang Juan Wang

subject

Cell cycle checkpoint Retinoic acid Connexin Antineoplastic Agents Tretinoin Odontología Cell Communication Connexins chemistry.chemical_compound Downregulation and upregulation Tretinoin medicine Tumor Cells Cultured Humans RNA Messenger General Dentistry neoplasms Mouth neoplasm Oral Medicine and Pathology organic chemicals Gap Junctions Cell cycle :CIENCIAS MÉDICAS [UNESCO]Ciencias de la salud biological factors Up-Regulation Gene Expression Regulation Neoplastic stomatognathic diseases Otorhinolaryngology chemistry Connexin 43 Immunology Cancer cell UNESCO::CIENCIAS MÉDICAS Cancer research Carcinoma Squamous Cell Surgery Mouth Neoplasms Research-Article medicine.drug

description

Objective: All-trans retinoic acid (ATRA) has been demonstrated to inhibit tumor growth by restoration of gap junctional intercellular communication (GJIC) via upregulation of connexin (Cx) expression in some solid tumors. However, the relationship between ATRA and GJIC remains unclear in oral squamous cell carcinoma (OSCC). The aim of this study was to investigate the effect of ATRA on the GJIC function of OSCC. Study design: We measured the effects of ATRA on the viability and cell cycle distribution of SCC9 and Tca8113 OSCC cells. The GJIC function was observed using the scrape-loading dye transfer technique, and the mRNA and protein levels of Cx32 and Cx43 were detected by qRT-PCR, Western blot, and immunofluorescence assays. Results: ATRA inhibited the growth of OSCC cells in a dose- and time-dependent manner (P <0.05) and caused cell cycle arrest. ATRA-treated cells showed a 2.69-fold and 2.06-fold enhancement of GJIC in SCC9 and Tca8113 cells, respectively (P <0.05). Moreover, ATRA induced upregulation of Cx32 and Cx43 at both the mRNA and protein levels in OSCC cells. Conclusion: Our results indicated that restoration of GJIC via enhanced Cx32 and Cx43 expression might serve as a novel mechanism for the anti-tumor effect of ATRA in OSCC. Key words:All-trans retinoic acid, oral squamous cell carcinoma, connexin, gap junctional intercellular communication.

year	journal	country	edition	language
2012-07-31

http://hdl.handle.net/10550/35658