Oral cancer cells sustainedly infected with Porphyromonas gingivalis exhibit resistance to Taxol and have higher metastatic potential
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Bok Hee Woo1, Da Jeong Kim1, Jeom Il Choi2, Sung Jo Kim2, Bong Soo Park3, Jae Min Song4, Ji Hye Lee1,5 and Hae Ryoun Park1,5
1Department of Oral Pathology & BK21 PLUS Project, School of Dentistry, Pusan National University, Mulgeum-up, Yangsan 50612, South Korea
2Department of Periodontology, School of Dentistry, Pusan National University, Mulgeum-up, Yangsan 50612, South Korea
3Department of Oral Anatomy, School of Dentistry, Pusan National University, Mulgeum-up, Yangsan 50612, South Korea
4Department of Oral and Maxillofacial Surgery, School of Dentistry, Pusan National University, Mulgeum-up, Yangsan 50612, South Korea
5Institute of Translational Dental Sciences, Pusan National University, Mulgeum-up, Yangsan 50612, South Korea
Hae Ryoun Park, email: email@example.com
Keywords: Porphyromonas gingivalis, oral cancer, Taxol, Notch1, metastasis
Abbreviations: oral squamous cell carcinoma, OSCC; cancer stem cell, CSC; Notch intracellular domain, NICD
Received: January 25, 2017 Accepted: March 03, 2017 Published: March 24, 2017
Major obstacles to improving the prognosis of patients with oral squamous cell carcinoma (OSCC) are the acquisition of resistance to chemotherapeutic agents and development of metastases. Recently, inflammatory signals are suggested to be one of the most important factors in modulating chemoresistance and establishing metastatic lesions. In addition, epidemiological studies have demonstrated that periodontitis, the most common chronic inflammatory condition of the oral cavity, is closely associated with oral cancer. However, a correlation between chronic periodontitis and chemoresistance/metastasis has not been well established. Herein, we will present our study on whether sustained infection with Porphyromonas gingivalis, a major pathogen of chronic periodontitis, could modify the response of OSCC cells to chemotherapeutic agents and their metastatic capability in vivo. Tumor xenografts composed of P. gingivalis–infected OSCC cells demonstrated a higher resistance to Taxol through Notch1 activation, as compared with uninfected cells. Furthermore, P. gingivalis–infected OSCC cells formed more metastatic foci in the lung than uninfected cells.
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