Gang Fu
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Gang Fu has a total of 6 co-authors. Here are the top co-authors by number of shared publications:
A Ren
Chongqing Key Laboratory for Oral Diseases and Biomedical Sciences, Chongqing Medical University, Chongqing, China
1 shared publicationAishu Ren
Chongqing Key Laboratory for Oral Diseases and Biomedical Sciences, Chongqing Medical University, Chongqing, 401147, PR China; Affiliated Hospital of Stomatology, Chongqing Medical University, Chongqing, 401147, PR China
1 shared publicationHongjuan Cui
State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, 400716, PR China
1 shared publication- Hongjuan Cui
Medical Research Institute, State Key Laboratory of Resource Insects, Southwest University, Chongqing 400715, China
1 shared publication Y Qiu
Chongqing Key Laboratory for Oral Diseases and Biomedical Sciences, Chongqing Medical University, Chongqing, China
1 shared publicationYu Qiu
Chongqing Key Laboratory for Oral Diseases and Biomedical Sciences, Chongqing Medical University, Chongqing, 401147, PR China; Affiliated Hospital of Stomatology, Chongqing Medical University, Chongqing, 401147, PR China
1 shared publication
Latest Publications
- 1 March 2015
- Published by Elsevier in Biochemical and Biophysical Research Communications
- Vol. 459 (1) , 10-17
Inhibition of H3K9 methyltransferase G9a induces autophagy and apoptosis in oral squamous cell carcinoma
- 1 March 2015
- Published by Elsevier in Biochemical and Biophysical Research Communications
- Vol. 459 (1) , 10-17
Inhibition of H3K9 methyltransferase G9a induces autophagy and apoptosis in oral squamous cell carcinoma
- 7 January 2015
- Published by Wiley in Oral Diseases
- Vol. 21 (5) , 558-564
Tigecycline exerts an antitumoral effect in oral squamous cell carcinoma
Objective To explore whether antibacterial drug tigecycline could exert an antitumoral effect in oral squamous cell carcinoma (OSCC). Materials and Methods Two OSCC cell lines Tca8113 and KB were used in this study. To investigate the cytostatic effects of tigecycline in OSCC, cell growth was tested by trypan blue staining, MTT assay, and Brdu immunofluorescence staining. Then, the apoptosis proportion was measured by FITC Annexin‐V and PI labeling, and cell cycle was determined by PI staining. The expression of caspase 3 (CASP3) and cell cycle regulatory protein was detected by Western blot assay. Finally, the clonogenesis and tumorigenesis capacity were analyzed by soft agar growth and xenograft model. Results Here, we showed that tigecycline significantly inhibited cell growth and proliferation in OSCC cell lines Tca8113 and KB. It did not induce cell apoptosis but led to an increase of cells in G0/G1 phase with down‐regulation of cyclin E2 (CCNE2) and cyclin‐dependent kinase4 (CDK4) protein expression. We also showed that tigecycline inhibited colony formation in soft agar and reduced tumor growth in a xenograft model. Conclusion Our results suggested that tigecycline might be used as a novel candidate agent for the treatment of OSCC.
- 7 January 2015
- Published by Wiley in Oral Diseases
- Vol. 21 (5) , 558-564
Tigecycline exerts an antitumoral effect in oral squamous cell carcinoma
Objective To explore whether antibacterial drug tigecycline could exert an antitumoral effect in oral squamous cell carcinoma (OSCC). Materials and Methods Two OSCC cell lines Tca8113 and KB were used in this study. To investigate the cytostatic effects of tigecycline in OSCC, cell growth was tested by trypan blue staining, MTT assay, and Brdu immunofluorescence staining. Then, the apoptosis proportion was measured by FITC Annexin‐V and PI labeling, and cell cycle was determined by PI staining. The expression of caspase 3 (CASP3) and cell cycle regulatory protein was detected by Western blot assay. Finally, the clonogenesis and tumorigenesis capacity were analyzed by soft agar growth and xenograft model. Results Here, we showed that tigecycline significantly inhibited cell growth and proliferation in OSCC cell lines Tca8113 and KB. It did not induce cell apoptosis but led to an increase of cells in G0/G1 phase with down‐regulation of cyclin E2 (CCNE2) and cyclin‐dependent kinase4 (CDK4) protein expression. We also showed that tigecycline inhibited colony formation in soft agar and reduced tumor growth in a xenograft model. Conclusion Our results suggested that tigecycline might be used as a novel candidate agent for the treatment of OSCC.