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YY1 targets tubulin polymerisation-promoting protein to inhibit migration, invasion and angiogenesis in pancreatic cancer via p38/MAPK and PI3K/AKT pathways.

Abstract

BACKGROUND

Pancreatic cancer (PDAC) is a highly invasive cancer with poor prognosis. Recent research has found that the transcription factor Yin Yang 1 (YY1) plays an inhibitory role in the development of pancreatic cancer. It has been reported that tubulin polymerisation-promoting protein (TPPP) plays an indispensable role in a variety of tumours, but its expression and role in pancreatic cancer have not yet been elucidated.

METHODS

In this study, we performed ChIP-sequencing and found that YY1 directly binds to the promoter region of TPPP. The expression of TPPP in pancreatic cancer was detected by western blotting and immunohistochemistry. Four-week-old male BALB/c-nude mice were used to assess the effect of TPPP on pancreatic cancer.

RESULTS

Immunohistochemistry revealed that TPPP was expressed at low levels in pancreatic cancer tissues, and was associated with blood vessel invasion. The results from vivo experiments have showed that TPPP could enhance the migration and invasion of pancreatic cancer. Further experiments showed that YY1 could inhibit the migration, invasion and angiogenesis of pancreatic cancer cells by downregulating TPPP via p38/MAPK and PI3K/AKT pathways.

CONCLUSION

Our study demonstrates that TPPP may act as a promoter and may serve as a novel target for the treatment of pancreatic cancer.

Authors+Show Affiliations

Pancreas Center, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China. Pancreas Institute, Nanjing Medical University, Nanjing, China.Pancreas Center, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China. Pancreas Institute, Nanjing Medical University, Nanjing, China.Pancreas Center, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China. Pancreas Institute, Nanjing Medical University, Nanjing, China.Pancreas Center, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China. Pancreas Institute, Nanjing Medical University, Nanjing, China.Pancreas Center, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China. Pancreas Institute, Nanjing Medical University, Nanjing, China.Pancreas Center, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China. Pancreas Institute, Nanjing Medical University, Nanjing, China.Pancreas Center, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China. Pancreas Institute, Nanjing Medical University, Nanjing, China.Pancreas Center, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China. Pancreas Institute, Nanjing Medical University, Nanjing, China.Pancreas Center, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China. Pancreas Institute, Nanjing Medical University, Nanjing, China.Pancreas Center, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China. miaoyi@njmu.edu.cn. Pancreas Institute, Nanjing Medical University, Nanjing, China. miaoyi@njmu.edu.cn.Pancreas Center, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China. jiangkuirongnjmu@sina.com. Pancreas Institute, Nanjing Medical University, Nanjing, China. jiangkuirongnjmu@sina.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31631174

Citation

Chen, Qun, et al. "YY1 Targets Tubulin Polymerisation-promoting Protein to Inhibit Migration, Invasion and Angiogenesis in Pancreatic Cancer Via p38/MAPK and PI3K/AKT Pathways." British Journal of Cancer, 2019.
Chen Q, Yang C, Chen L, et al. YY1 targets tubulin polymerisation-promoting protein to inhibit migration, invasion and angiogenesis in pancreatic cancer via p38/MAPK and PI3K/AKT pathways. Br J Cancer. 2019.
Chen, Q., Yang, C., Chen, L., Zhang, J. J., Ge, W. L., Yuan, H., ... Jiang, K. R. (2019). YY1 targets tubulin polymerisation-promoting protein to inhibit migration, invasion and angiogenesis in pancreatic cancer via p38/MAPK and PI3K/AKT pathways. British Journal of Cancer, doi:10.1038/s41416-019-0604-5.
Chen Q, et al. YY1 Targets Tubulin Polymerisation-promoting Protein to Inhibit Migration, Invasion and Angiogenesis in Pancreatic Cancer Via p38/MAPK and PI3K/AKT Pathways. Br J Cancer. 2019 Oct 21; PubMed PMID: 31631174.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - YY1 targets tubulin polymerisation-promoting protein to inhibit migration, invasion and angiogenesis in pancreatic cancer via p38/MAPK and PI3K/AKT pathways. AU - Chen,Qun, AU - Yang,Chuang, AU - Chen,Lei, AU - Zhang,Jing-Jing, AU - Ge,Wan-Li, AU - Yuan,Hao, AU - Meng,Ling-Dong, AU - Huang,Xu-Min, AU - Shen,Peng, AU - Miao,Yi, AU - Jiang,Kui-Rong, Y1 - 2019/10/21/ PY - 2019/04/16/received PY - 2019/09/27/accepted PY - 2019/08/21/revised PY - 2019/10/22/pubmed PY - 2019/10/22/medline PY - 2019/10/22/entrez JF - British journal of cancer JO - Br. J. Cancer N2 - BACKGROUND: Pancreatic cancer (PDAC) is a highly invasive cancer with poor prognosis. Recent research has found that the transcription factor Yin Yang 1 (YY1) plays an inhibitory role in the development of pancreatic cancer. It has been reported that tubulin polymerisation-promoting protein (TPPP) plays an indispensable role in a variety of tumours, but its expression and role in pancreatic cancer have not yet been elucidated. METHODS: In this study, we performed ChIP-sequencing and found that YY1 directly binds to the promoter region of TPPP. The expression of TPPP in pancreatic cancer was detected by western blotting and immunohistochemistry. Four-week-old male BALB/c-nude mice were used to assess the effect of TPPP on pancreatic cancer. RESULTS: Immunohistochemistry revealed that TPPP was expressed at low levels in pancreatic cancer tissues, and was associated with blood vessel invasion. The results from vivo experiments have showed that TPPP could enhance the migration and invasion of pancreatic cancer. Further experiments showed that YY1 could inhibit the migration, invasion and angiogenesis of pancreatic cancer cells by downregulating TPPP via p38/MAPK and PI3K/AKT pathways. CONCLUSION: Our study demonstrates that TPPP may act as a promoter and may serve as a novel target for the treatment of pancreatic cancer. SN - 1532-1827 UR - https://www.unboundmedicine.com/medline/citation/31631174/YY1_targets_tubulin_polymerisation-promoting_protein_to_inhibit_migration,_invasion_and_angiogenesis_in_pancreatic_cancer_via_p38/MAPK_and_PI3K/AKT_pathways L2 - http://dx.doi.org/10.1038/s41416-019-0604-5 DB - PRIME DP - Unbound Medicine ER -