PMID- 26927216
OWN - NLM
STAT- MEDLINE
DCOM- 20161213
LR  - 20190918
IS  - 1873-4316 (Electronic)
IS  - 1389-2010 (Linking)
VI  - 17
IP  - 6
DP  - 2016
TI  - Tumor Necrosis Factor-alpha, a Regulator and Therapeutic Agent on Breast Cancer.
PG  - 486-94
AB  - The cell-mediated immunity and cytotoxic agents play a significant role on tumor 
      cell apoptosis. Tumor necrosis factor-alpha (TNF-alpha) is an intricate linker between 
      inflammation and cancer through mediating the process of apoptosis and 
      cell-mediated immunity. A variety of evidences have confirmed the critical role 
      of TNF-alpha on tumor migration, proliferation, matrix degradation, tumor metastasis, 
      invasion, and angiogenesis. Through binding to receptors, TNF-alpha participates in 
      activating multiple cell signaling cascades that link inflammation, survival and 
      evolution towards breast cancer. TNF-alpha is an important agent for tumor 
      biotherapy, but its clinical application is limited for its severe fatal systemic 
      toxicity. The poly-lactic acid microspheres (PLAM) with intratumoral cytokine 
      release hold tremendous potential for the immunotherapy of breast cancer, and 
      TNF-alpha antagonists may offer therapeutic potential in solid tumors. In addition, 
      TNF-alpha is related with the blockage of estrogen and progesterone receptors. For 
      breast cancer treatment, it is necessary to understand the molecular signaling 
      pathways that mediate TNF-alpha and the aggressive behavior of negative breast 
      cancer. The aim of present review is to summarize the effect of TNF-alpha on breast 
      cancer cells.
FAU - Liu, Dongwu
AU  - Liu D
FAU - Wang, Xiaoqian
AU  - Wang X
FAU - Chen, Zhiwei
AU  - Chen Z
AD  - School of Life Sciences, Shandong University of Technology, 255049, Zibo, China. 
      12chen@163.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Netherlands
TA  - Curr Pharm Biotechnol
JT  - Current pharmaceutical biotechnology
JID - 100960530
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Breast Neoplasms/genetics/immunology/*metabolism
MH  - Humans
MH  - Immunotherapy
MH  - Polymorphism, Genetic
MH  - Receptors, Tumor Necrosis Factor/metabolism
MH  - Tumor Necrosis Factor-alpha/genetics/immunology/*metabolism
EDAT- 2016/03/02 06:00
MHDA- 2016/12/15 06:00
CRDT- 2016/03/02 06:00
PHST- 2015/03/24 00:00 [received]
PHST- 2015/08/21 00:00 [revised]
PHST- 2016/01/22 00:00 [accepted]
PHST- 2016/03/02 06:00 [entrez]
PHST- 2016/03/02 06:00 [pubmed]
PHST- 2016/12/15 06:00 [medline]
AID - CPB-EPUB-74062 [pii]
AID - 10.2174/1389201017666160301102713 [doi]
PST - ppublish
SO  - Curr Pharm Biotechnol. 2016;17(6):486-94. doi: 10.2174/1389201017666160301102713.