TNFR-1 on tumor cells contributes to the sensitivity of fibrosarcoma to chemotherapy
Protein & Cell
;
(12): 393-401, 2013.
Article
in English
| WPRIM
| ID: wpr-757801
ABSTRACT
Impaired tumor necrosis factor receptor-1 (TNFR-1) signaling has been found in some malignant tumors with poor prognosis. However, the exact role of TNFR-1 signaling in fibrosarcoma remains unclear. Here, we explored the question by comparing the growth of TNFR-1 deficient (Tnfr1 (-)) and TNFR-1 competent (Tnfr1 (+)) fibrosarcoma FB61 cells (FB61-m and FB61-R1) in mice. TNFR-1 expression on fibrosarcoma cells delayed their growth in vivo but not in vitro. Moreover, reduced FB61-R1 tumor growth was also obtained in TNFR-1 knockout mice. The mechanism relies mainly on the TNFR-1-mediated downregulation of vascular endothelial growth factor (VEGF) production by tumor cells. Importantly, treatment of FB61-m tumors with melphalan resulted in a short delay of tumor growth, followed by a quick remission. However, when FB61-R1 tumors were treated with melphalan, tumor growth was similarly delayed at first and then completely rejected. Our results reveal evidence for TNFR-1 on tumor cells as a prerequisite in chemotherapy for fibrosarcoma, and provide novel insight into the therapeutic approach against some types of tumors using TNFR-1 angonist.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pathology
/
Signal Transduction
/
Down-Regulation
/
Gene Expression Regulation, Neoplastic
/
Vascular Endothelial Growth Factor A
/
Receptors, Tumor Necrosis Factor, Type I
/
Drug Therapy
/
Molecular Targeted Therapy
/
Fibrosarcoma
/
Genetics
Type of study:
Diagnostic study
/
Prognostic study
Limits:
Animals
/
Humans
Language:
English
Journal:
Protein & Cell
Year:
2013
Type:
Article
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