Thyroid hormone-dependent pituitary tumor cell growth in serum-free chemically defined culture. A new regulatory role for apotransferrin

Biochemistry ◽  
1991 ◽  
Vol 30 (30) ◽  
pp. 7466-7477 ◽  
Author(s):  
David A. Sirbasku ◽  
Rajbabu Pakala ◽  
Hidetaka Sato ◽  
John E. Eby
Keyword(s):  
Thyroid Hormone ◽  
Cell Growth ◽  
Tumor Cell ◽  
Pituitary Tumor ◽  
Regulatory Role ◽  
Tumor Cell Growth ◽  
Serum Free ◽  
Defined Culture ◽  
Pituitary Tumor Cell

Octreotide treatment suppresses malignant somatotrophic pituitary tumor cell growth in rats.

2000 ◽  
Author(s):  
H Kondo ◽  
H Takino ◽  
K Akino ◽  
H Yamasaki ◽  
Y Yamaguchi ◽  
...  
Keyword(s):  
Cell Growth ◽  
Tumor Cell ◽  
Pituitary Tumor ◽  
Tumor Cell Growth ◽  
Octreotide Treatment ◽  
Pituitary Tumor Cell

scholarly journals MicroRNA-30d target TIMP3 induces pituitary tumor cell growth and invasion

Gland Surgery ◽  
2021 ◽  
Vol 0 (0) ◽  
pp. 0-0
Author(s):  
Bowen Sun ◽  
Congxin Dai ◽  
Shangfeng Zhao ◽  
Hao Dong ◽  
Haocheng Liu ◽  
...  
Keyword(s):  
Cell Growth ◽  
Tumor Cell ◽  
Pituitary Tumor ◽  
Tumor Cell Growth ◽  
Pituitary Tumor Cell

scholarly journals Trastuzumab inhibits pituitary tumor cell growth modulating the TGFB/SMAD2/3 pathway

2018 ◽  
Vol 25 (10) ◽  
pp. 837-852 ◽  
Author(s):  
Juan Pablo Petiti ◽  
Liliana del Valle Sosa ◽  
Florencia Picech ◽  
Gabriela Deisi Moyano Crespo ◽  
Jean Zander Arevalo Rojas ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cell Growth ◽  
Tumor Growth ◽  
Tumor Cell ◽  
Pituitary Adenomas ◽  
Pituitary Tumor ◽  
Transforming Growth Factor ◽  
Gh3 Cells ◽  
Tumor Cell Growth ◽  
Pituitary Tumor Cell

In pituitary adenomas, early recurrences and resistance to conventional pharmacotherapies are common, but the mechanisms involved are still not understood. The high expression of epidermal growth factor receptor 2 (HER2)/extracellular signal-regulated kinase (ERK1/2) signal observed in human pituitary adenomas, together with the low levels of the antimitogenic transforming growth factor beta receptor 2 (TBR2), encouraged us to evaluate the effect of the specific HER2 inhibition with trastuzumab on experimental pituitary tumor cell growth and its effect on the antiproliferative response to TGFB1. Trastuzumab decreased the pituitary tumor growth as well as the expression of ERK1/2 and the cell cycle regulators CCND1 and CDK4. The HER2/ERK1/2 pathway is an attractive therapeutic target, but its intricate relations with other signaling modulators still need to be unraveled. Thus, we investigated possible cross-talk with TGFB signaling, which has not yet been studied in pituitary tumors. In tumoral GH3 cells, co-incubation with trastuzumab and TGFB1 significantly decreased cell proliferation, an effect accompanied by a reduction in ERK1/2 phosphorylation, an increase of SMAD2/3 activation. In addition, through immunoprecipitation assays, a diminution of SMAD2/3-ERK1/2 and an increase SMAD2/3–TGFBR1 interactions were observed when cells were co-incubated with trastuzumab and TGFB1. These findings indicate that blocking HER2 by trastuzumab inhibited pituitary tumor growth and modulated HER2/ERK1/2 signaling and consequently the anti-mitogenic TGFB1/TBRs/SMADs cascade. The imbalance between HER2 and TGFBRs expression observed in human adenomas and the response to trastuzumab on experimental tumor growth may make the HER2/ERK1/2 pathway an attractive target for future pituitary adenoma therapy.

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