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首页> 外文期刊>Growth Factors >Stimulation of extracellular signal-regulated kinases and proliferation in the human gastric cancer cells KATO-III by obestatin.
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Stimulation of extracellular signal-regulated kinases and proliferation in the human gastric cancer cells KATO-III by obestatin.

机译：肥胖抑制素刺激人胃癌细胞KATO-III中细胞外信号调节激酶的增殖。

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摘要

Obestatin, the ghrelin-associated peptide, activates cell proliferation in the gastric cancer cell line KATO-III. The results showed that this peptide induced cell proliferation by mitogen-activated kinase kinase/extracellular signal-regulated kinases1/2 (ERK1/2) phosphorylation. A sequential analysis of the obestatin transmembrane signalling pathway indicated that the ERK1/2 activity is partially blocked after preincubation of the cells with pertussis toxin, as well as by wortmannin (an inhibitor of phosphoinositide 3-kinase (PI3K)), staurosporine (an inhibitor of protein kinase C (PKC)) and 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2, which inhibits the non receptor tyrosine kinase Src). Upon administration of obestatin, the intracellular levels of phospho-PKCepsilon- and theta-isoenzymes rise with similar time-courses, from which PKCepsilon appears to be the responsible for ERK1/2 response. Based on the experimental data, a signalling pathway involving the consecutive activation of G(i), PI3K, novel PKCepsilon and Src for ERK1/2 activation is proposed. These results point to a functionally active peptide that regulates proliferation of the gastric cancer cells KATO-III.
机译：生长抑素相关肽Obestatin激活胃癌细胞系KATO-III中的细胞增殖。结果表明，该肽通过有丝分裂原激活的激酶激酶/细胞外信号调节激酶1/2（ERK1 / 2）磷酸化诱导细胞增殖。对Obestatin跨膜信号通路的顺序分析表明，将细胞与百日咳毒素一起预孵育后，ERK1 / 2活性被部分阻断，而星形孢菌素（一种抑制剂，渥曼青霉素（一种磷酸肌醇3-激酶（PI3K）的抑制剂）蛋白激酶C（PKC））和4-氨基-5-（4-氯苯基）-7-（叔丁基）吡唑并[3,4-d]嘧啶（PP2，可抑制非受体酪氨酸激酶Src）。服用肥胖抑制素后，磷酸化PKCepsilon和theta同工酶的细胞内水平会随着相似的时程而上升，由此看来PKCepsilon可能是ERK1 / 2反应的原因。基于实验数据，提出了涉及G（i），PI3K，新型PKCepsilon和Src的ERK1 / 2激活连续激活的信号通路。这些结果指向了调节胃癌细胞KATO-III增殖的功能活性肽。

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