Calponin h1 suppresses tumor growth of Src-induced transformed 3Y1 cells in association with a decrease in angiogenesis.
Calponin h1 suppresses tumor growth of Src-induced transformed 3Y1 cells in association with a decrease in angiogenesis.
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DOI：
10.1111/j.1349-7006.2002.tb01340.x
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发表时间：
2002-08
期刊：
影响因子：
--
通讯作者：
Taniguchi S
中科院分区：
文献类型：
--
作者：
Kaneko M;Takeoka M;Oguchi M;Koganehira Y;Murata H;Ehara T;Tozuka M;Saida T;Taniguchi S
Calponin h1（CNhl）是一种碱性肌动蛋白结合蛋白，在平滑肌细胞中大量表达，并通过抑制肌动球蛋白MgATPase参与平滑肌收缩。在最近的研究中，注意到CNhl抑制平滑肌肉瘤中的细胞增殖和致瘤性以及纤维肉瘤细胞系中的肿瘤生长。为了进一步研究CNhl作为肿瘤抑制因子的功能，我们将人CNhl基因转染到v-src-转化的大鼠成纤维细胞系SR-3 Y1中。在裸鼠中，来自一个随机选择的CNh 1-转染子（C1）的肿瘤体积减少到来自一个随机选择的载体转染子（VI）的肿瘤体积的34.1%。在另一个独立的对（C2，V2）中观察到类似的趋势。病理学分析显示CNh 1转染子中有丝分裂细胞数量显著减少。此外，观察到CNhl转染子中血管数量的显著减少。与对照转染子（VI）相比，CNhl-转染子（Cl）中在无血清条件下的DNA合成显著降低，而在10%血清存在下的细胞生长中未观察到显著差异。还观察到CNhl转染子中体外细胞运动性的轻微但显著的降低。虽然CNhl转移对生长潜力和细胞运动性的抑制是显著的但部分的，但在CNhl转染子中观察到血管内皮生长因子（VEGF）mRNA和VEGF蛋白质分泌的显著减少。这些结果表明，CNhl在SR-3 Y1中主要通过降低体内VEGF表达和血管生成并且部分通过降低细胞增殖潜力和细胞运动性而起到肿瘤抑制剂的作用。
Calponin h1 (CNhl) is a basic actin‐binding protein that is abundantly expressed in smooth muscle cells and involved in smooth muscle contraction by inhibiting actomyosin MgATPase. In recent studies, CNhl was noted to suppress cell proliferation and tumorigenicity in leiomyosarcoma and tumor growth in fibrosarcoma cell lines. To further investigate the function of CNhl as a tumor suppressor, we transfected the human CNhl gene into a v‐src‐transformed rat fibroblast cell line SR–3Y1. The volume of the tumors derived from one randomly selected CNh1‐transfectant (C1) in nude mice was reduced to 34.1% of that from a randomly selected vector transfectant (VI). A similar tendency was observed in another independent pair (C2, V2). Pathological analysis showed a significant decrease in the number of mitotic cells in the CNh1‐transfectants. Further, a marked reduction in the number of vessels in the CNhl‐transfectant was observed. DNA synthesis under conditions without serum was significantly reduced in the CNhl‐transfectant (C1) compared with the control transfectant (VI), while no significant difference was seen in the cellular growth in the presence of 10% serum. A slight but significant reduction in in vitro cellular motility in the CNhl‐transfectant was also observed. While the suppression of growth potential and cell motility by CNhl transfer was significant but partial, a marked reduction in vascular endothelial growth factor (VEGF) mRNA and the secretion of VEGF protein was observed in the CNhl‐transfectant. These results suggest that CNhl plays a role as tumor suppressor in SR–3Y1 mainly by decreasing VEGF expression and angiogenesis in vivo and partially through reducing cellular proliferative potential and cell motility.
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影响因子：
3.6
作者：
Miyado, K;Sato, M;Taniguchi, S
通讯作者：
Taniguchi, S
影响因子：
8
作者：
Niu, GL;Wright, KL;Yu, H
通讯作者：
Yu, H
DOI：
10.1093/jnci/91.9.790
发表时间：
1999-05-05
期刊：
JOURNAL OF THE NATIONAL CANCER INSTITUTE
影响因子：
--
作者：
Horiuchi, A;Nikaido, T;Fujii, S
通讯作者：
Fujii, S
影响因子：
2.9
作者：
DUBAND, JL;GIMONA, M;SMALL, JV
通讯作者：
SMALL, JV
DOI：
10.1016/s0006-291x(86)80328-x
发表时间：
1986-11-26
影响因子：
3.1
作者：
TAKAHASHI, K;HIWADA, K;KOKUBU, T
通讯作者：
KOKUBU, T