Hypoxia-induced miR-210 in epithelial ovarian cancer enhances cancer cell viability via promoting proliferation and inhibiting apoptosis

Hypoxia-induced miR-210 in epithelial ovarian cancer enhances cancer cell viability via promoting proliferation and inhibiting apoptosis
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DOI:
10.3892/ijo.2014.2368
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发表时间:
2014-06-01
影响因子:
5.2
通讯作者:
Meng, Yuanguang
Meng, Yuanguang
中科院分区:
医学2区
文献类型:
--
作者:
Li, Li'an;Huang, Ke;Meng, Yuanguang

文献摘要

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miR-210在几种类型的癌症中以HIF-1 α依赖性方式上调。此外,上调的miR-210通过其抗凋亡作用促进癌症增殖。它对卵巢癌细胞在缺氧条件下miR-210的调节以及miR-210对卵巢癌生长的影响是盲目的。在本研究中,我们确定了miR-210在上皮性卵巢癌标本中的表达,以及在缺氧条件下的卵巢癌细胞系中的表达,并详细确定了miR-210过表达对肿瘤细胞增殖的影响,以及miR-210调节肿瘤生长的可能机制。研究表明,在上皮性卵巢癌标本以及上皮性卵巢癌细胞系中,miR-210表达上调,与HIF-1 α过表达相关。此外,上调的miR-210通过靶向PTPN 1和抑制凋亡促进体外肿瘤生长。因此,我们的研究结果揭示了卵巢癌适应缺氧的机制。
miR-210 is upregulated in a HIF-1 alpha-dependent way in several types of cancers. In addition, upregulated miR-210 promotes cancer proliferation, via its anti-apoptotic effects. It is blind to the regulation of miR-210 under hypoxia conditions for ovarian cancer cells and to the effect of miR-210 on ovarian cancer growth. In the present study, we determined the expression of miR-210 in epithelial ovarian cancer specimens, and in ovarian cancer cell lines under hypoxia conditions, and determined in detail the effect of miR-210 overexpression on tumor cell proliferation, and the possible mechanisms of tumor growth by miR-210 regulation. It was shown that miR-210 expression is upregulated, in response to hypoxia conditions in epithelial ovarian cancer specimens as well as epithelial ovarian cancer cell lines, with an association to HIF-1 alpha overexpression. Furthermore, upregulated miR-210 promoted tumor growth in vitro via targeting PTPN1 and inhibiting apoptosis. Therefore, our findings shed light on the mechanism of ovarian cancer adaptation to hypoxia.