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首页> 外文期刊>Pathobiology: journal of immunopathology, molecular and cellular biology >Hypoxia Induces Tumor Aggressiveness and the Expansion of CD133-Positive Cells in a Hypoxia-Inducible Factor-1alpha-Dependent Manner in Pancreatic Cancer Cells.
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Hypoxia Induces Tumor Aggressiveness and the Expansion of CD133-Positive Cells in a Hypoxia-Inducible Factor-1alpha-Dependent Manner in Pancreatic Cancer Cells.

机译：低氧诱导胰腺癌细胞低氧诱导因子-1α依赖性的肿瘤侵袭性和CD133阳性细胞的扩张。

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Background: Intratumoral hypoxia is known to lead to increased aggressiveness and distant metastasis. However, the interplay underlying these actions is still unknown. Objective: We explored whether cancer cells might acquire a stem-like phenotype under hypoxia, consequently leading to an aggressive phenotype, including invasiveness and metastasis. Methods: Under normoxia (20% O(2)) or hypoxia (1% O(2)), the expression of CD133 (cancer stem cell marker), CXC chemokine receptor 4 (CXCR4) and hypoxia-inducible factor-1alpha (HIF-1alpha) was examined by RT-PCR and immunostaining using human pancreatic cancer cell lines. We also examined if hypoxia facilitates the invasiveness of CD133+ cancer cells. Furthermore, we transfected dominant active HIF-1alpha (HIF-1alphaDeltaODD) by the retroviral gene transfer and examined the effects both in vitro and in vivo. Results: Compared with normoxia, hypoxia elevated the expression of CD133, CXCR4 and HIF-1alpha. Moreover, hypoxia facilitated the invasiveness of CD133+ pancreatic cancer cells. The behavior of HIF-1alphaDeltaODD-transfected cells under normoxia was compatible with that of the parent cells under hypoxia. Furthermore, a xenograft model of HIF-1alphaDeltaODD cells showed aggressiveness, including metastasis and highly tumorigenic ability. Conclusion: Hypoxia induces tumor aggressiveness associated with the expansion of CD133+ pancreatic cancer cells in a predominantly HIF-1alpha-dependent manner.
机译：背景：已知肿瘤内缺氧会导致侵略性增加和远处转移。但是，这些动作之间的相互作用仍然是未知的。目的：我们探讨了缺氧条件下癌细胞是否可能获得干样表型，从而导致侵袭性表型，包括侵袭性和转移性。方法：在常氧（20％O（2））或低氧（1％O（2））下，CD133（癌症干细胞标记），CXC趋化因子受体4（CXCR4）和低氧诱导因子-1α（HIF）的表达使用人胰腺癌细胞系通过RT-PCR和免疫染色检查了-1alpha）。我们还检查了缺氧是否促进了CD133 +癌细胞的侵袭性。此外，我们通过逆转录病毒基因转染了显性活跃的HIF-1alpha（HIF-1alphaDeltaODD），并在体内和体外检查了这种作用。结果：与正常氧相比，低氧使CD133，CXCR4和HIF-1α的表达升高。此外，低氧促进了CD133 +胰腺癌细胞的侵袭性。在常氧下转染HIF-1alphaDeltaODD的细胞的行为与在低氧下的亲本细胞的行为相容。此外，HIF-1alphaDeltaODD细胞的异种移植模型显示出侵袭性，包括转移和高度致瘤能力。结论：低氧主要通过HIF-1α依赖性方式诱导与CD133 +胰腺癌细胞的扩张相关的肿瘤侵袭性。

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