INSERM, U1065, Centre Méditerranéen de Médecine Moléculaire (C3M), Team 4, Inflammation, Cancer, Cellules Souches Cancéreuses, Nice, France.
Cancer Lett. 2013 Jun 1;333(1):76-88. doi: 10.1016/j.canlet.2013.01.020. Epub 2013 Jan 21.
The membrane-bound carbonic anhydrase isoforms CAIX and CAXII, underpin a pH-regulating system that enables hypoxic tumor cell survival. Here, we observed for the first time an upregulation of CAXII in T-cell acute lymphoblastic leukemia/lymphoma (T-ALL/LL) cells. First we showed that CAXII is overexpressed in thymocytes from tPTEN-/- mice suffering of T lymphoma and that its pharmacological inhibition decreased cell proliferation and induced apoptosis. The same results were observed with the SupT1 human T cell lymphoma line. In addition we observed an upregulation of CAXII in human T-ALL samples supporting the case that CAXII may represent a new therapeutic target for T-ALL/LL.
膜结合碳酸酐酶同工型 CAIX 和 CAXII 构成了一个 pH 调节系统，使缺氧肿瘤细胞能够存活。在这里，我们首次观察到 T 细胞急性淋巴细胞白血病/淋巴瘤（T-ALL/LL）细胞中 CAXII 的上调。首先，我们表明在患有 T 淋巴瘤的 tPTEN-/- 小鼠的胸腺细胞中过表达 CAXII，并且其药理学抑制降低了细胞增殖并诱导了细胞凋亡。人 T 细胞淋巴瘤系 SupT1 也观察到了相同的结果。此外，我们观察到人类 T-ALL 样本中 CAXII 的上调，这支持 CAXII 可能代表 T-ALL/LL 的新治疗靶点的情况。
