American Association for Cancer Research
00085472can123848-sup-supp_fig_10.pdf (84.07 kB)

Supplementary Figure 10 from HMGA2 Is a Driver of Tumor Metastasis

Download (84.07 kB)
journal contribution
posted on 2023-03-30, 21:29 authored by Asahiro Morishita, M. Raza Zaidi, Akira Mitoro, Devipriya Sankarasharma, Matthias Szabolcs, Yasunori Okada, Jeanine D'Armiento, Kiran Chada

Supplementary Figure 10 - PDF file 84K, HMGA2 mRNA expression in MCF7 and MDA-MB231 human breast cancer cells treated with TGFBeta 1 as detected by qRT-PCR



The non-histone chromatin-binding protein HMGA2 is expressed predominantly in the mesenchyme before its differentiation, but it is also expressed in tumors of epithelial origin. Ectopic expression of HMGA2 in epithelial cells induces epithelial–mesenchymal transition (EMT), which has been implicated in the acquisition of metastatic characters in tumor cells. However, little is known about in vivo modulation of HMGA2 and its effector functions in tumor metastasis. Here, we report that HMGA2 loss of function in a mouse model of cancer reduces tumor multiplicity. HMGA2-positive cells were identified at the invasive front of human and mouse tumors. In addition, in a mouse allograft model, HMGA2 overexpression converted nonmetastatic 4TO7 breast cancer cells to metastatic cells that homed specifically to liver. Interestingly, expression of HMGA2 enhanced TGFβ signaling by activating expression of the TGFβ type II receptor, which also localized to the invasive front of tumors. Together our results argued that HMGA2 plays a critical role in EMT by activating the TGFβ signaling pathway, thereby inducing invasion and metastasis of human epithelial cancers. Cancer Res; 73(14); 4289–99. ©2013 AACR.

Usage metrics

    Cancer Research



    Ref. manager