Modification of survival pathway gene expression in human breast cancer cells by tetraiodothyroacetic acid (tetrac)

Integrin-Mediated Actions of Thyroid Hormone Analogues on Tumor Cell Chemosensitivity, Integrin-Growth Factor Receptor Crosstalk and Inflammatory Gene Expression

“…Nanotetrac also downregulated expression of the chemokine CX3CL1 (fractalkine). We also know that nanoparticulate tetrac decreases expression of the epidermal growth factor receptor (EGFR) gene (Glinskii et al, 2009). EGFR engages in crosstalk with other signaling pathways involved in inflammation.…”

“…This desirable effect of tetrac and nanotetrac in the setting of experimental tumor growth is enhanced by other blood vessel-relevant activities of tetrac. Acting via the plasma membrane integrin, for example, tetrac formulations can induce expression of the thrombospondin 1 (TBSP1, TSP1) gene (Glinskii et al, 2009) that is almost invariably suppressed in cancer cells. The TBSP1 protein is an endogenous anti-angiogenic protein.…”

BCL2L14 (BCL2-like 14 (apoptosis facilitator))

“…A genome-wide RNAi screen has recently shown that BCL2L14 silencing in SKBR-3 results in resistance to the novel pan-ErbB inhibitor, neratinib (Seyhan et al, 2012). BCL2L14 has also been implicated in the anti-survival effects of nanoparticulate tetraiodothyroacetic acid on MDA-MB-231 cells (Glinskii et al, 2009). As regards genes involved in the post-translational modification of Bcl-G, FAU expression is downregulated and MELK expression is up-regulated in breast tumour tissue (Pickard et al, 2009).…”

“…BCL2L14 is itself a target gene for the apoptosis master regulator p53 (Miled et al, 2005), and it is one of a subset of proapoptotic genes whose expression is hyperactivated in response to interferon-α and -γ co-treatment of hepatoma cells (Zhang et al, 2006). Its expression is also increased in mammalian cells following exposure to a diverse range of apoptotic stimuli (including chemotherapeutic agents) such as: gamma-radiation therapy (Finnberg et al, 2008), UV-C irradiation (Pickard et al, 2011), arsenic trioxide (Galimberti et al, 2012), nanoparticulate tetraiodothyroacetic acid (Glinskii et al, 2009), etoposide and cisplatin (Benito et al, 2006). Mutations in pancreatic/duodenum homeobox protein 1 (PDX1) can result in human type 2 diabetes.…”

Radiosensitization and production of DNA double-strand breaks in U87MG brain tumor cells induced by tetraiodothyroacetic acid (tetrac)

“…10 It should also be noted that in the absence of T 4 and T 3 , tetrac can suppress angiogenesis promoted by vascular growth factors 6 and can also disable cancer cell survival gene expression. 11 As in the case of mouse glioma cells, 1 tetrac acts via αvβ3 integrin to inhibit proliferation in vitro of human glioblastoma U87MG cells. 9 Other investigators have described the presence of The LQ parameters for control cells were α = 0.225 (±0.023) and β = 0.016 (±0.002).…”