M2-like tumour-associated macrophages (TaMs) have been demonstrated to promote the growth of anaplastic thyroid carcinoma (aTc). However, the underlying mechanism of M2-like TaMs in aTc remains unclear. Thus, in the present study, the role and mechanism of M2-like TaMs in aTc were investigated. M2-like TaMs were induced by treatment with PMA, plus IL-4 and IL-13, and identified by flow cytometry. Transwell and sphere formation assays were applied to assess the invasion and stemness of aTc cells. The expression levels of insulin-like growth factor (iGF)-1 and iGF-2 were examined by eliSa and reverse transcription-quantitative Pcr. Proteins related to the epithelial-mesenchymal transition (eMT), stemness and the Pi3K/aKT/mTor pathway were examined via western blotting. immunohistochemistry (iHc) was used to detect the expression of the M2-like TaM markers cd68 and cd206 in aTc tissues and thyroid adenoma tissues. it was found that treatment with PMa plus il-4 and il-13 successfully induced M2-like TaMs. Following co-culture with M2-like TaMs, the invasive ability and stemness of ATC cells were significantly increased. The expression levels of the eMT-related markers n-cadherin and Vimentin, the stemness-related markers oct4, Sox2 and cd133, and the insulin receptor (ir)-a/iGF1 receptor (iGF1r) were markedly upregulated, whereas E-cadherin expression was significantly decreased. in addition, the production of iGF-1 and iGF-2 was significantly increased. Of note, exogenous IGF-1/IGF-2 promoted the invasion and stemness of c643 cells, whereas blocking iGF-1 and iGF-2 inhibited metastasis and stemness by repressing ir-a/iGF-1r-mediated Pi3K/aKT/mTor signalling in the co-culture system. iHc results showed that the expression of cd68 and cd206 was obviously increased in aTc tissues. To conclude, M2-like TaMs accelerated the metastasis and increased the stemness of aTc cells, and the underlying mechanism may be related to the section of iGF by M2-like TaMs, which activates the ir-a/iGF1r-mediated Pi3K/aKT/mTor signalling pathway.